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Long-term exposure to amiodarone, an antiarrhythmic drug, can induce different organ damage, including liver. Cell damage included by amiodarone is a consequence of mitochondrial damage, reactive oxygen species production, and cell energy depletion leading to programmed cell death. In the present study, hepatoprotective potential of neurohormone melatonin (50 mg/kg/day) was evaluated in a chronic experimental model of liver damage induced by a 4-week application of amiodarone (70 mg/kg/day). The obtained results indicate that amiodarone induces an increase in xanthine oxidase activity, as well as the content of the lipid and protein oxidatively modified products and p53 levels. Microscopic analysis further corroborated the biochemical findings revealing hepatocyte degeneration, apoptosis, and occasional necrosis, with the activation of Kupffer cells. Coadministration of melatonin and amiodaron prevented an increase in certain damage associated parameters, due to its multiple targets. In conclusion, the application of melatonin together with amiodarone prevented an increase in tissue oxidative damage parameters and moderately prevented liver cell apoptosis, indicating that the damage of hepatocytes provoked by amiodarone supersedes the protective properties of melatonin in a given dose. [ABSTRACT FROM AUTHOR]

Polymer microgels are smart materials used to fabricate and encapsulate different enzymes. Encapsulation of enzymes in the polymer gel particles prolong their life span, enhance and tune their activity in biomedical field to prevent cell damage and make possible tunable drug delivery. Enzymes are natural catalysts and have prodigious ability to make the reaction kinetically feasible. Enzymes encapsulated polymer microgels gained much attention due to their synergistic properties. Here, different methods adopted for the synthesis of enzyme encapsulated polymer microgels, their properties, and classification based on responsive behavior have been described in detail. Applications of these enzyme encapsulated polymer microgels in sensing, catalysis, environmental remediation, useful product formation, and biomedical field to prevent disabilities have also been elaborated with future directions. [ABSTRACT FROM AUTHOR]

Differential host responses in coronavirus disease 2019 (COVID-19) and multisystem inflammatory syndrome in children (MIS-C) remain poorly characterized. Here, we use next-generation sequencing to longitudinally analyze blood samples from pediatric patients with COVID-19 or MIS-C across three hospitals. Profiling of plasma cell-free nucleic acids uncovers distinct signatures of cell injury and death between COVID-19 and MIS-C, with increased multiorgan involvement in MIS-C encompassing diverse cell types, including endothelial and neuronal cells, and an enrichment of pyroptosis-related genes. Whole-blood RNA profiling reveals upregulation of similar pro-inflammatory pathways in COVID-19 and MIS-C but also MIS-C-specific downregulation of T cell-associated pathways. Profiling of plasma cell-free RNA and whole-blood RNA in paired samples yields different but complementary signatures for each disease state. Our work provides a systems-level view of immune responses and tissue damage in COVID-19 and MIS-C and informs future development of new disease biomarkers.

Microplastics (MPs) accumulate in tissues, including kidney tissue, while Bisphenol A (BPA) is a plasticizer of particular concern. At present, the combined effects of MPs and BPA are unexplored in human renal cells. Therefore, we exposed a proximal tubular cell line (PTECs) to polyethylene (PE)-MPs and BPA, both separately and in combination. When co-exposed, cells showed a significantly reduced cell viability (MTT test) and a pronounced pro-oxidant (MDA levels, NRF2 and NOX4 expression by Western blot) and pro-inflammatory response (IL1β, CCL/CCR2 and CCL/CCR5 mRNAs by RT-PCR), compared to those treated with a single compound. In addition, heat shock protein (HSP90), a chaperone involved in multiple cellular functions, was reduced (by Western Blot and immunocytochemistry), while aryl hydrocarbon receptor (AHR) expression, a transcription factor which binds environmental ligands, was increased (RT-PCR and immunofluorescence). Our research can contribute to the study of the nephrotoxic effects of pollutants and MPs and shed new light on the combined effects of BPA and PE-MPs.

A comprehensive knowledge of the physical and chemical properties of nanomaterials (NMs) is necessary to design them effectively for regulated use. Although NMs are utilized in therapeutics, their cytotoxicity has attracted great attention. Nanoscale quantitative structure–property relationship (nano-QSPR) models can help in understanding the relationship between NMs and the biological environment and provide new ways for modeling the structural properties and bio-toxic effects of NMs. The goal of the study is to construct fully validated property-based models to extract relevant features for estimating and influencing the zeta potential and obtaining the toxicity profile regarding cell damage in the treatment of cancer cells. To achieve this, QSPR modeling was first performed with 18 metal oxide (MeOx) NMs to measure their materials properties using periodic table-based descriptors. The features obtained were later applied for zeta potential calculation (imputation for sparse data) for MeOx NMs that lack such information. To further clarify the influence of the zeta potential on cell damage, a QSPR model was developed with 132 MeOx NMs to understand the possible mechanisms of cell damage. The results showed that zeta potential, along with seven other descriptors, had the potential to influence oxidative damage through free radical accumulation, which could lead to changes in the survival rate of cancerous cells. The developed QSPR and quantitative structure–activity relationship models also give hints regarding safer design and toxicity assessment of MeOx NMs.

In order to explore the effects of basigin (BSG) on the mitogen activated protein kinase (MAPK) signaling pathway and apoptosis in Qinchuan cattle muscle during postmortem maturation, the changes in BSG and related differentially expressed proteins were analyzed by 4D-label free quantification (4D-LFQ). The BSG inhibitor tunicamycin was injected into the longissimus dorsi of Qinchuan cattle after slaughter, and the expression levels of key proteins in the MAPK signaling pathway during storage at 4 ℃ were determined by Western blotting. An apoptosis detection kit was used to determine the change in the activity of caspase-3. The results showed that the expression of BSG increased first and then decreased during the postmortem storage period of Qinchuan cattle muscle. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, it was found that BSG and related differentially expressed proteins were significantly annotated to the oxidative phosphorylation pathway, calcium signal pathway and MAPK signaling pathway, indicating that BSG played an important role through the MAPK signaling pathway. In addition, for the tunicamycin group, the relative expression of the key proteins in the MAPK signaling pathway was significantly down-regulated, indicating that BSG inactivated the MAPK signaling pathway. This finding lays a good foundation for exploring the effect of BSG on the MAPK signaling pathway. After inhibiting BSG expression, caspase-3 activity in the tunicamycin group increased significantly, indicating that apoptosis was an important link in cell injury mechanism, and tunicamycin acted on the N-terminal structure of BSG to deglycosylate the protein and inhibited the folding of intracellular proteins and consequently their biological activity, thereby inducing cell apoptosis.

Simple Summary: The threat posed by microplastic toxicity to organisms is growing substantially, and the ramifications of daily microplastic usage cannot be disregarded. The extent of toxicological research pertaining to microplastics has increased due to the grave and alarming nature of microplastic pollution. We have, therefore, conducted research in an effort to determine the toxicological impact of microplastics on the cellular and genetic levels. The toxicity of accumulated polyethylene terephthalate microplastics on Drosophila melanogaster has been determined by our research. At higher concentrations of microplastics, cellular and reproductive toxicities have been observed, which correspond to elevated oxidative stress, identified through the analyses of various oxidative stress markers' activities. Furthermore, the levels of heat shock proteins have been identified, contributing to the understanding of the primary defense mechanism against the toxicity of microplastics. The study has provided significant and concerning insights into the escalating health risks posed by microplastics. It appears that microplastics are inducing genetic alterations; therefore, further investigation should be undertaken at the genetic level to clarify the potential transgenerational consequences that pose a significant risk to future generations. Microplastics and nanoplastics are abundant in the environment. Further research is necessary to examine the consequences of microplastic contamination on living species, given its widespread presence. In our research, we determined the toxic effects of PET microplastics on Drosophila melanogaster at the cellular and genetic levels. Our study revealed severe cytotoxicity in the midgut of larvae and the induction of oxidative stress after 24 and 48 h of treatment, as indicated by the total protein, Cu-Zn SOD, CAT, and MDA contents. For the first time, cell damage in the reproductive parts of the ovaries of female flies, as well as in the accessory glands and testes of male flies, has been observed. Furthermore, a decline in reproductive health was noted, resulting in decreased fertility among the flies. By analyzing stress-related genes such as hsp83, hsp70, hsp60, and hsp26, we detected elevated expression of hsp83 and hsp70. Our study identified hsp83 as a specific biomarker for detecting early redox changes in cells caused by PET microplastics in all the treated groups, helping to elucidate the primary defense mechanism against PET microplastic toxicity. This study offers foundational insights into the emerging environmental threats posed by microplastics, revealing discernible alterations at the genetic level. [ABSTRACT FROM AUTHOR]

Summary: The study aimed to assess the in vitro antibacterial effect of thymol (Thy) in conjunction with ultrasound (US) on Shewanella putrefaciens (S. putrefaciens). The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of Thy against S. putrefaciens were 0.50 and 1.00 mg mL−1, respectively. US was found to augment the antibacterial efficacy of Thy, resulting in a significant reduction of 2.36 log CFU mL−1 in the total colony count of S. putrefaciens, ensuring that the bacterial population maintained a consistently low growth rate. Quantitative detection of crystal violet revealed that the combined treatment exhibited a pronounced inhibitory effect on biofilm formation, with a clearance rate of mature biofilms reaching 91.60%. Alkaline phosphatase (AKPase), lactate dehydrogenase (LDHase), UV absorbing substance permeability, and other indicators were employed to measure changes in the bacterial cell membrane and internal environment. Scanning electron microscopy (SEM) was further used to observe the bacteria morphology before and after treated by US and Thy, a notable collapse of bacterial cells was observed, accompanied by ruptured outer membranes, damaged cell walls, and extensive leakage of cellular contents. This study presents a novel approach for controlling bacterial growth in food preservation methods. [ABSTRACT FROM AUTHOR]

Hexavalent chromium (Cr6+) is one of the stable oxidation states of chromium that has been reported to elicit various toxic effects in aquatic organisms. However, the mechanisms of Cr6+ toxicity are still poorly understood. Thus, the present study investigated the tissue accumulation, cytotoxic, oxidative stress, and immunotoxic effects of Cr6+ in juvenile Clarias gariepinus. The fish were exposed to waterborne Cr6+ concentrations (0, 0.42, 0.84, and 1.68 mg/L) for 28 days, after which they were sacrificed and various organs were harvested for the determination of Cr6+ levels. Other parameters that were indicators of oxidative stress, cytotoxicity, and immunotoxicity were measured. Cr6+ accumulated more in the kidney and liver of the exposed fish, especially at the highest concentration. The levels of lipid peroxidation and DNA fragmentation increased significantly in the exposed fish. The activities of superoxide dismutase and lactate dehydrogenase increased significantly in exposed fish compared to the control. The total white blood cells, lymphocytes, and neutrophils counts were significantly higher in the exposed fish compared to the control fish. The respiratory burst activity decreased significantly in the exposed fish while the myeloperoxidase content did not differ significantly. There were upregulations of TNF-α and HSP 70 while CYP II and MHC 2 were downregulated in the exposed fish. Also, exposure to Cr6+ resulted in various histopathological alterations in the architecture of the head kidney. The results indicate concentration-dependent toxic effects of Cr6+ in C. gariepinus. The study reveals the potentials of Cr6+ to accumulate in the different tissues of fish and caused cytotoxic, oxidative stress, and immunotoxic effects in the exposed fish. [ABSTRACT FROM AUTHOR]

Damage-associated molecular patterns (DAMPs) are endogenous danger molecules produced in cellular damage or stress, and they can activate the innate immune system. DAMPs contain multiple types of molecules, including nucleic acids, proteins, ions, glycans, and metabolites. Although these endogenous molecules do not trigger immune response under steady-state condition, they may undergo changes in distribution, physical or chemical property, or concentration upon cellular damage or stress, and then they become DAMPs that can be sensed by innate immune receptors to induce inflammatory response. Thus, DAMPs play an important role in inflammation and inflammatory diseases. In this review, we summarize the conversion of homeostatic molecules into DAMPs; the diverse nature and classification, cellular origin, and sensing of DAMPs; and their role in inflammation and related diseases. Furthermore, we discuss the clinical strategies to treat DAMP-associated diseases via targeting DAMP-sensing receptors. DAMPs represent important mediators in inflammation and inflammatory disease. Zhou et al. summarize the conversion route, classification, cellular origin, and sensing of DAMPs and their role in diseases. The strategies to treat inflammatory diseases via targeting DAMP-sensing receptors are also introduced. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Food Science & Biotechnology is the property of Journal of Food Science & Biotechnology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effects of casticin (CAS) on lipopolysaccharide-induced injury of human normal lung epithelial cells (BEAS-2B) and NF-κB-Keap1-Nrf2/ARE pathway. Methods: BEAS-2B cells were pretreated with different concentrations of casticin for 1 h, 2 h and 4 h, and then treated with 1 µg/ml liposolysaccharide to construct cell damage model. The contents of inflammatory factors in cell supernatant was detected by ELISA to screen the optimal concentration and time of casticin. The cells were divided into normal group, model group, Casticin group, ML385 group, Casticin+ML385 group and dexamethasone group. Cell apoptosis was detected by flow cytometry, the concentrations of inflammatory factors were detected by ELISA, and the levels of NF-κB p65, p-NF-κB p65, Keapl, Nrf2 and Nrf2 protein in cell nucleus were detected by Western blot. Results: The optimal concentration of CAS was 10 µmol/L and the optimal time was 2 h. Compared with normal group, the apoptosis rate, the contents of inflammatory factors, p-NF-κB p65 and Keap1 protein expression levels in model group were significantly increased (P<0.01), and Nrf2 protein expression levels in cells and nuclei were significantly decreased (P<0.01). Compared with model group, apoptosis rate and contents of inflammatory factors in casticin group and dexamethasone group were significantly decreased (P<0.01), protein expression levels of p-NF-κB p65 and Keap1 in Casticin group were significantly decreased (P<0.01). The expression level of Nrf2 protein in cells and nuclei was significantly increased (P<0.01). Compared with ML385 group, apoptosis rate, inflammatory factors contents, p-NF-κB p65 and Keap1 protein expression levels in Casticin+ML385 group were significantly decreased (P<0.01), the expression level of Nrf2 protein in cells and nuclei were significantly increased (P<0.01). Conclusion: CAS can inhibit cell inflammation induced by lipo-polysaccharide by regulating NF-κB-Keap1-Nrf2/ARE signaling pathway. [ABSTRACT FROM AUTHOR]

Recently, there has been an increasing demand for medicinal plants to control diseases for good health and well-being, as primary health facilities are inadequate in certain populations to cure infections. Since synthetic medicines are toxic to humans and other animals, the present research is thus focused on using traditional medicine for treating various ailments as they are harmless. Based on the above facts, the current study was conducted to assay the antimicrobial, anti-diabetic, anti-cholinesterase, anti-oxidant, anti-quorum sensing, and anti-antibiotic resistance modifying effect of extracts of Cyperus esculentus. This study found 37 and 30 chemicals in butanol and dichloromethane (DCM) extracts using a gas chromatograph mass spectrophotometer (GC-MS). Most active compounds identified were benzofuran, 2,3-dihydro-, 1,2,3-benzenetriol, 3-bornanone, oxime and oleic acid by extracts of butanol whereas dichloromethane extracted three major active compounds (2,3-dihydro-3,5-dihydroxy-, 4H-pyran-4-one 3-deoxy-d-mannoic lactone and 5-hydroxymethylfurfural). Both dichloromethane and butanol extracts showed the highest antimicrobial activity. Compared to aqueous extracts, dichloromethane, and butanol showed excellent anti-diabetic anti-cholinesterase activities and inhibited virulence factors regulated by quorum sensing (QS). Anti-oxidants increased in solvent extracts (DCM and butanol) compared to aqueous extracts. Results of scanning electron microscope (SEM) and Fourier Transmission Infrared (FTIR) indicated damage to the cell membrane of S. aureus by the formation of pits and breakage in functional groups exposed to the extracts of butanol and dichloromethane compared to aqueous extracts. The above results confirmed that C. esculentus can be an alternative medicine for treating diseases.

Abstract Applying extracts from plants is considered a safe approach in biomedicine and bio-nanotechnology. The present report is considered the first study that evaluated the seeds of Lasiurus scindicus and Panicum turgidum as biogenic agents in the synthesis of silver nanoparticles (AgNPs) which had bioactivity against cancer cells and bacteria. Assessment of NPs activity against varied cell lines (colorectal cancer HCT116 and breast cancer MDA MBA 231 and MCF 10A used as control) was performed beside the antibacterial efficiency. Different techniques (DLS, TEM, EDX and FTIR) were applied to characterize the biosynthesized AgNPs. The phytochemicals from both L. scindicus and Panicum turgidum were identified by GC–MS analysis. Spherical monodisperse NPs at average diameters of 149.6 and 100.4 nm were obtained from seed extract of L. scindicus (L-AgNPs) and P. turgidum, (P-AgNPs) respectively. A strong absorption peak at 3 keV is observed by the EDX spectrum in the tested NPs. Our study provided effective NPs in mitigating the tested cell lines and the lowest IC50 were 7.8 and 10.30 for MDA MB231 treated by L-AgNPs and P-AgNPs, respectively. Both fabricated NPs might differentially target the MDA MB231 cells compared to HCT116 and MCF10A. Ultrastructural changes and damage for the NPs-treated MDA MB231 cells were studied using TEM and LSM analysis. Antibacterial activity was also observed. About 200 compounds were identified in L. scindicus and P. turgidum by GC–MS analysis might be responsible for the NPs reduction and capping abilities. Efficient NPs against cancer cells and microbes were obtained, however large-scale screening is needed to validate our findings.

Da Ke,1 Jian Ni,1 Yuan Yuan,1 Mingzhen Cao,1 Si Chen,2 Heng Zhou1 1Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, People’s Republic of China; 2Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, 430060, People’s Republic of ChinaCorrespondence: Heng Zhou, Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, People’s Republic of China, Email hengzhou@whu.edu.cnPurpose: Studies have shown that neutrophil-mediated formation of neutrophil extracellular traps (NETs) leads to increased inflammatory response and cellular tissue damage during myocardial infarction (MI). We aimed to identify and validate possible hub genes in the process of NETs-mediated cell damage.Methods: We performed an immune cell infiltration analysis of the MI transcriptome dataset based on CIBERSORT and ssGSEA algorithms. Gene expression profiles of NETs formation (GSE178883) were used to analyze the physiological processes of peripheral blood neutrophils after phorbol myristate acetate (PMA) stimulation. Bioinformatics and machine learning algorithms were utilized to find candidate hub genes based on NETs-related genes and transcriptome datasets (GSE66360 and GSE179828). We generated the receiver operating curve (ROC) to evaluate the diagnostic value of hub genes. Next, the correlation between hub genes and immune cells was analyzed using CIBERSORT, ssGSEA and xCell algorithms. Finally, we used quantitative real-time PCR (qRT-PCR) and immunohistochemistry to verify gene expression.Results: Immune cell infiltration analysis revealed that inflammatory cells such as neutrophils were highly expressed in the peripheral blood of patients with MI. Functional analysis of differentially expressed genes (DEGs) in GSE178883 indicated that the potential pathogenesis lies in immune terms. Using weighted gene co-expression network analysis (WGCNA) and machine learning algorithms, we finally identified the seven hub genes (FCAR, IL1B, MMP9, NFIL3, CXCL2, ICAM1, and ZFP36). The qRT-PCR results showed that IL-1B, MMP9, and NFIL3 mRNA expression was up-regulated in the MI group compared to the control. Immunohistochemical results showed high MMP9, IL-1B, and NFIL3 expression in the infarcted area compared to the non-infarcted area and sham-operated groups.Conclusion: We identified seven hub genes associated with NETs-mediated cellular damage during MI. Our results may provide insights into the mechanisms of neutrophil-mediated cell injury during MI. Keywords: myocardial infarction, neutrophils, cell damage, neutrophil extracellular traps, bioinformatics, endothelial cells

Living Donor Liver Transplantation (LDLT) is a promising approach to treating end-stage liver diseases, however, some post-operatory complications such as pneumonia, bacteremia, urinary tract infections, and hepatic dysfunction have been reported. In murine models using partial hepatectomy (PHx), a model that emulates LDLT, it has been determined that the synthesis of hepatic cell proliferation factors that are associated with noradrenaline synthesis are produced in locus coeruleus (LC). In addition, studies have shown that PHx decreases GABA and 5-HT2A receptors, promotes loss of dendritic spines, and favors microgliosis in rat hippocampus. The GABA and serotonin-altered circuits suggest that catecholaminergic neurons such as dopamine and noradrenaline neurons, which are highly susceptible to cellular stress, can also be damaged. To understand post-transplant affections and to perform well-controlled studies it is necessary to know the potential causes that explain as a liver surgical procedure can produce brain damage. In this paper, we review several cellular processes that could induce gliosis in LC after rat PHx.

Applying extracts from plants is considered a safe approach in biomedicine and bio-nanotechnology. The present report is considered the first study that evaluated the seeds of Lasiurus scindicus and Panicum turgidum as biogenic agents in the synthesis of silver nanoparticles (AgNPs) which had bioactivity against cancer cells and bacteria. Assessment of NPs activity against varied cell lines (colorectal cancer HCT116 and breast cancer MDA MBA 231 and MCF 10A used as control) was performed beside the antibacterial efficiency. Different techniques (DLS, TEM, EDX and FTIR) were applied to characterize the biosynthesized AgNPs. The phytochemicals from both L. scindicus and Panicum turgidum were identified by GC–MS analysis. Spherical monodisperse NPs at average diameters of 149.6 and 100.4 nm were obtained from seed extract of L. scindicus (L-AgNPs) and P. turgidum, (P-AgNPs) respectively. A strong absorption peak at 3 keV is observed by the EDX spectrum in the tested NPs. Our study provided effective NPs in mitigating the tested cell lines and the lowest IC50 were 7.8 and 10.30 for MDA MB231 treated by L-AgNPs and P-AgNPs, respectively. Both fabricated NPs might differentially target the MDA MB231 cells compared to HCT116 and MCF10A. Ultrastructural changes and damage for the NPs-treated MDA MB231 cells were studied using TEM and LSM analysis. Antibacterial activity was also observed. About 200 compounds were identified in L. scindicus and P. turgidum by GC–MS analysis might be responsible for the NPs reduction and capping abilities. Efficient NPs against cancer cells and microbes were obtained, however large-scale screening is needed to validate our findings. [ABSTRACT FROM AUTHOR]

The ciliate Climacostomum virens produces the metabolite climacostol that displays antimicrobial activity and cytotoxicity on human and rodent tumor cells. Given its potential as a backbone in pharmacological studies, we used the fruit fly Drosophila melanogaster to evaluate how the xenobiotic climacostol affects biological systems in vivo at the organismal level. Food administration with climacostol demonstrated its harmful role during larvae developmental stages but not pupation. The midgut of eclosed larvae showed apoptosis and increased generation of reactive oxygen species (ROS), thus demonstrating gastrointestinal toxicity. Climacostol did not affect enteroendocrine cell proliferation, suggesting moderate damage that does not initiate the repairing program. The fact that climacostol increased brain ROS and inhibited the proliferation of neural cells revealed a systemic (neurotoxic) role of this harmful substance. In this line, we found lower expression of relevant antioxidant enzymes in the larvae and impaired mitochondrial activity. Adult offsprings presented no major alterations in survival and mobility, as well the absence of abnormal phenotypes. However, mitochondrial activity and oviposition behavior was somewhat affected, indicating the chronic toxicity of climacostol, which continues moderately until adult stages. These results revealed for the first time the detrimental role of ingested climacostol in a non-target multicellular organism. [ABSTRACT FROM AUTHOR]

Living Donor Liver Transplantation (LDLT) is a promising approach to treating end-stage liver diseases, however, some post-operatory complications such as pneumonia, bacteremia, urinary tract infections, and hepatic dysfunction have been reported. In murine models using partial hepatectomy (PHx), a model that emulates LDLT, it has been determined that the synthesis of hepatic cell proliferation factors that are associated with noradrenaline synthesis are produced in locus coeruleus (LC). In addition, studies have shown that PHx decreases GABA and 5-HT2A receptors, promotes loss of dendritic spines, and favors microgliosis in rat hippocampus. The GABA and serotonin-altered circuits suggest that catecholaminergic neurons such as dopamine and noradrenaline neurons, which are highly susceptible to cellular stress, can also be damaged. To understand post-transplant affections and to perform well-controlled studies it is necessary to know the potential causes that explain as a liver surgical procedure can produce brain damage. In this paper, we review several cellular processes that could induce gliosis in LC after rat PHx. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the protective effect of probucol on Müller cells exposed to high glucose conditions and examined potential mechanisms of action. Methods: Primary human retinal Müller cells were incubated with high glucose (HG, 35 mM) in the present or absence of different concentrations of probucol for 24 h. Cell viability was determined using the CCK-8 method. Mitochondrial membrane potential (MMP) was measured using JC-1 staining and cell cycle by flow cytometry. The expression of nuclear factor E2-related factor 2 (Nrf2), glutamate–cysteine ligase catalytic subunit, and p62 was quantified using quantitative polymerase chain reaction and western blot. Results: We found that HG inhibited cell proliferation, arrested cell cycle, and increased MMP in human Müller cells. Probucol activated the Nrf2/p62 pathway and upregulated the anti-apoptotic protein, Bcl2, and attenuated HG-mediated damage in Müller cells. Conclusions: Our results suggest that probucol may protect Müller cells from HG-induced damage through enhancing the Nrf2/p62 signaling pathway. [ABSTRACT FROM AUTHOR]

Spot blotch (caused by Bipolaris sorokiniana) is one of the main diseases of barley. In this study we evaluated the effect of silicon (Si) combined with the preventive application of a fungicide on the biochemical defense against spot blotch. For this purpose, we evaluated the activity of antioxidant system enzymes, accumulation of total soluble phenolics (TSPs), the lignin derivatives thioglycolic acid (DLTGA), and their influence in the host membrane damage by determining the electrolyte leakage (EL). Two barley cultivars, AnaG01 and BRS Cauê, both susceptible, were grown in soil not supplied (-Si) or supplied (+ Si) with Si and treated with the fungicide 7 or 15 days before inoculation (dbi). The highest disease severity (up to 29%) was observed for the -Si plants not treated with fungicide. Plants supplied with Si showed lower disease intensity due to an increase in the activity of SOD and reduction in CAT, which may have favored the hydrogen peroxide accumulation as well as increases in the TSP and DLTGA concentrations. The best disease control was achieved by combining Si in the soil and fungicide spray, especially when application occurred at 7 dbi. Furthermore, this combination increased the control at 15 dbi compared to -Si plants, indicating that defense mechanisms enhanced by Si may have favored the fungicidal control at the end of the protective period, reducing the disease intensity. In conclusion, the results of this study showed that Si supply to barley plants promoted the activation of biochemical mechanisms related to the plants' defense, enhancing the control of spot blotch severity by the fungicide. [ABSTRACT FROM AUTHOR]

Fractal analysis (FA) is a contemporary computational technique that can assist in identifying and assessing nuanced structural alterations in cells and tissues after exposure to certain toxic chemical agents. Its application in toxicology may be particularly valuable for quantifying structural changes in cell nuclei during conventional microscopy assessments. In recent years, the fractal dimension and lacunarity of cell nuclei, considered among the most significant FA features, have been suggested as potentially important indicators of cell damage and death. In this study, we demonstrate the feasibility of developing a random forest machine learning model that employs fractal indicators as input data to identify yeast cells treated with oxidopamine (6-hydroxydopamine, 6-OHDA), a powerful toxin commonly applied in neuroscience research. The model achieves notable classification accuracy and discriminatory power, with an area under the receiver operating characteristics curve of more than 0.8. Moreover, it surpasses alternative decision tree models, such as the gradient-boosting classifier, in differentiating treated cells from their intact counterparts. Despite the methodological challenges associated with fractal analysis and random forest training, this approach offers a promising avenue for the continued exploration of machine learning applications in cellular physiology, pathology, and toxicology. [ABSTRACT FROM AUTHOR]

Antibiotic resistance is one of the biggest public health problems of our time. The nanoparticles are a powerful alternative to these antibiotics. Engineered nanoparticles show toxic effects on bacteria by different mechanisms. The bacteria–cell interaction of engineered nanoparticles exerts their toxic effects through changes in cell wall, cell membrane, and cytoplasm content/density. Thus, death occurs as a result of cell deformation. In this study, the cellular damage of silver nanoparticles, which are known to have strong antibacterial properties, and zirconium oxide and silicon oxide engineering nanoparticles, which are less known, on periodontopathic (Prevotella intermedia and Aggregatibacter actinomycetemcomitans) bacteria, were investigated by ultrastructural changes. The lysis of the cytoplasm and separation of the membrane cytoplasm were observed. Both types of bacteria treated with Ag ENP show more hollow cytoplasm than bacteria treated with the other two nanoparticles. [ABSTRACT FROM AUTHOR]

Direct current (DC) electrical stimulation has been shown to have remarkable effects on regulating cell behaviors. Translation of this technology to clinical uses, however, has to overcome several obstacles, including Joule heat production, changes in pH and ion concentration, and electrode products that are detrimental to cells. Application of DC voltages in thick tissues where their thickness is >0.8 mm caused significant changes in temperature, pH, and ion concentrations. In this study, we developed a multifield and -chamber electrotaxis chip, and various stimulation schemes to determine effective and safe stimulation strategies to guide the migration of human vascular endothelial cells. The electrotaxis chip with a chamber thickness of 1 mm allows 10 voltages applied in one experiment. DC electric fields caused detrimental effects on cells in a 1 mm chamber that mimicking 3D tissue with a decrease in cell migration speed and an increase in necrosis and apoptosis. Using the chip, we were able to select optimal stimulation schemes that were effective in guiding cells with minimal detrimental effects. This experimental system can be used to determine optimal electrical stimulation schemes for cell migration, survival with minimal detrimental effects on cells, which will facilitate to bring electrical stimulation for in vivo use.

Microplastics and nanoplastics are abundant in the environment. Further research is necessary to examine the consequences of microplastic contamination on living species, given its widespread presence. In our research, we determined the toxic effects of PET microplastics on Drosophila melanogaster at the cellular and genetic levels. Our study revealed severe cytotoxicity in the midgut of larvae and the induction of oxidative stress after 24 and 48 h of treatment, as indicated by the total protein, Cu-Zn SOD, CAT, and MDA contents. For the first time, cell damage in the reproductive parts of the ovaries of female flies, as well as in the accessory glands and testes of male flies, has been observed. Furthermore, a decline in reproductive health was noted, resulting in decreased fertility among the flies. By analyzing stress-related genes such as hsp83, hsp70, hsp60, and hsp26, we detected elevated expression of hsp83 and hsp70. Our study identified hsp83 as a specific biomarker for detecting early redox changes in cells caused by PET microplastics in all the treated groups, helping to elucidate the primary defense mechanism against PET microplastic toxicity. This study offers foundational insights into the emerging environmental threats posed by microplastics, revealing discernible alterations at the genetic level.

Abstract Antibiotic resistance is one of the biggest public health problems of our time. The nanoparticles are a powerful alternative to these antibiotics. Engineered nanoparticles show toxic effects on bacteria by different mechanisms. The bacteria–cell interaction of engineered nanoparticles exerts their toxic effects through changes in cell wall, cell membrane, and cytoplasm content/density. Thus, death occurs as a result of cell deformation. In this study, the cellular damage of silver nanoparticles, which are known to have strong antibacterial properties, and zirconium oxide and silicon oxide engineering nanoparticles, which are less known, on periodontopathic (Prevotella intermedia and Aggregatibacter actinomycetemcomitans) bacteria, were investigated by ultrastructural changes. The lysis of the cytoplasm and separation of the membrane cytoplasm were observed. Both types of bacteria treated with Ag ENP show more hollow cytoplasm than bacteria treated with the other two nanoparticles.

Essential thrombocythemia (ET) is an uncommon situation in which the body produces too many platelets. This can cause blood clots anywhere in the body and results in various symptoms and even strokes or heart attacks. Removing excessive platelets using acoustofluidic methods receives extensive attention due to their high efficiency and high yield. While the damage to the remaining cells, such as erythrocytes and leukocytes is yet evaluated. Existing cell damage evaluation methods usually require cell staining, which are time‐consuming and labor‐intensive. In this paper, we investigate cell damage by optical time‐stretch (OTS) imaging flow cytometry with high throughput and in a label‐free manner. Specifically, we first image the erythrocytes and leukocytes sorted by acoustofluidic sorting chip with different acoustic wave powers and flowing speed using OTS imaging flow cytometry at a flowing speed up to 1 m/s. Then, we employ machine learning algorithms to extract biophysical phenotypic features from the cellular images, as well as to cluster and identify images. The results show that both the errors of the biophysical phenotypic features and the proportion of abnormal cells are within 10% in the undamaged cell groups, while the errors are much greater than 10% in the damaged cell groups, indicating that acoustofluidic sorting causes little damage to the cells within the appropriate acoustic power, agreeing well with clinical assays. Our method provides a novel approach for high‐throughput and label‐free cell damage evaluation in scientific research and clinical settings. [ABSTRACT FROM AUTHOR]

Transient receptor potential ankyrin 1 (TRPA1) is a nonselective ion channel implicated in thermosensation and inflammatory pain. It has been reported that expression of the TRPA1 channel is induced by cigarette smoke extract. Acrolein found in cigarette smoke is highly toxic and known as an agonist of the TRPA1 channel. However, the role of TRPA1 in the cytotoxicity of acrolein remains unclear. Here, we investigated whether the TRPA1 channel is involved in the cytotoxicity of acrolein in human lung cancer A549 cells. The IC50 of acrolein in A549 cells was 25 μM, and acrolein toxicity increased in a concentration- and time-dependent manner. When the effect of acrolein on TRPA1 expression was examined, the expression of TRPA1 in A549 cells was increased by treatment with 50 μM acrolein for 24 h or 500 μM acrolein for 30 min. AP-1, a transcription factor, was activated in the cells treated with 50 μM acrolein for 24 h, while induction of NF-κB and HIF-1α was observed in the cells treated with 500 μM acrolein for 30 min. These results suggest that acrolein induces TRPA1 expression by activating these transcription factors. Overexpression of TRPA1 in A549 cells increased acrolein sensitivity and the level of protein-conjugated acrolein (PC-Acro), while knockdown of TRPA1 in A549 cells or treatment with a TRPA1 antagonist caused tolerance to acrolein. These findings suggest that acrolein induces the TRPA1 channel and that an increase in TRPA1 expression promotes the cytotoxicity of acrolein. [ABSTRACT FROM AUTHOR]

Understanding the mitotic DNA damage response (DDR) is critical to our comprehension of cancer, premature aging and developmental disorders which are marked by DNA repair deficiencies. In this study we use a micro-focused laser to induce DNA damage in selected mitotic chromosomes to study the subsequent repair response. Our findings demonstrate that (1) mitotic cells are capable of DNA repair as evidenced by DNA synthesis at damage sites, (2) Repair is attenuated when DNA-PKcs and ATM are simultaneously compromised, (3) Laser damage may permit the observation of previously undetected DDR proteins when damage is elicited by other methods in mitosis, and (4) Twenty five percent of mitotic DNA-damaged cells undergo a subsequent mitosis. Together these findings suggest that mitotic DDR is more complex than previously thought and may involve factors from multiple repair pathways that are better understood in interphase.

Understanding the mitotic DNA damage response (DDR) is critical to our comprehension of cancer, premature aging and developmental disorders which are marked by DNA repair deficiencies. In this study we use a micro-focused laser to induce DNA damage in selected mitotic chromosomes to study the subsequent repair response. Our findings demonstrate that (1) mitotic cells are capable of DNA repair as evidenced by DNA synthesis at damage sites, (2) Repair is attenuated when DNA-PKcs and ATM are simultaneously compromised, (3) Laser damage may permit the observation of previously undetected DDR proteins when damage is elicited by other methods in mitosis, and (4) Twenty five percent of mitotic DNA-damaged cells undergo a subsequent mitosis. Together these findings suggest that mitotic DDR is more complex than previously thought and may involve factors from multiple repair pathways that are better understood in interphase.

Abstract Background Necroptosis and pyroptosis are newly identified forms of programmed cell death, which play a vital role in development of many gastrointestinal disorders. Although plant polyphenols have been reported to protect intestinal health, it is still unclear whether there is a beneficial role of plant polyphenols in modulating necroptosis and pyroptosis in intestinal porcine epithelial cell line (IPEC-1) infected with enterotoxigenic Escherichia coli (ETEC) K88. This research was conducted to explore whether plant polyphenols including protocatechuic acid (PCA) and quercetin (Que), attenuated inflammation and injury of IPEC-1 caused by ETEC K88 through regulating necroptosis and pyroptosis signaling pathways. Methods IPEC-1 cells were treated with PCA (40 μmol/L) or Que (10 μmol/L) in the presence or absence of ETEC K88. Results PCA and Que decreased ETEC K88 adhesion and endotoxin level (P

Objective To investigate the potential effects of long non-coding RNA (lncRNA) MINCR on lipopolysaccharide (LPS)-induced human alveolar epithelial cell line A549 damage and inflammation through targeted regulation of miR-223. Methods A549 cells were randomly divided into control group, LPS group, LPS+transfection group(Si NC group, Si MINCR group, miR-223 NC group, miR-223 mimic group, Si NC+miR-223 NC group, Si NC+miR-223 antagomir group, Si MINCR+miR-223 NC group, and Si MINCR+miR-223 antagomir group). RT-qPCR was performed to determine the expression levels of MINCR and miR-223; Flow cytometry was performed to determine the rate of apoptosis; ELISA was performed to determine the levels of serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6); Bioinformatics prediction and dual luciferase reporter gene assay were performed to verify the targeting relationship of MINCR and miR-223; Western blot was performed to test the expression levels of activated caspase-3 (cleaved caspase-3) and B-cell lymphoma-2(Bcl-2) proteins in the cells. Results There was a targeting relationship between MINCR and miR-223. Compared with the control group, the apoptosis rate, the level of TNF-α and IL-6, and the expression of MINCR, cleaved caspase-3 proteins in the LPS group were significantly increased (PPPPPPPConclusions Silencing the expression of lncRNA MINCR may target the activation of miR-223 expression, inhibit cell apoptosis and inflammation, and reduce LPS-induced damage of alveolar epithelial cells.

Abstract Three-dimensional (3D) bioprinting fabricates 3D functional tissues/organs by accurately depositing the bioink composed of the biological materials and living cells. Even though 3D bioprinting techniques have experienced significant advancement over the past decades, it remains challenging for 3D bioprinting to artificially fabricate functional tissues/organs with high post-printing cell viability and functionality since cells endure various types of stress during the bioprinting process. Generally, cell viability which is affected by several factors including the stress and the environmental factors, such as pH and temperature, is mainly determined by the magnitude and duration of the stress imposed on the cells with poorer cell viability under a higher stress and a longer duration condition. The maintenance of high cell viability especially for those vulnerable cells, such as stem cells which are more sensitive to multiple stresses, is a key initial step to ensure the functionality of the artificial tissues/organs. In addition, maintaining the pluripotency of the cells such as proliferation and differentiation abilities is also essential for the 3D-bioprinted tissues/organs to be similar to native tissues/organs. This review discusses various pathways triggering cell damage and the major factors affecting cell viability during different bioprinting processes, summarizes the studies on cell viabilities and functionalities in different bioprinting processes, and presents several potential approaches to protect cells from injuries to ensure high cell viability and functionality.

Respiratory viral diseases are among the most important causes of disability, morbidity, and death worldwide. Due to the limited efficacy or side effects of many current therapies and the increase in antiviral-resistant viral strains, the need to find new compounds to counteract these infections is growing. Since the development of new drugs is a time-consuming and expensive process, numerous studies have focused on the reuse of commercially available compounds, such as natural molecules with therapeutic properties. This phenomenon is generally called drug repurposing or repositioning and represents a valid emerging strategy in the drug discovery field. Unfortunately, the use of natural compounds in therapy has some limitations, due to their poor kinetic performance and consequently reduced therapeutic effect. The advent of nanotechnology in biomedicine has allowed this limitation to be overcome, showing that natural compounds in nanoform may represent a promising strategy against respiratory viral infections. In this narrative review, the beneficial effects of some promising natural molecules, curcumin, resveratrol, quercetin, and vitamin C, which have been already studied both in native form and in nanoform, against respiratory viral infections are presented and discussed. The review focuses on the ability of these natural compounds, analyzed in in vitro and in vivo studies, to counteract inflammation and cellular damage induced by viral infection and provide scientific evidence of the benefits of nanoformulations in increasing the therapeutic potential of these molecules. [ABSTRACT FROM AUTHOR]

As a non-thermal technology, high hydrostatic pressure (HHP) has been widely investigated for inactivating microorganisms in food. Few studies have been presented on the pressurization/depressurization rate and mode of microbial inactivation. In this study, effect of pressurization rate and mode on Escherichia coli and Staphylococcus aureus cell damage during HHP treatment was investigated. The results showed that fast pressurization + linear mode (FL) treatment has the best bactericidal effect on E. coli and S. aureus, followed by fast pressurization + stepwise mode (FS) and slow pressurization + stepwise mode (SS) treatments. FL treatment caused more morphological damage to the cell wall, cell membrane, and cytoplasmic components compared with FS and SS treatment detected by SEM and TEM. Additionally, the damage to membrane permeability of them was also enhanced after FL treatment. Therefore, our results indicated that FL treatment could be applied to enhance the bactericidal effect of HHP on bacteria by increasing the damage to cell morphological structure and membrane integrity. [ABSTRACT FROM AUTHOR]

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Purpose: The aim of this study was to investigate the protective effect of long non-coding lnc-PXMP4-2-4 on myocardial cell damage caused by acute myocardial infarction (AMI). Methods: Peripheral blood mononuclear cells (PBMC) were collected from 24 patients with AMI on the day of admission, the first day after percutaneous coronary intervention (PCI) and the third day after surgery, and 24 patients with clinical control group. Real-time quantitative PCR(QRT-PCR) was used to detect the expression of related genes. Then in human cardiomyocytes (AC16), Cell Counting Kit-8 (CCK-8) was used to determine cell viability, lactate dehydrogenase release assay (LDH) was used to determine the release of lactate dehydrogenase, PCR was used to detect the expression of genes, cell death was detected by flow cytometry, and the expression of related proteins was measured by Western blot. The effect of lnc-PXMP4-2-4 was further studied by silencing and overexpressing lnc-PXMP4-2-4. Results: Compared with clinical control group, the expression of lnc-PXMP4-2-4 in PBMC of AMI patients was significantly higher than it. Compared with pre-operation, the expression of lnc-PXMP4-2-4 was significantly up-regulated on day 1 after PCI, and recovered to pre-operation level on day 3 after surgery. In AC16 cells, lnc-PXMP4-2-4 inhibited the proliferation of AC16, promoted the release of LDH and increased cell death, aggravated the cardiomyocyte injury caused by H2O2, and inhibited the expression of JAK2 and STAT3 mRNA and protein. The up-regulation of lnc-PXMP-4-2-4 had the opposite effect. In addition, the inhibition of the signal pathway by JAK2/STAT3 pathway inhibitor AG490 partially weakened the enhanced viability of AC16 cells, decreased LDH release and apoptosis induced by lnc-PXMP4-2-4 overexpression, increased Bcl-2 expression and down-regulated Bax expression. Conclusion: Therefore, we conclude that lnc-PXMP4-2-4 protects cardiomyocytes from injury by activating the JAK2/STAT3 signaling pathway.

Objectives: As a universal cytoprotective protein, Hsp70 is used to monitor the effects of environmental temperature changes, increasing the survival rate of cells exposed to stress, as well as the role of protein in cardiovascular disease, body decay and cell aging. Our research aims to to examine whether changes in serum protein 70 (Hsp70) values due to exposure to water temperature (41 °C and 44 °C) may indicate a mechanism of cardiomyocyte damage due to hyperthermia. Methods: A total of 40 adult albino Wistar rats, of known gender and body weight from 250 g to 300 g were used as material in this research. Rats were housed in polypropylene cages with optimum environmental conditions. Depending on the temperature of the water (WT) to which they were exposed, rats were randomized into the following groups.WT 37 °C (n = 8); WT 41 °C, antemortem (n = 8), WT 41 °C, postmortem (n = 8); WT 44 °C, antemortem (n = 8), WT 44 °C, postmortem (n = 8). Blood samples for determination of Hsp70 were taken before and after the expiration of the given duration of the experiment of 20 min or death. The Hsp70 level was determined by Enzyme-Linked Immunosorbent Assay (ELISA) Results: Hsp70 basal values in serum were significantly different, p = 0.004 pg/ml, and in the groups depending on the duration of exposure to Hsp70, p = 0.002. Serum Hsp70 values after being exposed to water temperature were significantly different according to the group, p = 0.009. Significant lower Hsp70 levels were found in the control group according to G41 p = 0.006 and G44, p = 0.002. Insignificant differences in Hsp70 level were found among theseG41 and G44, p > 0.005. The concentration of Hsp70 in rat serum and ≥ 31.36 ng/ml indicates exposure to temperatures higher than 37 °C (sensitivity 85.71%, specificity 83.33%, PPV 96%, and NPV 55%, p = 0.002). Conclusions: Altered concentration of serum Hsp70 may show exposition to the elevated water temperature.

The ciliate Climacostomum virens produces the metabolite climacostol that displays antimicrobial activity and cytotoxicity on human and rodent tumor cells. Given its potential as a backbone in pharmacological studies, we used the fruit fly Drosophila melanogaster to evaluate how the xenobiotic climacostol affects biological systems in vivo at the organismal level. Food administration with climacostol demonstrated its harmful role during larvae developmental stages but not pupation. The midgut of eclosed larvae showed apoptosis and increased generation of reactive oxygen species (ROS), thus demonstrating gastrointestinal toxicity. Climacostol did not affect enteroendocrine cell proliferation, suggesting moderate damage that does not initiate the repairing program. The fact that climacostol increased brain ROS and inhibited the proliferation of neural cells revealed a systemic (neurotoxic) role of this harmful substance. In this line, we found lower expression of relevant antioxidant enzymes in the larvae and impaired mitochondrial activity. Adult offsprings presented no major alterations in survival and mobility, as well the absence of abnormal phenotypes. However, mitochondrial activity and oviposition behavior was somewhat affected, indicating the chronic toxicity of climacostol, which continues moderately until adult stages. These results revealed for the first time the detrimental role of ingested climacostol in a non-target multicellular organism.

Vitamin D, a secosteroid hormone, appears to have significant beneficial effects on various physiological systems, including the musculoskeletal system. Vitamin D assists in the regulation of numerous critical biological functions and physiological processes in humans, including inflammation, oxidative stress, and mitochondrial respiration, and is also linked to cardiac diseases. It is also reported that vitamin D plays a central role in molecular and cellular mechanisms, which reduce oxidative stress, and tissue damage and regulate cellular health. On the other side, hypovitaminosis D reduces mitochondrial activity and increases oxidative stress and inflammation in the body. Hypervitaminosis D increases the prevalence and severity of cellular damage. It has also been reported that vitamin D is involved in many functions of the reproductive system in human and critically play an important role in the reproductive tissues of women and men. Its role is very well defined, starting from female menarche to menopause, pregnancy, and lactation, and finally in male fertility. Hence, the appropriate amount of vitamin D is necessary to maintain the normal function of cell organelles. Based on recent studies, it is understood that vitamin D is involved in the biological activities of mitochondria in cells, especially in cardiomyocytes. In this review, we emphasized the role of vitamin D in mitochondrial respiration, which could significantly influence heart health and human reproduction.

The in vitro antioxidation and cytoprotection of abalone visceral peptides against oxidative damage were investigated. Results show that the DPPH· scavenging activities of the 16 chemically synthesized peptides were significantly and positively correlated with their reducing power. Their scavenging activities against ABTS·+ were positively correlated with their ability to inhibit linoleic acid oxidation. Only Cys containing peptides exhibited good DPPH· scavenging activity, while only Tyr containing peptides showed significant ABTS·+ scavenging activity. In the cytoprotection assay, all four representative peptides significantly increased the viability of H2O2-damaged LO2 cells and the activities of GSH-Px, CAT, and SOD, and all decreased MDA levels and LDH leakage, in which the Cys-containing peptides were more effective at increasing the activities of antioxidant enzymes, while the Tyr-containing peptides were more effective at decreasing MDA levels and LDH leakage. Abalone visceral peptides containing both Cys and Tyr exhibit strong in vitro and cellular antioxidation.

Pregnancies are a critical window period for environmental influences over the mother and the offspring. There is a growing body of evidence associating indoor and outdoor air pollution exposure to adverse pregnancy outcomes such as preterm birth and hypertensive disorders of pregnancy. Particulate matter (PM) could trigger oxi-inflammation and could also reach the placenta leading to placental damage with fetal consequences. The combination of strategies such as risk assessment, advise about risks of environmental exposures to pregnant women, together with nutritional strategies and digital solutions to monitor air quality can be effective in mitigating the effects of air pollution during pregnancy. [ABSTRACT FROM AUTHOR]

Background: Necroptosis and pyroptosis are newly identified forms of programmed cell death, which play a vital role in development of many gastrointestinal disorders. Although plant polyphenols have been reported to protect intestinal health, it is still unclear whether there is a beneficial role of plant polyphenols in modulating necroptosis and pyroptosis in intestinal porcine epithelial cell line (IPEC-1) infected with enterotoxigenic Escherichia coli (ETEC) K88. This research was conducted to explore whether plant polyphenols including protocatechuic acid (PCA) and quercetin (Que), attenuated inflammation and injury of IPEC-1 caused by ETEC K88 through regulating necroptosis and pyroptosis signaling pathways. Methods: IPEC-1 cells were treated with PCA (40 μmol/L) or Que (10 μmol/L) in the presence or absence of ETEC K88. Results: PCA and Que decreased ETEC K88 adhesion and endotoxin level (P < 0.05) in cell supernatant. PCA and Que increased cell number (P < 0.001) and decreased lactate dehydrogenases (LDH) activity (P < 0.05) in cell supernatant after ETEC infection. PCA and Que improved transepithelial electrical resistance (TEER) (P < 0.001) and reduced fluorescein isothiocyanate-labeled dextran (FD4) flux (P < 0.001), and enhanced membrane protein abundance of occludin, claudin-1 and ZO-1 (P < 0.05), and rescued distribution of these tight junction proteins (P < 0.05) after ETEC infection. PCA and Que also declined cell necrosis ratio (P < 0.05). PCA and Que reduced mRNA abundance and concentration of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8 (P < 0.001), and down-regulated gene expression of toll-like receptors 4 (TLR4) and its downstream signals (P < 0.001) after ETEC infection. PCA and Que down-regulated protein abundance of total receptor interacting protein kinase 1 (t-RIP1), phosphorylated-RIP1 (p-RIP1), p-RIP1/t-RIP1, t-RIP3, p-RIP3, mixed lineage kinase domain-like protein (MLKL), p-MLKL, dynamin- related protein 1 (DRP1), phosphoglycerate mutase 5 (PGAM5) and high mobility group box 1 (HMGB1) (P < 0.05) after ETEC infection. Moreover, PCA and Que reduced protein abundance of nod-like receptor protein 3 (NLRP3), nod-like receptors family CARD domain-containing protein 4 (NLRC4), apoptosis-associated speck-like protein containing a CARD (ASC), gasdermin D (GSDMD) and caspase-1 (P < 0.05) after ETEC infection. Conclusions: In general, our data suggest that PCA and Que are capable of attenuating ETEC-caused intestinal inflammation and damage via inhibiting necroptosis and pyroptosis signaling pathways. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effect of decursinol angelate in acute lung injury induced by lipopolysaccharide treatment. Methods: Human bronchial epithelial cells (BEAS-2B cells) and human pulmonary artery endothelial cells (HPAECs) were exposed to lipopolysaccharide to induce cell injury and then treated with 20, 40, or 60 µM decursinol angelate. Cell viability was quantified using a cell counting assay, while cell apoptosis was evaluated by western blot and flow cytometry. Colorimetric and enzyme-linked immunosorbent assay (ELISA) was used to measure oxidative stress. Expressions of tumor necrosis factor-alpha (TNF-α), interleukin-1β, and interleukin-6 were evaluated using quantitative real-time-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Phosphorylation levels of p65, IκBα, AKT, and phosphatidylinositol 3-kinase were assessed by western blot, while the entry of p65 into the nucleus was investigated by indirect immunofluorescence assay. Results: Treatment with 40 or 60 μM decursinol angelate increased cell viability after lipopolysaccharide-induced damage. B-cell lymphoma 2 (Bcl2) and Bax expression were regulated, and the rate of apoptosis was inhibited. The concentration of superoxide dismutase and glutathione was elevated, and the density of malondialdehyde and myeloperoxidase decreased significantly. Inflammation was also suppressed by decursinol angelate by regulating TNF-α, interleukin-1β, and interleukin-6 expressions. Furthermore, decursinol angelate significantly decreased the phosphorylation of p65, IκBα, AKT, and phosphatidylinositol 3-kinase. Finally, decursinol angelate inhibited p65 entry into the cell nucleus. Conclusion: Decursinol angelate alleviates cell damage and apoptosis, reduces oxidative stress, and attenuates inflammation after lipopolysaccharide-induced acute lung injury by inhibiting AKT/NF-κB signaling pathway. Thus, decursinol angelate is a potential candidate for the treatment of lung injury. [ABSTRACT FROM AUTHOR]

Introduction: Candida albicans is an opportunistic pathogenic fungus, which frequently causes systemic or local fungal infections in humans. The evolution of its drug-resistant mutants necessitate an urgent development of novel antimicrobial agents. Results: Here, we explored the antimicrobial activity and inhibitory mechanisms of X33 antimicrobial oligopeptide (X33 AMOP) against C. albicans. The oxford cup test results showed that X33 AMOP had strong inhibitory activity against C. albicans, and its MIC and MFC were 0.625 g/L and 2.5 g/L, respectively. Moreover, SEM and TEM showed that X33 AMOP disrupted the integrity of cell membrane. The AKP, ROS, H2O2 and MDA contents increased, while the reducing sugar, soluble protein, and pyruvate contents decreased after the X33 AMOP treatment. This indicated that X33 AMOP could damage the mitochondrial integrity of the cells, thereby disrupting the energy metabolism by inducing oxidative stress in C. albicans. Furthermore, transcriptome analysis showed that X33 AMOP treatment resulted in the differential expression of 1140 genes, among which 532 were up-regulated, and 608 were down-regulated. These DEGs were related to protein, nucleic acid, and carbohydrate metabolism, and their expression changes were consistent with the changes in physiological characteristics. Moreover, we found that X33 AMOP could effectively inhibit the virulence attributes of C. albicans by reducing phospholipase activity and disrupting hypha formation. Discussion: These findings provide the first-ever detailed reference for the inhibitory mechanisms of X33 AMOP against C. albicans and suggest that X33 AMOP is a potential drug candidate for treating C. albicans infections. [ABSTRACT FROM AUTHOR]

This study observed role of OZF5 for adsorption, transformation, biodegradation and detoxification and their effect in augmenting bean growth in metal amended pots. Brevibcillus parabrevis OZF 5 (accession number KX276150) significantly removed metals [Cr (VI) and Zn) by biosorption and Cr (VI) reduction. Gene amplification by PCR detected Cr (VI) reductase gene (ChR) and related protein in OZF5 which could be a mechanism responsible for Cr (VI) tolerance. Cytosolic reduction of Cr (VI) and biofilm formation may be actual mechanism of reduction. Bacterial strain OZF5 was also able to degrade wide variety of hydrocarbons in soil contaminated with petroleum. Inoculation of bean with OZF5 reduced production of eDNA [99.97% for both Cr (VI) and Zn], superoxide anions [89.18% for Cr (VI) and 84.61% for Zn], malondialdehyde (MDA) [41.48% for Cr (VI) and 45.88% for Zn], ascorbate [50.70% for Cr (VI) and 47.40% for Zn], catalase [22.51% for Cr (VI) and 51.93% for Zn] compared to un-inoculated but amended with Cr (VI) and Zn. Exopolysaccharide production did not decrease under metals stress. OZF5 completely prevented uptake of metals instead accumulated more nutrients which enhanced bean growth. Present study proved OZF5 to be a super-bioinoculant which could protect plants against oxidative damage. [ABSTRACT FROM AUTHOR]

The possession of a carbon concentrating mechanism (CCM) by a given phytoplankton species will in part determine its response to changes in the dissolved inorganic carbon concentrations in the global ocean. Earlier work on CCMs in the coccolithophore Emiliania huxleyi suggested that this species did not possess a CCM, though more recent studies indicate that a CCM is indeed present. Here we report work showing that another coccolithophore species, Gephyrocapsa oceanica, also possesses a functioning CCM, implying that increasing CO2 concentrations are unlikely to lead to enhanced growth rates. We discuss the protocol required for working with this species, noting that due to its liths being 10 or more times as massive as of those of Emiliania huxleyi, much lower centrifugation speeds (<400 × g) must be used to avoid damage to the cells. [ABSTRACT FROM AUTHOR]