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Polycystic ovary syndrome (PCOS) is a common metabolic disorder of the reproductive system in women of adolescent and childbearing age. In addition to ovulatory dysfunction, menstrual dysfunction and infertility, most patients suffer from endocrine abnormalities such as insulin resistance (IR), hyperandrogenemia (HA) and abdominal obesity. Ferroptosis, a highly iron-dependent programmed cell death mediated by the lipid peroxidation and the imbalance in the oxidative -antioxidant system is a hot research topic in reproductive medicine. The relevance of ferroptosis in PCOS has received much attention in recent years, and recent studies suggest that ferroptosis may be involved in the regulation of PCOS -associated metabolic disorders and affect reproductive function in women with PCOS by disrupting oocyte quality and uteroplacental function. To further enrich and improve the system of diagnosis, prevention, and prognosis assessment of PCOS, we summarize the mechanisms related to ferroptosis, systematically discusses the correlation between ferroptosis and the pathophysiology of PCOS, and its research progress in the treatment of PCOS. [ABSTRACT FROM AUTHOR]

Skeletal muscle aging is a biological process that occurs as the body ages, characterized by mass loss and functional decline. The involvement of metallomics, particularly copper metallomics, is pivotal in understanding its functional roles. Copper metallomics manifests as copper overload with aging. It triggers toxic effects that activate apoptosis, pyroptosis, ferroptosis, cuproptosis and also promote α-synuclein aggregation. The related signaling cascades can eventually promote metabolic turbulence and the loss of proteins, mitochondria, satellite cells and other cell contents in senescent myofibers, while causing the degeneration and abnormality of neuromuscular junctions. This is a new physiopathgical mechanism of aging-related atrophy in skeletal muscles. Here we firstly review the molecular biological functions of copper in the regulatory networks of aging-related atrophy for skeletal muscles, the potential mechanisms of copper overload in senescent skeletal muscles, and the novel role of multiple signaling transduction pathways associated with copper overload-induced cell death modes comprising apoptosis, pyroptosis, ferroptosis and cuproptosis in aging-related atrophy for skeletal muscles. We aim to provide potential molecular targets and option choices for clinically applying copper chelation to improve and treat aging-related atrophy in skeletal muscles. [ABSTRACT FROM AUTHOR]

BACKGROUND: silencing information regulatory 1 (SIRT1) regulates the function of related proteins in chondrocytes in a deacetylated manner and participates in chondrocyte proliferation and differentiation, thereby promoting cartilage defect repair. OBJECTIVE: To screen for signaling pathways with unclear action status after SIRT1 gene knockdown in chondrocytes, as well as diseases or functions that produce changes using high-throughput technology. METHODS: ATDC5 chondrocytes from mice in logarithmic growth phase were divided into two groups: the cells were transfected with SIRT1 gene knockdown negative control lentivirus in control group and SIRT1 gene knockdown lentivirus in experimental group. GeneChip® Mouse Genome 430 2.0 Array was used to detect the mRNA expression at 72 hours after transfection. Applied bioinformatics technology was also used to screen for unclear activation or inhibition signaling pathways and their related factors. Moreover, enrichment of disease or function modules was analyzed. RESULTS AND CONCLUSION: After knocking down the SIRT1 gene, there were 245 signaling pathways with unclear activation or inhibition status in the mouse ATDC5 chondrocytes. According to the ranking of -Log (P-value), we reported the factors in the top 20 signaling pathways with unclear activation or inhibition status, including IGFBP4, TGFBR1, CTGF, COL4A5, LHX2, IL1RL1, and KLF6. According to the ranking of -Log (P-value), there were significant changes in 14 disease or function modules, including cellular growth and proliferation, organism survival, cell death and survival. According to the number of differentially expressed genes, there were significant changes in three disease or function modules, including organismal injury and abnormalities, cancer, and cell death and survival. According to the comprehensive ranking of -Log (P-value) and the number of differentially expressed genes, the disease or function module related to intrinsic immune response was significantly activated. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality 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 observe the effect of Yupingfeng powder on ZBP1-mediated PANoptosis of alveolar macrophages so as to elucidate its molecular mechanism of inhibiting airway inflammation in asthma. Methods : Lipopolysaccharide was used to induce alveolar macrophages (MH-S) to construct an asthma cell model, and different concentration of Yupingfeng powder medicated Serum were given for intervention. CCK8 method was used to detect the activity of NH-S cells, ELISA method was used to detect the content of LDH, IL-1β and IL-18, flow cytometry was used to detect cell death, Western blot method was used to detect the expression of PANoptosis-related proteins and ZBP1 protein, and RT-qPCR method was used to detect the expression of ZBP1 gene. Results: Compared with the control group, the LDH release of alveolar macrophages, the content of IL-1β and IL-18 and the proportion of dead cells in the model group were significantly increased. The expressions of pyroptosis proteins (Cleaved caspase-1 and GSDMD-NT), necroptosis proteins (p-RIPK3 and p-MLKL), and apoptosis protein (Cleaved caspase-3) were significantly up-regulated (P<0.01). Compared with the model group, the expression of LDH release, the content of IL-1β and IL-18, and the proportion of dead cells in alveolar macrophages in the Yupingfeng powder group were significantly reduced, and the expression of Cleaved caspase-1, GSDMD-NT, p-RIPK3, p-MLKL, and Cleaved caspase-3 were significantly down-regulated (P<0.01). In addition, the expression of ZBP1 protein and ZBP1 mRNA in alveolar macrophages in the Yupingfeng powder group was significantly reduced compared with the model group, and the differences were statistically significant (P< 0.01). Conclusion: Yupingfeng powder ameliorates airway inflammation by inhibiting the expression of ZBP1 in alveolar macrophages, thereby suppressing the level of PANoptosis. [ABSTRACT FROM AUTHOR]

AIM: To explore the impact of histidine triad nucleotide-binding protein 2 (HINT2) on atherosclerosis (AS), and to elucidate its underlying mechanisms. METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from patients with chest pain and induced to differentiate into macrophages for assessing HINT2 expression. In vitro, RAW264. 7 mouse macrophages were cultured to evaluate inflammatory cytokine levels and cell death in supernatants. An apolipoprotein E gene knockout (apo mouse model of AS was developed to analyze plaque formation, lipid metabolism and macrophage foaminess in the aortic root. Pyroptosis-related protein expression in cultured RAW264. 7 cells and the aorta of apo mice was determined by RT-qPCR and Western blot. RESULTS: Significantly reduced HINT2 expression was observed in PBMCs from patients with acute coronary syndrome, which was negatively correlated with pro-inflammatory and positively correlated with anti-inflammatory serum factors, suggesting HINT2's potential role in mitigating AS-related inflammation. In vitro experiments demonstrated that HINT2 overexpression inhibited lipid accumulation and foam cell formation in macrophages induced by oxidized low-density lipoprotein (ox-LDL). It also reduced secretion of inflammatory cytokines, including interleukin-6 (IL-6), IL-lp, IL-18 and tumor necrosis factor-a, and decreased cell death and pyroptosis-related protein expression. In vivo experiments in apo mice confirmed that H1NT2 overexpression lessened plaque burden in the aortic root, reduced macrophage foaminess, and inhibited the expression of pyroptosis-related proteins such as nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3), caspase-1, gasdermin D (GSDMD), IL-ip and IL-18. CONCLUSION: HINT2 potentially inhibits ox-LDL-induced macrophage pyroptosis, attenuates inflammatory responses in AS, and may slow the progression of this disease. [ABSTRACT FROM AUTHOR]

Ferroptosis is a new type of iron-dependent cell death and is involved in many biological processes. Multiple ferroptosis signals affect enzymes and metabolites during glucose metabolism, altering the metabolic pathways of macrophages. In addition, macrophages with different polarization phenotypes have different resistance to ferroptosis, which affects the occurrence and signal transmission of ferroptosis. Therefore, the important process of glucose metabolism in macrophages is targeted to regulate the sensitivity of macrophages to ferroptosis through energy metabolism. In this paper, we review the recent research progress on the effect of ferroptosis signaling on the reprogramming of glucose metabo, lism in macrophages and the regulatory effects of various compounds. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy 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.)

The pathogenesis of psoriasis is complex, so it is very important to explore the pathogenesis for the treatment of psoriasis. The Nrf2/HO-1 pathway has a protective effect on cells and is closely related to physiological and pathological aspects such as oxidative stress, immunity, abnormal proliferation of blood vessels, epidermal imbalance and cell death. Currently, some studies have confirmed that Nrf2/HO-1 pathway may have an inhibitory effect on psoriatic lesion, and it may be involved in psoriasis pathogenesis through multiple pathways. This paper reviews the mechanism of Nrf2/HO-1 pathway in psoriasis and the research progress in the treatment of psoriasis through the intervention of traditional Chinese medicine. [ABSTRACT FROM AUTHOR]

Ferroptosis suppressor protein 1 (FSP1) is a key suppressor in the process of ferroptosis, which can prevent cell death and has important biological functions and potential value in clinical application. In this article, the discovery background, gene localization and structural characteristics of FSP1, as well as its dual role in inhibiting ferroptosis and promoting apoptosis were explicitly discussed. In clinical researches, FSP1 inhibitors, such as iFSP1 and icFSP1, have been developed. Subsequently, the regulatory mechanisms of FSP1 expression, its association with tumor immune escape, and its potential as a monitoring indicator for tumor prognosis and therapeutic response will be investigated. [ABSTRACT FROM AUTHOR]

Background and objective Targeted therapies are ineffective in lung squamous cancer (LUSC), and the low response rate of immunotherapy hampers its application in LUSC, so it is urgent to explore new strategies for LUSC treatment. Ferroptosis plays an important role in tumour suppression. The aim of this study was to investigate the role and mechanism of targeting 3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1) in regulating ferroptosis in LUSC cells, in order to provide a new research direction for LUSC therapy. Methods The expression of HMGCS1 in LUSC was analysed by The Cancer Genome Atlas (TCGA) and Clinical Proteomic Tumor Analysis Consortium (CPTAC) online databases; the relationship between HMGCS1 and survival time of lung cancer was analysed by the Kaplan-Meier Plotter online survival database; the expression level of HMGCS1 in LUSC tissues was verified by immunohistochemistry. After interfering with HMGCS1 expression by small interfering RNA (siRNA), cell activity and cell migration ability were detected by CCK8 and Transwell assay; apoptosis was detected by flow cytometry after interfering with HMGCS1 or after treatment with the HMGCS1 inhibitor of hymeglusin; Fe2+, reactive oxygen species (ROS) and lipid peroxidation levels were detected by flow cytometry and highcontent confocal fluorescence imaging systems, respectively in SKMES cells after inhibition of HMGCS1; and Western blot was performed to detect the expression of ACSL4, GPX4 and SLC7A11, which are markers of the ferroptosis pathway after inhibition of HMGCS1. Results HMGCS1 mRNA and protein levels were significantly high in LUSC; siRNA interference with HMGCS1 expression inhibited the proliferative activity and migration ability of LUSC cells, but had no significant effect on apoptosis. Interference with HMGCS1 or treatment with the HMGCS1 inhibitor of hymeglusin significantly promoted intra- cellular Fe2+, ROS and lipid peroxidation levels in SKMES cells, and induced ferroptosis in LUSC cells; Western blot assay showed that inhibition of HMGCS1 significantly promoted the expression of ACSL4. Conclusion Inhibition of HMGCS1, a target of LUSC, promotes ferroptosis in lung cancer cells and provides a research basis for screening new therapeutic targets for LUSC. [ABSTRACT FROM AUTHOR]

Gasdermin D (GSDMD) is a widely expressed protein that can be activated by inflammatory factors within hepatocytes. Once activated, the N terminal domain of GSDMD (GSDMD N) will form pores, leading to rupture of cell membranes and leakage of cytoplasm, ultimately leading to cell death. Pyrozosis is the most characteristic mode of inflammatory lytic cell death mediated by GSDMD. Recent studies have found that activation of GSDMD amplifies the inflammatory response and induces pyrosis of liver cells, thereby accelerating the progression of acute liver failure. This article focuses on the pathogenic mechanism and potential therapeutic targets of GSDMD mediated hepatocyte pyrozosis in acute liver failure, in order to provide new ideas for finding potential intervention targets for the effective treatment of acute liver failure. [ABSTRACT FROM AUTHOR]

Objective Tumor is a major public health problem harmful to people's health. Cell copper death provides a new idea for the basic research of tumor. This paper reviews the latest progress of cell copper death in the field of tumor prevention and treatment. Methods The literatures related to copper death in tumor prevention and treatment were summarized, and the research status of copper death related genes in different types of tumors was reviewed. Results Ferredoxin 1 (FDXl), lipoic acid synthase (LIAS), dihydro lipocyte answers (DLAT), and dihydro lipoamide S-succinyl transferase (DLST) were the key regulatory genes of copper death, which were abnormally expressed in lung cancer, hepatocellular carcinoma, and breast cancer. Among them, the low expression of FDXl in tumor patients was related to the poor prognosis of the disease, while the overall survival time of cancer patients with high expression of DLA T and DLST genes was decreased. In addition, targeting copper death protein and promoting cell copper death inhibited the proliferation of cancer cells in vivo and in vitro. Conclusion Several genes related to copper death, such as FDXl, LIAS, DLAT, and DLST, are abnormally expressed in cancer patients and are related to the occurrence, development, metastasis, and prognosis of the tumor. Targeted promotion of cell copper death and inhibition of cancer cell proliferation provide a new direction for future basic research in the field of tumor, which has public health significance for tumor prevention and treatment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Hainan Medical University is the property of Journal of Hainan Medical College 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.)

Cardiomyopathy is a group of heterogeneous myocardial diseases with a variety of specific phenotypes that can lead to cardiovascular death or progressive heart failure in severe cases. Because of the severity and complexity of these diseases, the search for new regulatory mechanisms to prevent and treat cardiomyopathy is particularly urgent. Iron death is a form of programmed cell death that differs from other forms of iron dependence and is characterized by the accumulation of iron-dependent lipid peroxides. Studies have shown that iron death can be involved in the occurrence and progression of cardiomyopathy through different signaling pathways. Therefore, targeted regulation of iron death is a new strategy to prevent cardiomyopathy. In this paper, the mechanism of iron death and its important role in cardiomyopathy were reviewed to find the potential relationship between iron death and cardiomyopathy and provide more ideas for the treatment of various cardiomyopathies in the future. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC) is one of the malignant tumors with high morbidity and mortality worldwide. Ferroptosis is a new type of programmed cell death caused by abnormal accumulation of iron-dependent reactive oxygen species (ROS) leading to lipid peroxidation. It involves the balance between iron metabolism, lipid metabolism, oxygen free radical reaction and lipid peroxidation. Recent studies have found that ferroptosis is closely related to the occurrence and development of NSCLC. Due to the emergence of chemotherapy resistance and radiotherapy resistance in the treatment of NSCLC, there is an urgent need to develop new effective drugs and treatment strategies. Traditional Chinese medicine has unique advantages in the prevention and treatment of NSCLC due to its multi-targets and minimal side effects. In this review, we summarize the mechanism of ferroptosis in NSCLC, and discuss the research status of active ingredients of traditional Chinese medicine, single-herb traditional Chinese medicine and Chinese herbal compounds in the intervention of NSCLC through ferroptosis, in order to provide a new theoretical basis for the research of ferroptosis pathway and the prevention and treatment of NSCLC by targeted ferroptosis of traditional Chinese medicine. [ABSTRACT FROM AUTHOR]

Lipid metabolism may play a role in the onset and progression of Parkinson's disease (PD), involving various pathological mechanisms such as abnormal folding and accumulation of α-synuclein (α-Syn), ferroptosis, GBA1 gene mutation, and mitochondrial dysfunction, etc.. This article reviews the lipid metabolism abnormalities associated with Parkinson's disease and explores potential related pathophysiological mechanism, aiming to provide new insights into the early diagnosis and treatment of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Ferroptosis is an iron-dependent form of regulated cell death, which is distinct from apoptosis, necrosis, and pyroptosis. Recent studies have found that activators of ferroptosis, such as Erastin, can activate autophagy-related proteins, induce the formation of autophagosomes, and ultimately release ferric ions to mediate ferroptosis. This process, called ferritinophagy, is initiated by the binding of an autophagic cargo receptor protein, nuclear receptor coactivator 4（NCOA4）, to iron-laden ferritin. The transfer of NCOA4-ferritin to the lysosome by ferritinophagy results in the proteolysis of ferritin, and, in turn, the release of its iron content and lipid-reactive oxygen species (ROS) accumulation. Ferritinophagy has been closely associated with central nervous system disorders, circulatory system diseases, and cancer. Furthermore, the regulation mechanism of ferritinophagy is also a hot topic in the study of iron-dependent cell death process. With the in-depth study of ferritinophagy, great progress has been made in the study of key components of ferritinophagy as well as its molecular mechanisms and processes. However, a comprehensive summary of the methods for detecting ferritinophagy is still unclear. To further deepen the understanding of ferritinophagy and its detection methods, this review focuses on the concept, characteristics, methods, and precautions during detection of ferritinophagy. This review provided experimental reference for subsequent researchers and promoting the progress of research related to ferritinophagy. [ABSTRACT FROM AUTHOR]

Ferroptosis is defined as an iron-dependent regulated form of cell death driven by lipid peroxidation, which is not only regulated by a variety of cellular metabolic pathways, but it is also related to neurodegenerative diseases, tumors, cardiovascular diseases and so on. Recent studies have found that ferroptosis plays a crucial part in the process of atherosclerosis. This article reviews the role and molecular mechanism of ferroptosis in the pathological processes of atherosclerosis, such as vascular endothelial cell dysfunction, macrophage polarization, foam cell formation, vascular smooth muscle cell proliferation and migration, and summarizes the ferroptosis inhibitors and related targets that may have therapeutic effects on atherosclerosis. The aim is to provide a new therapeutic direction for atherosclerosis from the perspective of ferroptosis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy 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.)

In 2023, numerous theoretical advancements and technological breakthroughs have been achieved in the field of immunology research. In this article, we summarized representative research achievements in the field of immunology both domestically and internationally in 2023, and discussed the challenges and opportunities for future research. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology 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 Practical Oncology Journal is the property of Journal of Practical Oncology 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.)

Vascular calcification is age dependent and a risk factor for cardiovascular all-cause mortality. Recently, growing evidences have shown that novel forms of programmed cell death including ferroptosis, pyroptosis, and autophagy play an important role in the development of vascular calcification. This review introduces the molecular mechanism of programmed cell death and its relationship with vascular calcification, elucidates the evidence of anti-vascular calcification by regulating the cell death pathway key molecules. [ABSTRACT FROM AUTHOR]

Mixed lineage kinase domain-like protein （MLKL） serves as the terminal effector in the necroptosis pathway. Upon phosphorylation by receptor-interacting protein kinase 3 （RIPK3）, MLKL translocates to the plasma membrane, compromising the membrane integrity, thus inducing lytic cell death. This process epitomizes the classical mechanism of MLKL-driven necroptosis. Additionally, MLKL possesses several non-necroptotic functions, such as the regulation of autophagy and endosomal transport. This review summarizes the structural characteristics of MLKL, its mechanism in mediating necroptosis and recent research advances in its non-necroptotic functions, as well as the diverse functionalities of MLKL in connection with its phosphorylation sites, subcellular location, and non-RIPK3-dependent activation pathways. [ABSTRACT FROM AUTHOR]

AA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD ceBackground and objective Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2. Methods Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bio-informatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PR^AA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PR^AA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PR^lls were measured using the L-ROS tests to determine the effects of miR-186-5p and PRAA2. Resuits The expression of PR^AA2 is up-regulated, and a high level of PR^AA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRAA2. Conclusion miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRAA2, thus inhibiting the proliferation, invasion and migration of LUAD. [ABSTRACT FROM AUTHOR]

The fundamental aspect of tissue injury was the structural changes and functional disorders caused by a great deal of cell death, it might further develop into organ damage in severe cases. At present, the treatment of tissue injury was more focused on improving the micro-environment and promoting cell renewing. Insufficient attention was paid to the repair of cell damage, this oversight could exacerbate disease conditions and create difficulties in achieving healing. Thus, treating tissue injury should be based on repairing cell damage. In order to systematically grasp the research status and drug development of cell damage and repair, this article provided a systematic review of the damaging causes, repair mechanisms, and drug development from the perspectives of DNA damage, RNA damage, protein damage, mitochondrial damage, membrane damage and cell death. It was expected to contribute to promoting the research and development of repair medicines.

Lung cancer is one of the most common cancers in the world, and its treatment strategy is mainly surgery combined with radiotherapy and chemotherapy. However, long-term chemotherapy will result in drug resistance, which is also one of the difficulties in the treatment of lung cancer. Ferroptosis is an iron-dependent and lipid peroxidation-driven non-apoptotic cell death cascade, occurring when there is an imbalance of redox homeostasis in the cell. Nuclear factor erythroid 2-related factor 2 (Nrf2) is key for cellular antioxidant responses. Numerous studies suggest that Nrf2 assumes an extremely important role in regulation of ferroptosis, for its various functions in iron, lipid, and amino acid metabolism, and so on. In this review, a brief overview of the research progress of ferroptosis over the past decade will be presented. In particular, the mechanism of ferroptosis and the regulation of ferroptosis by Nrf2 will be discussed, as well as the role of the Nrf2 pathway and ferroptosis in tumor drug resistance, which will provide new research directions for the treatment of drug-resistant lung cancer patients. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy 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 Journal of China Medical University is the property of Journal of China Medical University 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.)

Necroptosis is a major discovery in the field of cell death in recent decades. At present, in the field of ophthalmology, the activation of necroptosis pathway has been found from corneal diseases, glaucoma, retinal diseases and so on. In addition to Necrostatin-1（Nec-1）, a necroptosis inhibitor targeting receptor-interacting protein1（RIP1）, drugs such as GSK2399872A（GSK872）, a receptor-interacting protein3（RIP3） inhibitor, and TC13172, a novel inhibitor targeting mixed lineage kinase domain-like protein （MLKL）, have made major breakthroughs in cell death mechanisms. Currently in the field of ophthalmology, necroptosis inhibitors have demonstrated their protective effects in a variety of disease models. This article focuses on the molecular mechanism of necroptosis and the research results of its inhibitors in ophthalmology, discusses the potential of necroptosis as a new target for the treatment of ophthalmic diseases, and puts forward suggestions for its further research in the field of ophthalmology. [ABSTRACT FROM AUTHOR]

Copper is an essential trace element in human body and plays an important role in maintaining health in humans. Copper is involved in various metabolic pathways in human body, and copper metabolism disorder may lead to metabolic disorders such as impaired glucose tolerance and dyslipidemia. The liver plays a key role in maintaining copper homeostasis, and copper deficiency or excess may cause cell damage and liver dysfunction. Recent studies on copper metabolism have shown that copper metabolism disorder may result in cell damage by affecting oxidative stress, proteasome, cuproptosis, and angiogenesis and help to clarify the assumed mechanisms of liver diseases and metabolic disorders due to copper metabolism disorder. This article reviews the recent research advances in copper metabolism disorder in cell damage/death and chronic liver diseases, including Wilson’s disease, nonalcoholic fatty liver disease, and hepatocellular carcinoma, which helps to identify future research priorities. [ABSTRACT FROM AUTHOR]

Thioridazine, a phenothiazine drug, has a potential to induce tumor immunogenic cell death (ICD) and activate a tumor-specific immune response. In this study, we examined the ICD effect induced by Thioridazine and elucidated its underlying mechanisms using lung adenocarcinoma A549 and H1299 cells. Various concentrations of Thioridazine were employed to treat A549 and H1299 cells. The cell inhibition rate was determined using the methyl thiazol tetrazolium (MTT) assay, apoptosis rate was assessed by Flow Cytometry, extracellular ATP release was measured by using an ATP Assay Kit, and the presence of calreticulin (CRT) on the cell surface was evaluated via immunofluorescence. Furthermore, Western blot analysis was conducted to assess the expression levels of apoptosis-related proteins, including cleaved caspase 3, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and cytochrome C (Cyt C). Our findings revealed a significant, dose-dependent inhibition of A549 and H1299 cell proliferation and a marked increase in the apoptosis rate upon treatment with Thioridazine. Additionally, there was an elevation in extracellular ATP secretion and CRT expression on the cell surface, indicative of ICD occurrence. Consistently, the expression level of Bcl-2 decreased, while Bax, Cyt C, and cleaved caspase 3 were up-regulated that further indicate the induction apoptosis of tumor cell by Thiolidazine. Collectively, our results confirm that Thioridazine inhibits the proliferation of lung adenocarcinoma cells by inducing ICD through the mitochondrial stress signaling pathway. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is one of the most common malignant tumors in the world, and the current lung cancer screening and treatment strategies are constantly improving, but its 5-year survival rate is still very low, which seriously endangers human health. Therefore, it is critical to explore new biomarkers to provide personalized treatment and improve the prognosis. Cuproptosis is a newly discovered type of cell death, which is due to the accumulation of excess copper ions in the cell, eventually leading to cell death, which has been suggested by studies to be closely related to the occurrence and development of lung adenocarcinoma (LUAD). Based on The Cancer Genome Atlas (TCGA) database, this study explored the association between cuproptosis-related genes (CRGs) and LUAD prognosis, established a prognostic risk model, and analyzed the interaction between CRGs and LUAD immune cell infiltration. Methods The RNA-seq data of LUAD tissue and paracancerous or normal lung tissue were downloaded from the TCGA database; the RNA-seq data of normal lung tissue was downloaded from the Genotype-tissue Expression (GTEx) database, and the data of 462 lung adenocarcinoma cases were downloaded from the Gene Expression Omnibus repository (GEO) as verification. T the risk score model to assess prognosis was constructed by univariate Cox and Lasso-Cox regression analysis, and the predictive ability of the model was evaluated by receiver operating characteristic (ROC) curve and calibration curve. Immune-related and drug susceptibility analysis was further performed on high- and low-risk groups. Results A total of 1656 CRGs and 1356 differentially expressed CRGs were obtained, and 13 CRGs were screened out based on univariate Cox and Lasso-Cox regression analysis to construct a prognostic risk model, and the area under the curves (AUCs) of ROC curves 1-, 3- and 5- year were 0.749, 0.740 and 0.689, respectively. Further study of immune-related functions and immune checkpoint differential analysis between high- and low-risk groups was done. High-risk groups were more sensitive to drugs such as Savolitinib, Palbociclib, and Cytarabine and were more likely to benefit from immunotherapy. Conclusion The risk model constructed based on 13 CRGs has good prognostic value, which can assist LUAD patients in individualized treatment, and provides an important theoretical basis for the treatment and prognosis of LUAD. [ABSTRACT FROM AUTHOR]

Objective: In order to explore the function and influence of long non-coding RNA SNAI3-AS1(LncRNA SNAI3-AS1,SNAI3-AS1) in the progression of osteoarthritis(OA). Methods: LncRNA SNAI3-AS1 was screened by whole-transcriptome sequencing,and its expression in cell model of chondrocyte degeneration was detected by real-time quantitative fluorescence polymerase chain reaction(q RT-PCR). Transfecting SNAI3-AS1-specific si-RNA or eukaryotic overexpression plasmid in chondrocytes to knock down or overexpress SNAI3-AS1 separately. The proliferation activity of chondrocytes was detected by MTT assay, plate colony assay and EdU assay, and the expression of inflammatory and extracellular matrix proteins was detected by Western Blot. The lncRNA-miRNA and miRNA-m RNA interactions were predicted by bioinformatics website, and verified by dual luciferase reporter gene and RIP assay. Results: Compared with normal human chondrocytes, the expression level of SNAI3-AS1 was significantly down-regulated in OA. And knockdown of SNAI3-AS1 in chondrocytes can reduce chondrocyte proliferation and promote chondrocyte degeneration, while overexpression of SNAI3-AS1 in chondrocytes of OA model can enhance chondrocyte proliferation and inhibit chondrocyte degeneration. In terms of mechanism, SNAI3-AS1 can act as a competitive endogenous RNA(ceRNA), which indirectly up-regulates PRELP by sponging miR-2278, and plays a role in promoting chondrocyte proliferation and inhibiting its degeneration. Conclusion: LncRNA SNAI3-AS1 is involved in the occurrence and development of osteoarthritis through the lncRNA SNAI3-AS1/miR-2278/PRELP axis. [ABSTRACT FROM AUTHOR]

The aim of this study is to establish the IPEC-J2 cell line with MDH2 gene knockout by CRISPR/Cas9 genome editing technology and investigate whether MDH2 gene knockout confers resistance to deoxynivalenol. sgRNA sequences targeting MDH2 gene were designed and cloned into PX459 vector; the recombinant plasmid PX459-sgRNA-MDH2 was introduced into the IPEC-J2 cells by electroporation，and puromycin was added to screen KO cell colony generations. The MDH2 KO single cell colony generations were isolated by limited dilution method and validated by genotype sequencing, quantitative PCR and Western blotting to obtain MDH2-KO monoclonal cell colony generation. Finally, the cell viability was detected by CCK8 kit and apoptosis and necrosis assay kit to determine the resistance of MDH2 knockout cell colony generation to deoxynivalenol. The sequencing results showed that the MDH2 knockout vector was successfully constructed. The obtained cell colony generations were validated as MDH2 knockout monoclonal cell colony generations by RT-qPCR and immunoblotting. The CCK8 cell viability assay showed that knockout of MDH2 increased the viability of IPEC-J2 cells by 18.67%, 19.59%, 26.36%, and 27.01% at different concentrations of deoxynivalenol（4, 2, 1, and 0.5 μg/mL）for 5 d compared with wild-type cells. Flow cytometry assays showed that knockout of MDH2 reduced the mortality rate of IPEC-J2 cells by 30.33%, 15.81%, 16.00%, and 14.70% at different concentrations of deoxynivalenol respectively compared with wild-type cells for 5 d. We obtained the MDH2-KO monoclonal cell colony generation by editing the MDH2 gene in IPEC-J2 cells using the CRISPR/Cas9 system. The resistance of MDH2-KO cell colony generation to deoxynivalenol was demonstrated by cell viability and cell death assays, which provids insight into the toxic mechanism of deoxynivalenol-induced cell death and offers a new strategy for the prevention and treatment of deoxynivalenol. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Oil Crop Sciences is the property of Oil Crops Research Institute of Chinese Academy of Agricultural Sciences 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.)

Type III secreted effectors are the key pathogenic factors secreted by Acidovorax citrulli, the pathogen of bacterial fruit blotch （BFB）. To identify the T3SE gene aop2 with GNAT（Gcn5-related N-acetyltransferase）superfamily domain, which is specific for Acidovorax citrulli, and to analyze the way that its encoded protein affects plant immunity, will lay a foundation for further understanding the role of this gene in pathogen pathogenesis. Bioinformatics was applied to analyze the sequence characteristics . Fluorescence quantitative PCR was used to analyze the expression regulation of aop2 and its relationship with the expression of disease-resistant genes. Gene mutation and gene function complementation was to analyze the gene function, including pathogenicity and host reactive oxygen species accumulation. Transient expression technique was used to investigate the ability of Aop2 inhibitory elicitor to induce necrosis and its subcellular localization. There was a core gene binding site of Type III secretion system（T3SS）in the promoter region of aop2 gene, and there was no signal peptide or transmembrane helical region in the encoded protein, and there was a GNAT family acetyltransferase domain but no homologous protein. The expression of aop2 gene in hrpG/hrpX mutant of T3SS significantly decreased. The mutant with aop2 gene deletion decreased the pathogenicity of host cucumber, but increased the accumulation of reactive oxygen species in cucumber cotyledon. Aop2 can be localized to whole tobacco cells and inhibited programmed cell death（PCD）induced by NIP. The expression of Aop2 enhanced the expression of genes involved in SA and JA signaling pathways triggered by pathogen-related molecular patterns in tobacco leaves. The results showed that Aop2 was a specific T3SE containing GNAT domain in A. citrulli. Aop2 played the function of virulence factor in the interaction with cucumber and was involved in the regulation of plant cell death and PTI and phytohormone-related disease resistance in the interaction with tobacco. [ABSTRACT FROM AUTHOR]

In order to investigate the effects of cinnamaldehyde(CA)on salt tolerance of tomato seedlings, we used tomato ‘Cooperative 903' as experimental material, and investigated the characteristics of germination and seedling growth of tomato under NaCl(100 mmol·L-1)stress compared with the treatment of adding CA(100 μg·L-1). We set up four groups of treatments in the experiment: Control(CK, distilled water), NaCl(100 mmol·L-1), NaCl+CA(100 mmol·L-1 NaCl + 100 μg·L-1 CA), and CA(100 μg·L-1). The results were as follows:(1)With the application of CA, the germination potential and the germination rate of tomato seeds were both improved. The root length and fresh weight of tomato seedlings were also significantly increased under NaCl(100 mmol·L-1)stress.(2)CA could effectively alleviate the excessive accumulation, oxidative damage and cell death of total ROS caused by salt stress in roots of tomato seedlings. To sum up, CA can improve the salt tolerance of tomato during germination and seedling stage by alleviating the degree of oxidative damage of seedlings, and CA has the potential in field production as a new preparation. [ABSTRACT FROM AUTHOR]

BACKGROUND: The chondrogenic differentiation of human adipose-derived mesenchymal stem cells is affected by many factors. Studies have confirmed that long noncoding RNAs (lncRNAs) play important roles in epigenetic regulation, transcription and post-transcriptional regulation. However, there are few reports on the changes of its expression profile and its regulatory role during the chondrogenic differentiation of human adipose-derived mesenchymal stem cells. OBJECTIVE: To preliminarily analyze the differentially expressed lncRNAs and their potential functions during the chondrogenesis of human adipose-derived mesenchymal stem cells. METHODS: The human adipose-derived mesenchymal stem cells at 0 day (undifferentiated group) and 14 days (differentiated group) after chondrogenic differentiation were used as research objects. RNA-seq was used to screen lncRNAs and messenger RNAs (mRNAs) with expressed fold change larger than twice between groups. Quantitative real time PCR (qRT-PCR) was used to verify the sequencing results. Bioinformatics analyses including GO function analysis and KEGG pathway analysis were performed for differentially expressed genes to screen adjacent genes and co-expressed genes of lncRNAs. RESULTS AND CONCLUSION: (1) Compared with the undifferentiated group, a total of 816 lncRNAs and 5 138 mRNAs were significantly differentially expressed in the differentiated group. (2) GO function and KEGG signaling pathway analysis showed that differentially expressed genes were enriched in several biological processes including cellular processes, biological regulation, and metabolic processes, and multiple pathways including focal adhesion kinase, insulin signaling pathway, and Wnt signaling pathway. (3) Analysis results of adjacent genes and co-expressed genes of differentially expressed lncRNAs indicated that some lncRNAs such as SNHG16 and XLOC_003886 might play critical roles in the chondrogenic differentiation of adipose-derived mesenchymal stem cells and cartilage degeneration. (4) These findings suggest that the expression profiles of lncRNAs were significantly altered during the chondrogenesis of adiposederived mesenchymal stem cells. The biological functions of differentially expressed lncRNAs may be closely related to the functions of adjacent genes and coexpressed genes, thereby regulating the chondrogenic differentiation of adipose-derived mesenchymal stem cells. However, further experiments should be employed to uncover the regulatory roles and underlying molecular mechanisms of differentially expressed lncRNAs. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology 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 Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine 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.)

Ferroptosis, as a regulated and non-apoptotic form of cell death, provides a new research direction for tumor therapy. Ferroptosis is involved in the development of drug resistance in some tumors and also in the treatment process of many tumor therapies, which is a neglected mechanism in tumor therapy. This article will introduce the relationship between ferroptosis and different tumor treatment therapies from the aspects of tumor chemotherapy, tumor radiation therapy and tumor immunotherapy, and summarize the strategies of improving tumor treatment effect by ferroptosis, in order to provide reference for tumor treatment.

Objective To explore the role of STX17 protein in Aβ-induced death of mouse hippocampal neuronal cells. Methods Based on Weighted correlation network analysis (WGCNA), the modules significantly related to Alzheimer's disease (AD) were selected, and key genes were screened for cross-fertilization with autophagy gene bank and SNARE family genes. Aβ31-35 at a concentration of 1 g/L was used to inject the C57BL/6 mouse hippocampal tissue, and HT22 hippocampal neuronal cells were treated with 5 μmol/L Aβ31-35. Then the protein expression of STX17, LC3 Ⅱ and P62 was detected by Western blotting. The survival rate of the HT22 hippocampal neuronal cells treated by using Aβ31-35 was detected by CCK-8 assay. Protein expression of LC3Ⅱ and P62 were determined by Western blotting after overexpression STX17 in HT22 hippocampal neuronal cells. Results The Salmon and Black modules significantly associated with AD crossed with autophagic gene pool and SNARE subfamily intersection STX17, respectively. Under the action of Aβ31-35 mouse hippocampal tissue and mouse HT22 hippocampal neuronal cells, and the survival rate of HT22 cells [(81.81±11.65)% vs (100.00±12.89)%, P < 0.05] were decreased significantly, and the expression of STX17 was significantly reduced in both tissue and cells (P < 0.05). The expression of tissue LC3Ⅱ and P62 proteins were significantly elevated in the tissue (P < 0.05), and in the cells (P < 0.05). After lentivirus-mediated overexpression of STX17 in HT22 hippocampal neuronal cells, the protein expression upregulation of LC3II and P62 induced by Aβ31-35 was significantly reversed, and the survival rate was improved in Aβ31-35-induced HT22 hippocampal neuronal cells [(101.91±13.81)% vs (79.21±8.75)%, P < 0.05]. Conclusion STX17 improves Aβ-induced death of mouse hippocampal neuronal cells by promoting autophagy.

Glioma is the most common primary malignant tumor in the central nervous system, and ferroptosis is a newly discovered form of cell death that has been linked to cancer, including glioblastoma (GBM). Drugs that target different molecules associated with ferroptosis and stimulate this process have been described as a potential adjuvant anti-cancer treatment option. In GBM, ferroptosis stimulates inhibition of tumor growth, improves patient survival, and increases the efficacy of radiation and chemotherapy. This article summarizes the current research progress on the regulation of ferroptosis in glioblastoma. [ABSTRACT FROM AUTHOR]

To investigate the mechanism of Zhuangfang Rougan Huaxian Granule on liver tissue pathology in rats with liver fibrosis. Eighty male Wistar rats were randomly divided into normal control group, pathological model group, low, medium and high dose groups of Rougan Huaxian Granules, with 16 rats in each group. Carbon tetrachloride compound factors were used to make models, observe and record the morphology of rat liver, observe the changes of rat liver tissue and collagen fibers with HE staining and Masson staining, detect the values of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) indicators, and analyze the contents of glutathione peroxidase (GSH-Px), hydroxyproline (HYP), superoxide dismutase (SOD) and malondialdehyde (MDA) in rat liver tissue. The degree of liver cell degeneration, necrosis and fibrotic tissue proliferation of rats in the low, middle and high dosage groups of Rougan Huaxian granules were significantly reduced compared with those in the pathological model group. Compared with the pathological model group, the levels of serum ALT, AST, HYP and MDA in liver tissue in the low, middle and high dose groups of Rougan Huaxian Granules decreased in a dose-dependent manner (P<0.001), while the levels of GSH-Px and SOD in the high dose group of Rougan Huaxian Granules were significantly higher than those in the pathological model group(P<0.001). Rugan Huaxian Granule can effectively improve the damage of hepatocytes in rats with liver fibrosis, reduce the degree of inflammation of their liver tissues, and has certain liver protection and anti fibrosis effects on rats with liver fibrosis. Its mechanism may be related to increasing the level of GSH-Px and SOD, reducing the content of HYP and MDA, reducing the level of oxidative stress, regulating lipid metabolism, and reducing the synthesis of collagen in the body. [ABSTRACT FROM AUTHOR]

As a novel star molecule, gasdermin D (GSDMD)plays an important role in the amplification of immune inflammatory response and the process of pyroptosis. After being cleaved and activated by caspase - 1,the N - terminal of GSDMD is rapidly released, which anchors on the cell membrane and forms pores, thereby leading to pyroptosis, accompanied by the release of a large amount of the strong proinflammatory factors IL - 1ß and IL - 18. Acute / chronic liver inflammatory response and cell death are the common pathological features of liver diseases such as viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease, autoimmune liver disease, liver failure, and hepatocellular carcinoma. This article summarizes the basic structural characteristics of GSDMD and elaborates on its important role in the pathological progression of various liver diseases. In addition, it is proposed that prevention and treatment strategies with GSDMD as a potential therapeutic target can provide new ideas for further studies on the clinical prevention and treatment of liver diseases. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of quercetin on microcirculation and liver lesions in cirrhotic rats based on Bcl-2/CytC regulatory network. Methods: Forty-five clean SD rats were selected and divided into group A, LC group, QUE Low group, QUE High group, ETV group, 10 rats per group by random number table method. Liver cirrhosis model was established except for 10 healthy rats. QUE Low group was given quercetin 50 mg/kg intragastric administration. QUE High group was given quercetin 100 mg/kg intragastric administration, ETV group was given Entecavir dispersible tablets 0.5 mg/time intragastric administration, group A and LC were given normal saline intragastric administration, once A day, for A total of 14 days. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG) and the contents of thrombin A2 (TXA2), angiotensin II (Ang ii) and prostacyclin (PGI2) in serum of rats were detected by ELISA. Liver morphology of each group was compared by HE staining. West- ern blotting was used to detect the expression of bcl-2, Bax and cytochrome C (CytC) proteins in rat liver tissue. Results: Compared with A group, ALT, AST, TC, TG, TXA2 and AngII expressions were higher in LC group, while PGI2, CytC and Bax were lower (P<0.05). Compared with LC group, ALT, AST, TC, TG, TXA2 and AngII in QUE Low group were decreased, while PGI2, CytC and Bax were increased (P<0.05). Compared with QUE Low group, ALT, AST, TC, TG, TXA2 and Angll of ETV group decreased, while PGI2, CytC and Bax increased (P<0.05). Compared with ETV group, ALT, AST, TC, TG, TXA2 and Angll in QUE High group were decreased, while PGI2, CytC and Bax were increased (P<0.05). The liver tissues of group A were intact. The liver tissue of LC group rats was severely damaged. QUE Low group rats still had fibrous tissue hyperplasia and inflammatory infiltration in liver interstitium. ETV group still had hepatocyte degeneration and inflammatory factors. In QUE High group, the degeneration reaction of liver tissue and inflammation of portal area were decreased. Compared with A group, LC group had obvious liver fibrosis, liver cell degeneration and necrosis and inflammatory cell infiltration (P<0.05). Compared with LC group, liver fibrosis was alleviated in QUE Low group (P<0.05); Compared with QUE Low group, liver fibrosis, degeneration necrosis and inflammatory cell infiltration were alleviated in ETV group (P<0.05). Compared with ETV group, liver fibrosis, degeneration necrosis and inflammatory cell infiltration were improved in QUE High group (P<0.05). Conclusion: Quercetin has a protective effect on liver tissue of cirrhotic rats, improving liver function, liver microcirculation and liver lesions, and its mechanism may regulate bcl-2, Bax, CytC and other related proteins. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy 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 Practical Oncology Journal is the property of Journal of Practical Oncology 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.)