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Cyanra cardunclus L. var. ferocissima is widely used in Morocco as a food and in traditional medicine. Therefore, this study aimed to determine, for the first time, the phytochemical content and antioxidant and anti-inflammatory activities of this variety. Qualitative tests were used to screen for the phytochemical compounds present in the extract, and spectrophotometric methods were used for quantification. The sugar profiles were determined using HPLC. Antioxidant activity was determined in vitro using DPPH, FRAP, and total antioxidant activity assays, and anti-inflammatory activity was assessed using serum albumin denaturation and membrane stabilization assays. The extract contained a high amount of total polyphenols, hydrocinnamic acids, anthocyanins, chlorophyll, ortho-diphenols, terpenoids, and triterpenoids. In addition, five sugars were identified with high amounts of raffinose and sucrose. The extract exerted considerable antioxidant activity by scavenging radicals and reducing power. It exerts anti-inflammatory effects by inhibiting protein denaturation and heat-inducing hemolysis. From the correlation results, anthocyanin, polyphenol, and triterpenoid contents were strongly correlated with DPPH free radical scavenging activity. Orthodiphenols, flavonols, and chlorophyll α were strongly correlated with FRAP, whereas orthodiphenols, hydrocinnamic acids, and triterpenoids were strongly correlated with total antioxidant activity. In terms of anti-inflammatory activity, orthodiphenols, hydrocinnamic acids, and triterpenoids correlated strongly with inhibition of bovine serum albumin denaturation activity, whereas terpenoids, flavonols, and chlorophyll correlated strongly with red cell membrane-stabilizing activity. In conclusion, the Moroccan Cynara cardunclus var. ferocissima leaf methanolic extract constitutes a promising source of phytochemicals with considerable antioxidant and anti-inflammatory activity., Competing Interests: Declarations Human and Animal Participants This article does not contain any studies with human or animal subjects. Competing Interests The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Hyperlipidemia, a condition characterized by elevated levels of lipids in the blood, poses a significant risk factor for various health disorders, notably cardiovascular diseases. Phytochemical compounds are promising alternatives to the current lipid-lowering drugs, which cause many undesirable effects. Based on in vivo and clinical studies, combining phytochemicals with other phytochemicals, prebiotics, and probiotics and their encapsulation in nanoparticles is more safe and effective for managing hyperlipidemia than monotherapy. To this end, the results obtained and the mechanisms of action of these combinations were examined in detail in this review., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. All authors declare having no conflict of interest or personal relationships that could influence this work., (Copyright © 2023. Published by Elsevier Ltd.)

Background: Oxidative stress and chronic inflammation, at both the systemic and the central level, are critical early events in atherosclerosis and Alzheimer's disease (AD)., Purpose: To investigate the oxidative stress-, inflammation-, and Tau-phosphorylation-lowering effects of pomegranate polyphenols (PPs) (punicalagin, ellagic acid, peel, and aril extracts)., Methods: We used flow cytometry to quantify the protein expression of proinflammatory cytokines (IL-1β) and anti-inflammatory mediators (IL-10) in THP-1 macrophages, as well as M1/M2 cell-specific marker (CD86 and CD163) expression in human microglia HMC3 cells. The IL-10 protein expression was also quantified in U373-MG human astrocytes. The effect of PPs on human amyloid beta 1-42 (Aβ 1-42 )-induced oxidative stress was assessed in the microglia by measuring ROS generation and lipid peroxidation, using 2',7'-dichlorofluorescein diacetate (DCFH-DA) and thiobarbituric acid reactive substance (TBARS) tests, respectively. Neuronal viability and cell apoptotic response to Aβ 1-42 toxicity were assayed using the MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) assay and the annexin-V-FITC apoptosis detection kit, respectively. Finally, flow cytometry analysis was also performed to evaluate the ability of PPs to modulate Aβ 1-42 -induced Tau-181 phosphorylation (pTau-181)., Results: Our data indicate that PPs are significantly ( p < 0.05) effective in countering Aβ 1-42 -induced inflammation through increasing the anti-inflammatory cytokines (IL-10) in U373-MG astrocytes and THP1 macrophages and decreasing proinflammatory marker (IL-1β) expression in THP1 macrophages. The PPs were also significantly ( p < 0.05) effective in inducing the phenotypic transition of THP-1 macrophages and microglial cells from M1 to M2 by decreasing CD86 and increasing CD163 surface receptor expression. Moreover, our treatments have a significant ( p < 0.05) beneficial impact on oxidative stress, illustrated in the reduction in TBARS and ROS generation. Our treatments have significant ( p < 0.05) cell viability improvement capacities and anti-apoptotic effects on human H4 neurons. Furthermore, our results suggest that Aβ 1-42 significantly ( p < 0.05) increases pTau-181. This effect is significantly ( p < 0.05) attenuated by arils, peels, and punicalagin and drastically reduced by the ellagic acid treatment., Conclusion: Overall, our results attribute to PPs anti-inflammatory, antioxidant, anti-apoptotic, and anti-Tau-pathology potential. Future studies should aim to extend our knowledge of the potential role of PPs in Aβ 1-42 -induced neurodegeneration, particularly concerning its association with the tauopathy involved in AD.

Accumulating evidence proves that children with autism have gastrointestinal problems. However, a significant difference in gut microbiota (GM) exists between autistic and non-autistic children. These changes in the GM may stem from several factors. Recently, researchers focused on nutritional factors, especially vitamin deficiency. Thus, our systematic review investigates the connections among autism, GM alterations, and vitamin A deficiency (VAD), by analyzing studies sourced from PubMed and Embase databases spanning from 2010 to 2022. Adhering to PRISMA guidelines, we meticulously selected 19 pertinent studies that established links between autism and GM changes or between autism and VAD. Our findings uniformly point to significant alterations in the GM of individuals with autism, indicating these changes as promising biomarkers for the disorder. Despite the consistent association of GM alterations with autism, our analysis revealed no notable differences in GM composition between individuals with autism and those experiencing VAD. This suggests that VAD, especially when encountered early in life, might play a role in the onset of autism. Furthermore, our review underscores a distinct correlation between reduced levels of retinoic acid in children with autism, a disparity that could relate to the severity of autism symptoms. The implications of our findings are twofold: they not only reinforce the significance of GM alterations as potential diagnostic markers but also spotlight the critical need for further research into nutritional interventions. Specifically, vitamin A supplementation emerges as a promising avenue for alleviating autism symptoms, warranting deeper investigation into its therapeutic potential.

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders defined by a lack of social behaviors, repetitive behaviors and nonverbal interactions, such as limited eye contact, facial expression, and body gesturing. It is not a single condition, but rather a multi-factorial disorder caused by hereditary and non-genetic risk factors, as well as their interaction. According to several studies, the gut microbiota may have a role in the pathophysiology of autism spectrum disorder. Various studies have found differences in the composition of the gastrointestinal (GI) microbiota in children with ASD compared to unaffected siblings and/or healthy unrelated controls. The processes that relate the gut microbiota to brain dysfunctions (the gut-brain axis) in ASD are yet to be fully understood. However, the differences in the gastrointestinal composition might be due to vitamin A deficiency because vitamin A (VA) plays a role in the regulation of the intestinal microbiota. This narrative review discusses the impact of vitamin A deficiency on the gut microbiota composition and tries to understand how this may contribute for the development and severity of ASD.

Modern research achievements support the health-promoting effects of natural products and diets rich in polyphenols. Pomegranate (PG) ( Punica granatum L.) contains a considerable number of bioactive compounds that exert a broad spectrum of beneficial biological activities, including antimicrobial, antidiabetic, antiobesity, and atheroprotective properties. In this context, the reviewed literature shows that PG intake might reduce insulin resistance, cytokine levels, redox gene expression, blood pressure elevation, vascular injuries, and lipoprotein oxidative modifications. The lipid parameter corrective capabilities of PG-ellagitannins have also been extensively reported to be significantly effective in reducing hyperlipidemia (TC, LDL-C, VLDL-C, and TAGs), while increasing plasma HDL-C concentrations and improving the TC/HDL-C and LDL-C/HDL-C ratios. The health benefits of pomegranate consumption seem to be acheived through the amelioration of adipose tissue endocrine function, fatty acid utilization, GLUT receptor expression, paraoxonase activity enhancement, and the modulation of PPAR and NF-κB. While the results from animal experiments are promising, human findings published in this field are inconsistent and are still limited in several aspects. The present review aims to discuss and provide a critical analysis of PG's bioeffects on the components of metabolic syndrome, type-2 diabetes, obesity, and dyslipidemia, as well as on certain cardiovascular-related diseases. Additionally, a brief overview of the pharmacokinetic properties, safety, and bioavailability of PG-ellagitannins is included.

Graphene oxide (GO) is a graphene derivative used for numerous applications in which biomedical uses are significant. However, for this application, the security of GO is doubtful. In this work, we synthesized this nanoparticle to assess its toxicity in male mice. In addition, we studied the effects of this nanomaterial on behavior by administering GO intraperitoneally to mice at different doses (2 mg/kg and 5 mg/kg) for five days. Subsequently, we performed biochemical analyses of blood serum and measured peroxidase and malondialdehyde (MDA) activity. Then, we performed histological sections to evaluate the brain's and liver's pathological and morphological changes. The data showed that the open field tests did not alter the locomotor activity. Furthermore, the elevated cross-maze tests showed no anxiety effect in the GO doses in the animals. The biochemical analyses indicated that GO influenced the level of biochemical parameters. Although, the oxidative stress assay showed an increase in peroxidase and MDA activity after GO intoxication. However, histopathological analysis of liver sections showed that GO caused liver inflammation, whereas, at the brain level, GO did not affect neuronal cells. The results indicate that GO caused toxic effects and that its toxicity could be mediated by oxidative stress., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)