Background and Objectives. Environmental pollution with the different Aluminum (Al) containing compounds has been increased. Liver and kidney are two vital organs targeted by Al accumulation. The aim of this study was to assess the possible protective and curative effects ofLepidium sativumLinn (LS) against Al-induced impairment of liver and kidney in albino rat and to explore the mechanism behind this effect.Materials and Methods. This experimental animal-based study included fifty albino rats divided into five groups, the control, LS-treated (20 mg/kg), AlCl₃-treated (10 mg/kg), AlCl₃then LS, and AlCl₃plus LS-treated, simultaneously for 8 weeks. At the end of the experiment, hepatic and renal functions as well as the biomarkers of antioxidants activities were assessed in the serum. Both liver and kidney were dissected out and histopathologically examined.Results. This study showed that administration of AlCl₃caused a significant (p<0.05) reduction in rats body weight. It significantly increased serum AST, ALT, ALP, bilirubin, urea, and creatinine levels and decreased total protein and albumin. AlCl₃significantly reduced enzymatic (catalase), nonenzymatic (reduced glutathione), and ferric reducing antioxidant power (FRAP) in the serum. Histopathologically, it induced necrosis and degeneration of hepatocytes, glomeruli, and renal tubules. Administration of LS after or along with AlCl₃significantly restored the serum biomarkers of liver and kidney functions to their near-normal levels and had the ability to overcome Al-induced oxidative stress and preserved, to some extent, the normal hepatic and renal structure. The coadministration of LS had a superior effect in alleviating Al-induced changes.Conclusion. Exposure to AlCl₃induced a set of functional and structural changes in the liver and kidney of rats evident through both biochemical and histopathological assessment. The antioxidant activity of LS seeds mediated a protective and curative effect of LS against such changes. Further study through a rigorous clinical trial to prove LS activity on human is recommended.

Background: Bioaccumulation of aluminum in the brain is associated with adverse neuroinflammatory and neurodegenerative changes, such as those seen in Alzheimer’s disease (AD). Objective: This study aimed to assess the impact of the administration of Lepidium sativum (LS) extract on behavioral, biochemical, and cerebral histopathological changes in rats with AlCl₃-induced AD and explore the mechanism behind this effect. Materials and Methods: This study was conducted on 40 male albino rats divided into four groups (n=10): LS (control, 20 mg/kg body weight for 8 weeks), AD (AlCl_3, 10 mg/kg body weight), and an LS-treated AD group. Behavioral assessment included radial armed maze and active avoidance training tests. Proinflammatory cytokines, oxidant/antioxidant markers, Aβ, AchE, tau protein, TGFβ₁, homocysteine, folic acid, and vitamin B₁₂ were biochemically assessed in the serum. The cerebral cortex was histopathologically examined. Results: AlCl₃ administration significantly impaired rats’ memory, indicating AD-like behavioral changes, significantly increased (P< 0.001) oxidative stress markers, enhanced proinflammatory cytokines, and significantly increased AChE (P< 0.001) adding to cytotoxic effects and neuronal loss in the cerebral cortex. LS administration significantly improved the antioxidant parameters, reduced proinflammatory cytokines, and alleviated AD-associated histopathological changes. Conclusion: LS ameliorated AlCl₃-induced changes through its antioxidant, anti-inflammatory, and antiapoptotic effects, suggesting that it has a neuroprotective effect.

Background. The association between hypothyroidism and renal diseases has been described in many studies. Nigella Sativa was among the recently reported natural product that has the potential to prevent renal tissue damage and fibrosis. The aim of this study was to evaluate the possible protective effect of thymoquinone on the structure of the renal cortex of hypothyroid rats and explore the mechanism behind it. Methods. An experimental model of hypothyroidism was induced in adult male Wistar rats by administration of propylthiouracil (6 mg/kg/body weight). One hypothyroid group was treated with thymoquinone at the dose of 50 mg/kg/body weight and compared to the untreated group. Thyroid function and oxidant/antioxidant status were assessed in the serum. Catalase gene expression was assessed using the real-time polymerase chain reaction. The kidney was assessed both histologically and immunohistochemically. Results. Administration of propylthiouracil resulted in a significant decrease in the serum levels of nitric oxide, reduced glutathione, and superoxide dismutase activity while the level of malondialdehyde significantly (p<0.001) increased. Administration of thymoquinone alleviated this effect on the thyroid hormones and significantly increased the serum levels of antioxidants. Thymoquinone significantly (p<0.001) upregulated catalase transcription by about 24-fold and could block the hypothyroidism-induced glomerular and tubular injury. Conclusion. Thymoquinone may have a potential protective effect against hypothyroidism-induced renal injury acting through the attenuation of the oxidative stress and upregulation of renal catalase gene expression.

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease of old age. Accumulation of β-amyloid peptide (Aβ) and mitochondrial dysfunction results in chronic microglial activation, which enhances neuroinflammation and promotes neurodegeneration. Microglia are resident macrophages of the brain and spinal cord which play an important role in maintaining brain homeostasis through a variety of phenotypes, including the pro-inflammatory phenotype and anti-inflammatory phenotypes. However, persistently activated microglial cells generate reactive species and neurotoxic mediators. Therefore, inhibitors of microglial activation are seen to have promise in AD control. The modified TPP/MoS₂ QD blend is a mitochondrion-targeted nanomaterial that exhibits cytoprotective activities and antioxidant properties through scavenging free radicals. In the present study, the cell viability and cytotoxicity of the DSPE-PEG-TPP/MoS₂ QD blend on microglial cells stimulated by Aβ were investigated. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were also assessed. In addition, pro-inflammatory and anti-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), transforming growth factor beta (TGF-β), inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-I) were measured in the presence or absence of the DSPE-PEG-TPP/MoS₂ QD blend on an immortalized microglia cells activated by accumulation of Aβ. We found that the DSPE-PEG-TPP/MoS₂ QD blend was biocompatible and nontoxic at specific concentrations. Furthermore, the modified TPP/MoS₂ QD blend significantly reduced the release of free radicals and improved the mitochondrial function through the upregulation of MMP in a dose-dependent manner on microglial cells treated with Aβ. In addition, pre-treatment of microglia with the DSPE-PEG-TPP/MoS₂ QD blend at concentrations of 25 and 50 μg/mL prior to Aβ stimulation significantly inhibited the release and expression of pro-inflammatory cytokines, such as IL-1β, IL-6, TNF-α, and iNOS. Nevertheless, the anti-inflammatory cytokines TGF-β and Arg-I were activated. These findings suggest that the modified TPP/MoS₂ QD blend reduced oxidative stress, inflammation and improved the mitochondrial function in the immortalized microglial cells (IMG) activated by Aβ. Overall, our research shows that the DSPE-PEG-TPP/MoS₂ QD blend has therapeutic promise for managing AD and can impact microglia polarization.

Background: By the end of 2019, the COVID-19 pandemic spread all around the world with a wide spectrum of clinical presentations ranging from mild to moderate to severe or critical cases. T cell subtype dysregulation is mostly involved in the immunopathogenic mechanism. The present study aimed to highlight the role of monitoring T cell subtypes and their activation (expression of CD38) in COVID-19 patients compared to healthy subjects and their role in predicting severity and patients’ outcomes. Materials: The study involved 70 adult COVID-19 confirmed cases stratified into three groups: a mild/asymptomatic group, a clinically moderate group, and a clinically severe/critical group. Flow cytometry analysis was used for the assessment of CD3⁺ cells for total T cell count, CD4⁺ cells for helper T cells (Th), CD8⁺ cells for cytotoxic T cells (Tc), CD4⁺CD25⁺ cells for regulatory T cells (T reg), and CD38 expression in CD4⁺ T cells and CD8⁺ T cells for T cell activation. Results: A statistically significant difference was found between COVID-19 cases and healthy controls as regards low counts of all the targeted T cell subtypes, with the lowest counts detected among patients of the severe/critical group. Furthermore, CD38 overexpression was observed in both CD4⁺ and CD8⁺ T cells. Conclusion: Decreased T cell count, specifically CD8⁺ T cell (Tc), with T cell overactivation which was indicated by CD38 overexpression on CD4⁺ and CD8⁺ T cells had a substantial prognostic role in predicting severity and mortality among COVID-19 patients. These findings can provide a preliminary tool for clinicians to identify high-risk patients requiring vigilant monitoring, customized supportive therapy, or ICU admission. Studies on larger patient groups are needed.