Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the increased risk of some life-threatening complications such as pulmonary embolism, myocardial infarction, and ischemic stroke. In this regard, overproduction of proinflammatory cytokines such as IL-6, IL-1β, and TNF-α induce cytokine storms, increase the risk of clot formation, platelet activation, and multiorgan failure that may eventually lead to death among these patients. Surface S protein of SARS-CoV-2 binds to its target transmembrane receptor, named as angiotensin converting enzyme 2 (ACE2(, on various cells such as lymphocyte, alveolar cells, monocytes/macrophages, and platelets. Notably, the activation of the coagulation cascade occurs through tissue factor (TF)/FVIIa-initiated hemostasis. Accordingly, TF plays the major role in the activation of coagulation system during viral infection. In viral infections, the related coagulopathy multiple factors such as inflammatory cytokines and viral specific TLRs are involved, which consequently induce TF expression aberrantly. SARS-COV-2 may directly infect monocytes/ macrophages. In addition, TF expression/release from these cells may play a critical role in the development of COVID-19 coagulopathy. In this regard, the use of TF- VIIa complex inhibitor may reduce the cytokine storm and mortality among COVID-19 patients.

Background. Cisplatin is a powerful chemotherapeutic drug mainly used in the treatment of solid tumors. Aggregation of the drug in renal proximal tubule cells causes nephrotoxicity and renal failure. Investigations showed nephrotoxicity as Cisplatin’s dose‐limiting side effect. One of the Cisplatin toxicity mechanisms is generation of reactive oxygen species, which leads to oxidative stress and renal damage. The purpose of this study was evaluation of the modulating effects of Gallic acid on Cisplatin‐induced variations including Caspase‐3 and Clusterin expression and histopathological and biochemical parameters in adult male Wistar rats. Method. Rats were kept under standard condition of temperature, light, and humidity. The animals were divided into 4 groups: GpI: control group (received distilled water for 10 days); GpII: Gallic acid (alone) (50 mg/kg bw, once a day for 10 days); GpIII: Cisplatin (alone), single dose (6 mg/kg bw, I.P. on 5th day of study); GpIV: Gallic acid (50 mg/kg bw, once a day for 10 days) and also injected with single dose of Cisplatin (6 mg/kg bw, I.P., on 5th day of study). After 10 days, all rats were anaesthetized and plasma collected to estimate urea, creatinine, and uric acid. The right kidneys were removed for the study of gene expression and biochemical parameters. The left kidneys were used for histopathological studies. Results. The Cisplatin‐induced nephrotoxicity was evident from the elevated levels of creatinine, urea, uric acid, and renal tissue MDA and also decreased levels of SOD, CAT, GPX, and GSH in renal tissue. Administration of Gallic acid significantly modulated nephrotoxicity markers, gene expression variations, and histopathological damage. Conclusion. Outcomes of the present investigation suggest that Gallic acid provides protection against CP‐induced nephrotoxicity, but for application in people, further studies are needed.

Introduction: Multiple sclerosis (MS) is a chronic, autoimmune, and neurodegenerative disease that affects the central nervous system. Royal jelly (RJ), a nutrient-rich substance known for its anti-inflammatory and antioxidant properties, holds potential in impeding disease progression by mitigating inflammatory processes and oxidative stress. This study was undertaken to explore the impact of RJ on oxidative stress and inflammatory markers in individuals diagnosed with MS. Methods: This randomized clinical trial involved the allocation of 35 MS patients into two groups: intervention (n = 19) and control (n = 16). The intervention group received daily 500 mg RJ capsules for a duration of 2 months, while the control group received placebo capsules. Prior to and following the intervention, the Expanded Disability Status Scale (EDSS) was ascertained for the patients. Furthermore, the serum levels of inflammatory markers interleukin (IL-1B), IL-6, tumor necrosis factor (TNF), and interferon (IFN), in addition to the oxidative stress indices catalase (CAT), malondialdehyde (MDA), superoxide dismutase, and nitric oxide were evaluated. The data were analyzed using the GraphPad Prism software. Results: After the intervention, the mean EDSS score significantly decreased in the case group compared to pre-intervention (P < 0.05). Levels of MDA, IL-1B, TNF, and IFN significantly decreased in the case group post-intervention (P < 0.05). Additionally, a significant increase in CAT enzyme levels was observed in the case group after two months (P < 0.05). In contrast, the control group showed a significant increase in MDA levels after 2 months compared to baseline (P < 0.05). Conclusion: Our findings suggest that RJ supplementation may have beneficial effects on inflammatory markers, oxidative stress indices and quality of life in MS patients.

Background: Areas with a higher prevalence of vitamin D deficiency have reported a higher frequency of severe coronavirus disease 2019 (COVID-19) infections. Objectives: This study aimed to assess the possible association between vitamin D and COVID-19. Methods: This study examined the vitamin D status, hepatic, serologic, and hematologic parameters of COVID-19 patients who tested positive upon admission to a major referral center in southwest Iran. A total of 50 cases and 50 controls were enrolled in the study after obtaining informed consent. The patients did not receive a vitamin D supplement during their hospitalization. Results: Patients with insufficiency and deficiency of vitamin D3 had a longer hospitalization time, a higher likelihood of ICU admission, and a greater risk of death compared to cases with sufficient levels of vitamin D. Conclusions: The results of this study showed that vitamin D deficiency is associated with increased severity and mortality rates. Therefore, using a vitamin D supplement may help reduce the severity of COVID-19.