The World Health Organization has described the 2019 Coronavirus disease caused by an influenza-like virus called SARS-CoV-2 as a pandemic. Millions of people worldwide are already infected by this virus, and severe infection causes hyper inflammation, thus disrupting lung function, exacerbating breath difficulties, and death. Various inflammatory mediators bio-synthesized through the arachidonic acid pathway play roles in developing cytokine storms, injuring virus-infected cells. Since pro-inflammatory eicosanoids, including prostaglandins, and leukotrienes, are key brokers for physiological processes such as inflammation, fever, allergy, and pain but, their function in COVID-19 is not well defined. This study addresses eicosanoid's crucial role through the arachidonic pathway in inflammatory cascading and recommends using bioactive lipids, NSAIDs, steroids, cell phospholipase A2 (cPLA2) inhibitors, and specialized pro-resolving mediators (SPMs) to treat COVID-19 disease. The role of soluble epoxide hydrolase inhibitors (SEHIs) in promoting the activity of epoxyeicosatrienoic acids (EETs) and 17-hydroxide-docosahexaenoic acid (17-HDHA) is also discussed. Additional research that assesses the eicosanoid profile in COVID-19 patients or preclinical models generates novel insights into coronavirus-host interaction and inflammation regulation.

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An influenza-like virus named SARS-CoV-2 is responsible for COVID-19 disease and spread worldwide within a short time. COVID-19 has now become a significant concern for public health. Obesity is highly prevalent worldwide and is considered a risk factor for impairing the adaptive immune system. Although diabetes, hypertension, cardiovascular disease, and renal failure are considered the risk factors for COVID-19, obesity is not yet well-considered. This study approaches establishing a systemic association between the prevalence of obesity and its impact on immunity concerning the severe outcomes of COVID-19 utilizing existing knowledge. Overall study outcomes documented the worldwide prevalence of obesity, its effects on immunity, and a possible underlying mechanism covering obesity-related risk pathways for the severe outcomes of COVID-19. Overall understanding from the present study is that being an immune system impairing factor, the role of obesity in the severe outcomes of COVID-19 is worthy.

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The present research study was designed to evaluate the effect of zinc supplementation on body weight, serum triglyceride, cholesterol, glucose homeostasis, oxidative stress, and hepatic function in mice. Mice were treated with zinc sulphate at an equivalent weight of 6.5 mg/kg-body weight elemental zinc for four weeks. Bodyweight, serum glucose, triglyceride, cholesterol, serum MDA, nitric oxide, vitamin C, and hepatic enzymes level were determined at the end of the study period. Data from this study showed that supplementation with zinc in mice maintained a balanced blood glucose homeostasis throughout the experimental period. Moreover, treatment with zinc showed a significant (p <0.05) decrease in serum triglyceride and cholesterol level along with a decrease in the body weight compared to control. Treatment with zinc significantly attenuated the rate of lipid peroxidation whereas increased the level of vitamin C and NO level. The protective effect of zinc on liver activity was observed. Treatment with zinc showed a strong negative association with serum total cholesterol (r= -0.934, p = 0.02), triglycerides level (r= -0.709, p = 0.05), and body weight (r= -0.899, p = 0.01). The present findings demonstrate that zinc supplementation can be helpful to maintain a glucose homeostasis, ameliorate hyperlipidemia, oxidative stress, and liver dysfunction. Therefore, zinc supplementation can be suggested to alleviate diseases associated with metabolic syndrome and oxidative stress. Dhaka Univ. J. Pharm. Sci. 20(1): 59-66, 2021 (June)