Background: Coronavirus-19 (COVID-19) pandemic is a worldwide public health problem that has been known in China since December 25, 2019. Phospholipids are structural components of the mammalian cytoskeleton and cell membranes. They suppress viral attachment to the plasma membrane and subsequent replication in lung cells. In the virus-infected lung, phospholipids are highly prone to oxidation by reactive oxygen species, leading to the production of oxidized phospholipids (OxPLs). Objective: This study was carried out to explain the correlation between the level of plasma phospholipids in patients with COVID-19 infection and the levels of cytokine storms to assess the severity of the disease. Methods: Plasma samples from 34 enrolled patients with mild, moderate, and severe COVID-19 infection were collected. Complete blood count (CBC), plasma levels of D-dimer, ferritin, C-reactive protein (CRP), cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), phospholipids, secretory phospholipase A2 (sPLA2)α2, and cytokine storms were estimated, and lung computed tomography (CT) imaging was detected. Results: The CBC picture showed the presence of leukopenia, lymphopenia, and eosinopenia in patients with COVID-19 infection. Furthermore, a significant increase was found in plasma levels of D-dimer, CRP, ferritin, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-13 as well as sPLA2α2 activity compared to normal persons. However, plasma levels of phospholipids decreased in patients with moderate and severe COVID-19 infection, as well as significantly decreased in levels of triacylglycerols and HDL-C in plasma from patients with severe infection only, compared to normal persons. Furthermore, a lung CT scan showed the presence of inflammation in a patient with mild, moderate, and severe COVID-19 infection. Conclusions: This study shows that there is a correlation between plasma phospholipid depletion and elevated cytokine storm in patients with COVID-19 infection. Depletion of plasma phospholipid levels in patients with COVID-19 infection is due to oxidative stress, induction of cytokine storm, and systemic inflammatory response after endothelial cell damage promote coagulation. According to current knowledge, patients with COVID-19 infection may need to administer surfactant replacement therapy and sPLA2 inhibitors to treat respiratory distress syndrome, which helps them to maintain the interconnected surfactant structures.

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Gentamicin is an aminoglycoside antibiotic widely used against infections caused by Gram-negative microorganisms. Nephrotoxicity is the main limitation to its therapeutic use. The objective of this study was to evaluate the potential protective effect of astaxanthin on the renal damage generated by gentamicin in rats, in an attempt to understand its mechanism of action, which may pave the way for possible therapeutic applications. The daily oral administration of the astaxanthin at a concentration of 50 mg/kg for 15 days to gentamicin (80 mg/kg.b.w) treated rats showed a significant decrease (p<0.05) in plasma creatinine, urea, TNF-α as well as plasma and renal MDA and HP. The treatment also resulted in a significant increase in hemoglobin, plasma sodium, potassium and TAS as well as renal total protein, GSH, Pr-SHs, G6PD, SOD, GPx, CAT and GR levels. The histological examinations of renal tissues in this study revealed damage and glomerular infiltration in gentamicin treated rats. The presented data suggest that astaxanthin has a significant prophylactic action against gentamicin-induced nephrotoxicity in rats. The effect was more pronounced in case of astaxanthin pre-treatment compared with administration of astaxanthin post-treatment. Taken together, astaxanthin has a potential as a protective and therapeutic agent for nephrotoxicity and deserves clinical trial in the near future as an adjuvant therapy in patients treated with gentamicin.

These results suggested that mechanistic-based evidence substantiating the traditional claims of cucurbitacin E glucoside (1) and its derivatives (2 and 3) to be applied for the treatment of inflammation-related disorders, such as oxidative liver damage and inflammation diseases.

Objective This study aimed to assess the correlation between body mass index (BMI) and plasma lipid profile levels in mild and severe COVID-19 patients. Method This was a prospective, observational, cohort study, conducted in a medical referral center specializing in management of COVID-19 cases. Patients were divided into two groups according to infection severity (mild and severe). Blood samples were obtained from all patients who tested positive to a PCR test for measuring biochemical and inflammatory markers such as lactate dehydrogenase, ferritin, C-reactive protein, and d -dimer, as well as lipid profile, including total cholesterol, triacylglycerols, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), which were analyzed and compared between the two groups. Pearson’s correlation was used to assess the correlation between BMI and plasma lipid profile among mild and severe cases. Results The levels of plasma triacylglycerols, d -dimer, lactate dehydrogenase, ferritin, and C-reactive protein with severe infection were significantly different between patients with mild and severe COVID-19 symptoms ( p = 0.036, 0.03, 0.001, 0.014, and 0.006, respectively). A positive correlation between BMI and triglyceride levels was observed only in the severe infection group. However, HDL-C was negatively correlated with BMI. Conclusion A routine lipid profile test might help as a marker of inflammation and risk stratification in patients with COVID-19. Especially in middle- or low-income countries, the test can rapidly help clinicians to delineate prognostic measures and hence management and treatment plans for this disease as the levels of the lipid profile were correlated with the patients’ BMI and infection severity.