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COVID-19 emerged in December 2019 in Wuhan, China, spread worldwide rapidly, and caused millions of deaths in a short time. Many preclinical and clinical studies were performed to discover the most efficient therapy to reduce the mortality of COVID-19 patients. Among various approaches for preventing and treating COVID-19, mesenchymal stem cell (MSC) therapy can be regarded as a novel and efficient treatment for managing COVID-19 patients. In this review, we explain the pathogenesis of COVID-19 infection in humans and discuss the role of MSCs in suppressing the inflammation and cytokine storm produced by COVID-19. Then, we reviewed the clinical trial and systematic review studies that investigated the safety and efficacy of MSC therapy in the treatment of COVID-19 infection. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection leads to the development of coronavirus disease 2019 (COVID-19), which causes endothelial dysfunction (ED), oxidative stress (OS), and inflammatory disorders. These changes cause hypoxia and cytokine storm with the development of cardio-pulmonary complications. Bioactive lipids and other polyunsaturated fatty acids participate in a vital role in the SARS-CoV-2 infection process. One of these mediators is the anti-inflammatory compound, lipoxin (LX). LXs are produced from arachidonic acid (AA) by collaboration between 5-lipoxygenase (5-LO) and 12–15 LO during cell interactions. Thus, our goal was to review the probable role of LXs in COVID-19 regarding the effects of LXs on the inflammatory signaling pathways that are linked with COVID-19 pathogenesis and complications. [ABSTRACT FROM AUTHOR]

COVID-19 is one of the viral diseases that has caused many deaths and financial losses to humans. Using the available information, this virus appears to activate the host cell-death mechanism through Calpain activation. Calpain inhibition can stop its downstream cascade reactions that cause cell death. Given the main roles of Calpain in the entry and pathogenicity of the SARS-CoV-2, its inhibition can be effective in controlling the COVID-19. This review describes how the virus activates Calpain by altering calcium flow. When Calpain was activated, the virus can enter the target cell. Subsequently, many complications of the disease, such as inflammation, cytokine storm and pulmonary fibrosis, are caused by virus-activated Calpain function. Calpain inhibitors appear to be a potential drug to control the disease and prevent death from COVID-19. [ABSTRACT FROM AUTHOR]

The inflammatory process is a biological response of the organism to remove injurious stimuli and initiate homeostasis. It has been recognized as a key player in the most severe forms of SARS-CoV-2, characterized by significantly increased pro-inflammatory cytokine levels, the so-called "cytokine storm" that appears to play a pivotal role in this disease. Therefore, the aim of this systematic review was to select clinical trials with anti-inflammatory plants and relate the activity of these plants to inflammatory markers of SARS-CoV-2 infection. PRISMA guidelines are followed, and studies of interest are indexed in PubMed and ClinicalTrials.gov databases. As a result, 32 clinical trials encompassing 22 plants were selected. The main anti-inflammatory mechanisms described in the studies are the inhibition of inflammatory cytokines, such as IL-6, TNF-a, IFN-γ, and IL-1; decreased CRP and oxidative marker levels; increased endogenous antioxidant levels; modulation of cardiovascular risk markers. The data found are not directly related to SARS-CoV-2 infection. However, they provide possibilities for new studies as plants have a wide array of phytochemicals, and detecting which ones are responsible for anti-inflammatory effects can provide invaluable contribution to studies aiming to evaluate efficacy in scenarios of SARS-CoV-2 infection. [ABSTRACT FROM AUTHOR]

In the current scenario, most countries are affected by COVID-19, a pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has a massive impact on human health. Previous studies showed that some traditionally used medicinal herbs and their combinations showed synergistic anti-viral and anti-inflammatory activity against SARS-CoV-2 type infections. Therefore, the goal of this study is to demonstrate the anti-viral and anti-inflammatory effects of a novel polyherbal formulation, hereinafter referred to as Imusil, on Vero E6 cell lines and Raw 264.7 murine macrophage cells respectively. The Imusil was subjected to identify its chemical characterisations such as UV–Visible spectrum profile, Fourier transform infrared spectroscopy (FT-IR) and gas chromatography–mass spectroscopic (GC–MS) analysis. FT-IR analysis of Imusil peak values with various functional compounds such as alcohol, esters, aliphatic and carboxylic acids. GC–MS analysis of compounds with totally 87 compounds major chemical compounds were identified, such as 3-(Octanoyloxy) propane-1,2-diyl bis(decanoate), Succinic acid, 2-methylhex-3-yl 2,2,2-trifluoroethyl ester, Neophytadiene, 3,5,9-Trioxa-4-phosphaheneicosan-1-aminium, 4-hydroxy-N,N,N-trimethyl-10-oxo-7-[(1-oxododecyl)oxy]-, hydroxide, inner salt, 4-oxide, (R)-. The anti-viral activity of Imusil against SARS-CoV-2 was assessed using plaque reduction assay and anti-inflammatory study was conducted on lipopolysaccharide (LPS)-induced RAW 264.7 cells. The results obtained from the study reveal that Imusil significantly inhibited SARS-CoV-2 replication in Vero E6 cells and the production of inflammatory mediator's cyclooxygenase-2 and pro-inflammatory cytokines like tumour necrosis factor-α and interleukin- 6 were significantly reduced, along with thwarting the significant oxidative stress by preventing the expression of NOX-2 thereby inhibiting the reactive oxygen species formation. Hence, considering the current study as a novel strategy for mediating the COVID-19 associated aliments, inceptive scientific evidence of Imusil promises its potential therapeutic implications against COVID-19 and inflammatory conditions. [ABSTRACT FROM AUTHOR]