Stem Cells Therapy as a Possible Therapeutic Option in Treating COVID-19 Patients.

An unfortunate emergence of a new virus SARS-CoV-2, causing a disease known as COVID-19, has spread all around the globe and has caused a pandemic. It primarily affects the respiratory tract and lungs in some cases causing severe organ damage and pneumonia due to overwhelming immune responses. Clinical reports show that the most commons symptoms are fever, dry cough, and shortness of breath, along with several other symptoms. It is thought that an immense cytokine dysregulation in COVID-19 patients is caused following the virus infection. Notably, if patients present with pre-existing specific comorbidities like diabetes or high blood pressure, rates of COVID-19 induced complications and deaths are escalated. Mesenchymal stem cell (MSC) therapy has been shown to alleviate pneumonia and acute respiratory syndrome (ARDS) symptoms, through their immunomodulatory activities in COVID-19 patients. Although more research studies and clinical trial results are needed to elucidate the exact mechanism by which MSCs provide relief to COVID-19 infected patients. Results from clinical trials are encouraging as patients treated with MSCs, regain lung functions and have restored levels of cytokines and trophic factors underscoring the fact that stem cell therapy can be, at least, a complementary therapy to alleviate sufferings in COVID-19 patients. This review discusses the possible therapeutic uses of MSCs for treating COVID-19. Graphical Abstract.

Ethyl linoleate from garlic attenuates lipopolysaccharide-induced pro-inflammatory cytokine production by inducing heme oxygenase-1 in RAW264.7 cells.

In the present study, an essential fatty acid, ethyl linoleate (ELA), was isolated from the cloves of Allium sativum, and its structure was elucidated by NMR and GC-MS analyses. In vitro systems were used to evaluate the anti-inflammatory activity of ELA. Our results indicate that ELA down-regulates inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression and thereby reduces nitric oxide (NO) and prostaglandin E2 production in lipopolysaccharide (LPS)-activated RAW 264.7 cells. Immunofluorescent microscopy and western blot analyses revealed that these effects were mediated by impaired translocation of nuclear factor (NF)-κB and inhibition of phosphorylation of mitogen activated protein kinases. Furthermore, ELA exerted its anti-inflammatory activity by inducing heme oxygenase-1 (HO-1) expression, as determined by HO-1 small interfering (Si) RNA system. Si RNA-mediated knock-down of HO-1 abrogated the inhibitory effects of ELA on the production of NO, TNF-α, IL-1ß, and IL-6 in LPS-induced macrophages. These findings indicate the potential therapeutic use of ELA as an anti-inflammatory agent.