Cellular preconditioning and mesenchymal stem cell ferroptosis

In this editorial,we comment on the article published in the recent issue of the World Journal of Stem Cells.They focus on stem cell preconditioning to prevent ferroptosis by modulating the cystathionineγ-lyase/hydrogen sulfide(H_(2)S)pathway as a novel approach to treat vascular disorders,particularly pulmonary hypertension.Preconditioned stem cells are gaining popularity in regenerative medicine due to their unique ability to survive by resisting the harsh,unfavorable microenvironment of the injured tissue.They also secrete various paracrine factors against apoptosis,necrosis,and ferroptosis to enhance cell survival.Ferroptosis,a regulated form of cell death characterized by iron accumulation and oxidative stress,has been implicated in various pathologies encompassing dege-nerative disorders to cancer.The lipid peroxidation cascade initiates and sustains ferroptosis,generating many reactive oxygen species that attack and damage multiple cellular structures.Understanding these intertwined mechanisms provi-des significant insights into developing therapeutic modalities for ferroptosis-related diseases.This editorial primarily discusses stem cell preconditioning in modulating ferroptosis,focusing on the cystathionase gamma/H_(2)S ferroptosis pathway.Ferroptosis presents a significant challenge in mesenchymal stem cell(MSC)-based therapies;hence,the emerging role of H_(2)S/cystathionase gamma/H_(2) S signaling in abrogating ferroptosis provides a novel option for therapeutic intervention.Further research into understanding the precise mechanisms of H_(2)S-mediated cytoprotection against ferroptosis is warranted to enhance the thera-peutic potential of MSCs in clinical settings,particularly vascular disorders.

Mesenchymal stem cells’“garbage bags”at work:Treating radial nerve injury with mesenchymal stem cell-derived exosomes

Unlike central nervous system injuries,peripheral nerve injuries(PNIs)are often characterized by more or less successful axonal regeneration.However,structural and functional recovery is a senile process involving multifaceted cellular and molecular processes.The contemporary treatment options are limited,with surgical intervention as the gold-standard method;however,each treatment option has its associated limitations,especially when the injury is severe with a large gap.Recent advancements in cell-based therapy and cell-free therapy approaches using stem cell-derived soluble and insoluble components of the cell secretome are fast-emerging therapeutic approaches to treating acute and chronic PNI.The recent pilot study is a leap forward in the field,which is expected to pave the way for more enormous,systematic,and well-designed clinical trials to assess the therapeutic efficacy of mesenchymal stem cell-derived exosomes as a bio-drug either alone or as part of a combinatorial approach,in an attempt synergize the best of novel treatment approaches to address the complexity of the neural repair and regeneration.

Effect of aspirin on glucose-D transport in intestine of rat

Objective: The present study was designed to evaluate the effect a commonly prescribed Non Steroidal Anti Inflammatory Drug(NSAID) i.e.aspirin on brush border membrane in terms of changes in the intestinal transport level of glucose which is monosaccharide with absolute requirement in the body and hence its absorption is directly proportional on the morphology of the intestinal mucosa.Method: Albino rats(Rattus Norvegicus) were divided into two different groups,Group I(Control),Group II(aspirin-treated,50 mg aspirin/kg of body weight).The treatment was continued for 28 days.On the 29th day after overnight fasting,intestine was removed from animals of both groups.Changes in transport of glucose-D in intestine were studied.Result: The results indicated a significant decrease in the transport of glucose-D in aspirin treated group as compared to the control group.Conclusion: Cautious use of NSAID is recommended in commonly observed symptom such as headache and to those patients who are given as a prophylaxis for thrombosis.

The pharmacological mechanism of quercetin as adjuvant therapy of COVID-19

The emergence of novel severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)has caused the global outbreak and major public health concern.After the outbreak human-to-human transmission was confirmed with or without symptoms of upper and lower respiratory tract involvement.Up to date,there has been evidence that COVID-19 is beyond that of a typi­cal pulmonary disease and revealing pathomechanics of COVID-19-associated acute respiratory distress syndrome(CARDS),which include severe inflammation and pulmonary edema leading to impaired alveolar homeostasis,and resulting in an alter­ation of lung physiology,lung fibrosis,inflammation of endothelium,vascular thrombosis,as well as exaggerated immune re­sponse.Concerning this pathophysiology,the use of quercetin as phytotherapeutic may merit in the management of COVID-19 patients.In this review,the authors wish to elaborate on the molecular effect of quercetin on SARS-CoV-2 by giving a detailed mechanism of quercetin against the binding of the S-protein of the virus to angiotensin-converting enzyme 2(ACE2)recep­tors,the main protease(M^(pro))or 3C-like protease(3CL^(pro)),papain-like protease(PL^(pro)),and RNA-dependent RNA polymerase(RdRP).Recent clinical evidence supporting the use of quercetin in COVID-19 management is also discussed in this paper.