Protective Effects Of Losartan Potassium On Skeletal Muscle Cell And Its Mechanism

The treatment of sarcopenia is still in the exploratory stage.Clinically,patients have been found to have improved mobility after losartan potassium treatment,but the specific mechanism is still unclear.We aim to explore the protective effects of losartan potassium on skeletal muscle cell injury and its mechanism at the cellular level.Methods: Public data were used to analyze gene expression changes before and after resistance training in the elderly;deprivation serum method induced L6 myoblasts to differentiate into myotubes;CCK-8 kit and Western Blot to determine the appropriate losartan cell treatment concentration;palmitic acid construction Myotube aging model,q PCR was used to detect the expression levels of P53,P21,MURF1 and MAFbx m RNA;Western Blot was used to detect the expression levels of apoptosis-related proteins,endoplasmic reticulum stressrelated proteins and autophagy-related proteins.Results: Analysis of public data found that down-regulation of angiotensin Ⅱ type 1 receptor can be used in the treatment of sarcopenia patients;successfully induced L6 myoblasts to differentiate into myotubes and successfully constructed a model of myotube cells aging with palmitic acid.Potassium potassium can reduce myotube apoptosis after palmitic acid treatment,and at the same time,reduce endoplasmic reticulum stress.Adding endoplasmic reticulum stress inhibitors to myotubes treated with palmitic acid can also be used as chlorine Satan potassium generally inhibits myotube apoptosis;however,losartan potassium does not affect the autophagy pathway of myotubes and the expression of MAFbx m RNA.Conclusion Losartan potassium inhibits the expression of cleaved caspase 3 and its substrate cleaved PARP,reduces the apoptosis of myotubes and exerts a protective effect.This protective effect may be achieved through the endoplasmic reticulum stress pathway rather than the autophagy pathway.