Molecular Mechanism Of Aluminum-induced Myocardial Damage In Mice And Antagonism Of Selenium

Aluminum(Al)is one of the most abundant metal elements in the earth’s crust Due to its excellent physical and chemical properties,Al products are widely used in production and life.With the deepening of the toxicity of Al3+on human and animal organisms,Al has been found to be myocardial.It can also exhibit its toxic effects,but the research on its mechanism of action is still in its infancy.Selenium is an essential trace element,plays an important role in maintaining the body’s life activities,and can alleviate the poisoning of certain metal elements.Therefore,whether selenium can be used to antagonize the cardiotoxicity of aluminum is worthy of further study.To this end,In this paper,male Kunming mice were used as test subjects,and aluminum trichloride(AlCl3)and selenium-enriched yeast(SeY)were used for the test.The myocardial pathological changes of mice were observed.The antioxidative ability,ATPase activity and ion concentration of myocardial tissue were detected.The mRNA expression level of the Keap1/Nrf2 pathway,inflammation related factors,nuclear receptor and CYP450 enzyme system were detected by RT-PCR,to preliminarily explore the molecular mechanism of aluminum-induced myocardial injury in mice Then,AlCl3 and SeY were simultaneously fed,and a control group was set to observe the antagonistic effect of selenium on myocardial injury induced by aluminum in mice The results showed that:1 Long-term intake of aluminum can induce pathological changes in mouse myocardial tissue,induce thrombosis;activate nuclear receptors,increase CYP450 enzyme transcription level;cause peroxidation of cardiac tissue to activate Keap1/Nrf2 pathway;up-regulate inflammatory factors Expression aggravates the inflammatory response;increasing ATPase gene expression increases ATPase activity and causes abnormal changes in cardiac ion concentration2 Increased selenium intake can effectively reduce the degree of aluminum-induced heart damage,antagonize the toxicity of aluminum to alleviate myocardial tissue oxidative stress;reduce the transcription of Keapl/Nrf2 pathway;reduce aluminum-induced inflammatory factor overexpression to reduce inflammatory response;The induced ATPase expression was abnormally increased,and the ATPase activity was restored to restore the ion concentration to normal3 The effect of additional selenium intake alone on the antioxidant function,inflammatory factor expression,ion balance,ATPase activity and subunit expression of the mouse heart was not significant.