Protective Effect And Mechanism Of PQQ On Myocardial Injury In Mice With Exhaustive Exercise

Objective:This study based on exercise injury in mice by PQQ stress,antioxidant supplements drugs improve the mouse exhaustive cardiac muscle,from the angle of relationship between oxidative stress and inflammatory reaction and cell apoptosis of PQQ on myocardial protective effect,to further understand the molecular mechanism of protective effect of PQQ on myocardium,at the same time drug supplement on prevention and treatment of myocardial injury after exhaustive and provide new experimental evidence.Methods:1.60 healthy Kunming mouse with 8 week old were randomly divided into normal control group(group NC),exhaustive exercise group(E group),low dose of PQQ(5mg/kg/d)exhaustive exercise group(group LE),PQQ(lOmg/kg/d)dose in the exhaustive exercise group(group ME),PQQ high dose(20mg/kg/d)exhaustive exercise group(HE group),10 rats in each group.In addition to the normal control group,the rest mouse in each group were loaded with 3%body weight at the rear,6 days a day,1 times a day for exhaustive swimming.According to the Thomas exhaustion standard,they worked for 2 weeks.The normal control group were taken directly,the other groups were immediately after exercise motive force.2.the content of serum and cardiac troponin I(C Tn I)in the serum and myocardium of the mice was detected by ELISA.3.the content of creatine kinase(CK)in serum was detected by the method of health disc detection.4.the expression of IL-6,IL-1 beta,CXCL10,Caspase-3,Bax and Bcl-2 genes in the myocardium of mice was detected by fluorescence quantitative PCR.5.the expression of NF--kappa B(p65)and p-NF--kappa B(p65)protein in the myocardium of mice was detected by Western Blot.Results:1 Compared with group NC,the levels of serum CK,cTnI and MDA increased significantly in group E,with statistical significance(P<0.05).There was no significant change in serum CK,cTn I and HE content in LE group,ME group and HE group.Compared with E group,LE group,ME group and HE group serum CK activity decreased significantly(P<0.05);LE group and ME group of mice serum cTn I content decreased significantly(P<0.05),HE grouphad no obvious change;LE group,ME group and HE group serum MDA content decreased significantly(P<0.01).2Compared with group NC,the activity of SOD in myocardium of E group was significantly decreased(P<0.01)and GSH-PX activity was significantly decreased(P<0.05),but there was no significant change in LE,ME and HE group.Compared with group E,the activity of SOD and GSH-PX in myocardium of LE group,ME group and HE group increased significantly(P<0.05),and the activity of ME group increased significantly(P<0.01),while the activity of GSH-PX in HE group increased significantly.3 Compared with group NC,the expression of IL-6,IL-1?,CXCL10 and Caspase-3mRNA in myocardium of E group increased(P<0.01),and the expression level of Bcl-2/Bax mRNA decreased significantly(P<0.01).Compared with group E,the myocardial IL-6,IL-1?,CXCL10 and Caspase-3 mRNA in group LE,group ME and group HE were significantly decreased(P<0.05 or P<0.01),and the expression of Bcl-2/Bax increased significantly(P<0.05 or P<0.01).4Compared with the NC group,the expression of NF-kappa B(p65)and p-NF-kappa B(p65)protein in group E mice was significantly enhanced(P<0.05 or P<0.01).Compared with the E group,the expression of NF-kappa B(p65)and p-NF--kappa B(p65)protein in LE,ME and HE groups decreased significantly(P<0.05 or P<0.01).Conclusions:1 Exhaustive exercise injure myocardial.Oxidative stress,inflammatory response and apoptosis are involved in the occurrence of myocardial injury induced by exhaustive exercise.2Supplementation of PQQ can reduce myocardial injury caused by exhaustive exercise.Its mechanism may be related to the inhibition of oxidative stress,the reduction of inflammatory response and the inhibition of apoptosis.3 Supplementation of low,medium and high doses of PQQ can protect myocardial injury to varying degrees,but there is no dose effect.