北沙参多糖调控AMPK-SIRT1通路改善小鼠运动性疲劳学习记忆的机制研究OA

This study aimed to investigate whether Glehnia littoralis polysaccharides could ameliorate learn-ing and memory deficits induced by exercise-induced fatigue via regulating the AMPK-SIRT1 signaling pathway and further modulating the Bax/Bcl-2/Caspase-3 apoptotic pathway.A total of 50 C57BL/6J mice were randomly divided into blank control group,model group,and low-,medium-and high-dose Glehnia littoralis polysaccharides groups(50,100,200 mg/kg).Except for the blank control group,mice in other groups were subjected to weight-loaded swimming to establish exercise-induced fatigue models.The feed-ing experiment lasted for 4 weeks,followed by a 6-day Morris water maze test.The Morris water maze test was performed to evaluate spatial learning and memory capacity.The contents of hepatic glycogen(LG),muscle glycogen(MG),glutathione(GSH)and lipid peroxide(LPO)in serum were determined.Pathological changes of hippocampal tissues were observed under light microscope via H.E.staining and Nissl staining.Western blot was adopted to detect the protein expression levels of P-AMPK,AMPK,SIRT1,Bax,Bcl-2 and Caspase-3 in hippocampal tissues.The results demonstrated that intervention with Glehnia littoralis polysaccharides signifi-cantly shortened escape latency and elevated the percentage of residence time in the target quadrant(P<0.05),alleviated morphological structural damage of hippocampal neurons,markedly increased the contents of LG,MG and GSH(P<0.05),and remarkably reduced LPO content(P<0.05).In a dose-dependent manner,Glehnia littoralis polysaccharides significantly up-regulated the protein expression of P-AMPK/AMPK,SIRT1 and Bcl-2(P<0.05),while significantly down-regulating the protein expression of Bax and Caspase-3(P<0.05).In conclusion,Glehnia littoralis polysaccharides may relieve exercise-induced fatigue and improve learning and memory functions by acti-vating the AMPK-SIRT1 pathway,inhibiting the mitochondrial apoptotic pathway and enhancing antioxi-dant capacity.