摘要
Heat stress(HS)reaction can lead to serious physiological dysfunction associated with cardiovascular and various organ diseases.Ginsenoside Rg3(G-Rg3)is a representative component of ginseng rare saponin and can protect against multiple organs,also used as functional food to adjust the balance of the human body,but the therapeutic effect and molecular mechanism of G-Rg3 on male diseases under HS are underexplored.The aim of the present study,G-Rg3 was prepared through the efficient conversion of ginsenoside Rd and investigate the contribution of G-Rg3 to testicular injury induced exposure to HS.All mice were divided into four groups as follows:normal group,HS group,and HS+G-Rg3(5 and 10 mg/kg)groups.G-Rg3 was administered orally for 14 days,then exposed to a single scrotal heat treatment(43°C,18min)on the 7th day.After HS treatment,the morphology of testis and epididymis changes,and caused a significant loss of multinucleated giant cells,desquamation of germ cells in destructive seminiferous tubules,and degenerative Leydig cells,further destroying the production of sperm.After administration G-Rg3(5 and 10 mg/kg/day)for 2 weeks,the spermatogenic-related indexes of testosterone levels and superoxide dismutase(SOD)activity,glutathione(GSH)content significantly(p<0.01)increase compared with the HS group.Moreover,G-Rg3 treatment effectively ameliorated the production of malondialdehyde(MDA)(p<0.05 or p<0.01).Importantly,G-Rg3 exhibited the protective potential against HS-induced injury not only suppressing the protein levels of heme oxygenase-1(HO-1),hypoxia-inducible factor-1α(HIF-1α),and heat shock protein 70(HSP70)but also modulating the Bcl-2 family(p<0.01 or p<0.001)and activation of mitogen-activated protein kinase(MAPK)signaling pathways(p<0.01).For most of the parameters tested,the HS+G-Rg3(10 mg/kg)group exhibited potent effects compared with those exhibited by the low dose(5 mg/kg)group.In conclusion,the present study demonstrated that G-Rg3 exerted protective effects against HS-induced testicular dysfunction via inhibiting the MAPK-mediated oxidative stress and apoptosis in mice.
出处
《BIOCELL》
SCIE
2020年第4期655-669,共15页
生物细胞（英文）
基金
the grants of the Jilin Science&Technology Development Plan(Nos.20170101011JC,20200301037RQ and 20190103092JH)
the Open Fund of Key Laboratory of Biotechnology and Bioresources Utilization(KF202004).
