淫羊藿总黄酮通过AMPK/SIRT1/NFκB信号通路减轻自然衰老大鼠睾丸组织炎症反应

Total Flavonoids of Epimedium Reduce Inflammatory Reaction via AMPK/SIRT1/NFκB Signaling Pathway in Testes of Natural Aging Rats

探讨淫羊藿总黄酮(Total flavonoids of Epimedium,TFE)对自然衰老大鼠睾丸组织中AMPK/SIRT1/NFκB信号通路的影响及其抗炎作用。将40只18月龄雄性SD大鼠随机分为TFE低、中、高剂量组和自然衰老组,每组10只。另取10只2月龄雄性SD大鼠作为青年对照组。TFE低、中、高剂量组分别以10、20、40 mg/kg剂量灌胃给药,青年对照组和自然衰老组大鼠均灌胃给予质量分数为1%羧甲基纤维素钠溶液,持续给药4个月。HE染色观察大鼠睾丸组织形态,Western blot法检测各组大鼠睾丸组织中AMPK、p-AMPK、SIRT1、acetylNFκBp65、IL-1β、TNFα蛋白表达水平。结果显示,与自然衰老组相比,TFE低、中、高剂量组大鼠睾丸组织形态结构均有明显改善,TFE可促进大鼠睾丸组织内p-AMPK和SIRT1蛋白表达,显著降低acetyl-NFκBp65及其下游炎症因子IL-1β、TNFα蛋白表达水平。实验结果表明,TFE可减轻自然衰老大鼠睾丸组织炎症反应,其机制可能与调控AMPK/SIRT1/NFκB信号通路有关。

This study was to investigate the effect of total flavonoids of Epimedium(TFE)on AMPK/SIRT1/NFκB signaling pathway and its anti-inflammatory effect in the testes of natural aging rats.Forty 18-month-old male SD rats were randomly divided into TFE low-,medium-and high-dose group and natural aging group.Ten 2-month-old SD male rats were used as young control group.TFE low-,medium-and high-dose groups were given 10,20 and 40 mg/kg dose for 4 months by stomach lavaging,respectively.However,young control group and natural aging group were given the same concentration of 1%sodium carboxymethyl cellulose solution,lasting for 4 months.The testicular histology was observed by haematoxylin-eosin(HE)staining.The relative protein expression levels of AMPK,p-AMPK,SIRT1,acetyl-NFκBp65,IL-1βand TNFαin the testes of rats were detected by Western blot.These data showed that TFE treatment significantly improved the change of testicular histomorphology with aging.In addition,TFE significantly increased the protein expression levels of p-AMPK and SIRT1,and decreased the protein expression levels of acetyl-NFκBp65 when compared with the natural aging group.Furthermore,TFE significantly downregulated inflammatory factors IL-1β,TNFαlevels with aging.Taken together,TFE reduce the inflammatory response of testes in natural aging rats,and its mechanism may be related to the regulation of AMPK/SIRT1/NFκB signaling pathway.