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目的:探讨淫羊藿总黄酮对自然衰老雄性大鼠睾丸生殖细胞凋亡的影响及其延缓睾丸衰老的作用机制。方法:将30只18月龄SD雄性大鼠随机分为自然衰老组及淫羊藿总黄酮低、高剂量组,每组各10只,10只3月龄SD大鼠作为青年对照组。淫羊藿总黄酮低、高剂量组分别以10、20 mg/kg剂量灌胃给药,同时青年对照组和自然衰老组大鼠均灌胃给予1%羧甲基纤维素钠,共持续给药6个月。HE染色观察各组大鼠睾丸组织形态,TUNEL法检测各组大鼠睾丸细胞凋亡情况,Western Blot检测各组大鼠睾丸组织中Bcl-2、Bax、p-P53、p-P38蛋白表达情况。结果:与自然衰老组大鼠比较,淫羊藿总黄酮低、高剂量组大鼠睾丸的形态结构均有明显改善,且发生凋亡的生殖细胞数明显减少。此外,淫羊藿总黄酮还可显著升高自然衰老组睾丸组织中Bcl-2蛋白表达,显著降低Bax、p-P53、p-P38蛋白表达。结论:淫羊藿总黄酮对自然衰老大鼠睾丸细胞凋亡有较好的保护作用,其机制可能是通过抑制p38活化进而减少P53磷酸化,从而减少睾丸内生殖细胞的凋亡,以延缓睾丸衰老。
Objective: To investigate the effect of Epimedium Flavonoids on testicular germ cell apoptosis in natural aging rats and its mechanism of delaying testicular senescence. Methods: Thirty male Sprague-Dawley rats of 18 months old were randomly divided into low-dose and high-dose groups of natural aging and epimedium total flavonoids, 10 rats in each group and 10 3-month-old SD rats as youth control group. Epimedium total flavonoids low and high dose groups were administered by gavage at the dose of 10 and 20 mg / kg, respectively. Meanwhile, the rats in the youth control group and the natural aging group were intragastrically given 1% sodium carboxymethyl cellulose, Medicine for 6 months. The morphological changes of testis were observed with HE staining. TUNEL method was used to detect the apoptosis of testicular cells in each group. Western Blot was used to detect the expression of Bcl-2, Bax, p-P53 and p-P38 in testis . Results: Compared with the rats of the natural aging group, the morphology and structure of the testis in both the low and high dose epimedium flavonoids groups were significantly improved, and the number of apoptotic germ cells was significantly decreased. In addition, Epimedium Flavonoids can significantly increase the Bcl-2 protein expression in testis tissue of the natural aging group, and significantly reduce the protein expression of Bax, p-P53 and p-P38. CONCLUSION: Epimedium Flavonoids can protect testis cells from apoptosis in natural aging rats. The mechanism may be that it inhibits the activation of p38 and then reduces the phosphorylation of P53, thereby reducing the apoptosis of germ cells in testes and delaying the testicular senescence.