论文部分内容阅读
目的:研究竹节参总皂苷对衰老大鼠肠道上皮细胞紧密连接蛋白表达的调节作用及其可能机制。方法:SPF级SD大鼠分为成年组(6月龄)、衰老模型组(24月龄)及竹节参总皂苷高、中、低剂量组5组。免疫组织化学方法检测各组大鼠回肠上皮细胞间紧密连接蛋白Occludin、ZO-1,抗氧化应激相关蛋白Nrf2、HO-1、NQO-1,线粒体相关蛋白Sirt1、PGC-1α,及p-AMPK蛋白的表达情况。结果:与成年组大鼠比较,自然衰老大鼠Occludin、ZO-1、Nrf2、HO-1、NQO-1、Sirt1、PGC-1α、p-AMPK蛋白表达均显著降低(P<0.01)。与自然衰老大鼠比较,竹节参总皂苷各组大鼠Occludin、ZO-1、Nrf2、HO-1、NQO-1、Sirt1、PGC-1α、p-AMPK表达显著升高(P<0.05或P<0.01)。结论:自然衰老大鼠细胞间紧密连接蛋白表达减少引起的回肠黏膜屏障功能障碍可能与线粒体氧化应激密切相关,而竹节参总皂苷可能通过调节衰老大鼠线粒体氧化应激的水平,从而上调肠上皮细胞间紧密连接蛋白的表达,改善衰老大鼠肠道黏膜屏障功能障碍。
Objective: To study the regulation effect of Sasa saponin on the expression of Claudin in aging rat intestinal epithelial cells and its possible mechanism. Methods: SPF SD rats were divided into five groups: adult group (6 months old), aging model group (24 months old) and SSP group high, medium and low dose groups. Immunohistochemistry was used to detect the expression of Occludin, ZO-1, Nrf2, HO-1, NQO-1, mitochondria related proteins Sirt1 and PGC- AMPK protein expression. Results: Compared with adult rats, the expression of Occludin, ZO-1, Nrf2, HO-1, NQO-1, Sirt1, PGC-1α and p-AMPK in the aged rats were significantly decreased (P <0.01). Compared with the natural aged rats, the expressions of Occludin, ZO-1, Nrf2, HO-1, NQO-1, Sirt1, PGC-1alpha and p-AMPK in SSP group were significantly increased P <0.01). CONCLUSION: Dysfunction of ileal mucosal barrier caused by decreased expression of claudin may be closely related to mitochondrial oxidative stress, and SSP may up-regulate mitochondrial oxidative stress in aging rats Intestinal epithelial cells between the tight junction protein expression, improve aging rats intestinal mucosal barrier dysfunction.