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目的:探讨氧化应激介导的NF-κB信号通路在系膜增生性肾小球肾炎大鼠中的影响及参地颗粒对其干预作用。方法:建立系膜增生性肾炎(Ms PGN)模型,将38只SD大鼠随机分为参地颗粒组(n=8)、贝那普利组(n=9)、模型组(n=8)和正常组(n=13)。参地颗粒组按0.4 g/(100 g·d)灌胃,贝那普利组按0.15 mg/(100 g·d)灌胃,模型组及正常组每日给予等量生理盐水灌胃,疗程12周。检测各组大鼠24 h尿蛋白定量(U-Pro/24 h)水平,采用酶联免疫吸附(ELISA)法检测肾脏组织中ROS、MDA、SOD的含量,免疫组织化学法检测肾脏组织中NF-κB p65、MCP-1、FN的表达情况。结果:参地颗粒组、贝那普利组、模型组U-Pro/24 h、ROS、MDA含量及肾组织中NF-κB p65、MCP-1、FN表达均高于正常组(P<0.01或P<0.05),SOD含量低于正常组(P<0.05);治疗后与模型组比较,参地颗粒组和贝那普利组可显著降低U-Pro/24 h、ROS、MDA含量及肾组织中NF-κB p65、MCP-1、FN水平(P<0.01或P<0.05),升高SOD含量(P<0.05),参地颗粒组优于贝那普利组(P<0.05)。结论:Ms PGN大鼠的发病过程有氧化应激介导NF-κB信号活化的参与,参地颗粒在延缓Ms PGN大鼠肾小球硬化进程中发挥了积极的作用,其机制与抑制氧化应激介导的NF-κB信号活化有关。
Objective: To investigate the effects of oxidative stress-mediated NF-κB signaling pathway in mesangial proliferative glomerulonephritis rats and its intervention effect. Methods: The mesangial proliferative glomerulonephritis (Ms PGN) model was established and 38 SD rats were randomly divided into three groups: Shendi Granule group (n = 8), benazepril group (n = 9), model group ) And normal group (n = 13). The ginseng group was gavaged at 0.4 g / (100 g · d), while the benazepril group was gavaged at 0.15 mg / (100 g · d). The rats in the model group and the normal group were given the same amount of normal saline intragastrically, Treatment for 12 weeks. The levels of 24 h urinary protein (U-Pro / 24 h) were measured in each group. The content of ROS, MDA and SOD in renal tissues were detected by enzyme linked immunosorbent assay (ELISA) -κB p65, MCP-1, FN expression. RESULTS: The levels of U-Pro / 24 h, ROS and MDA in Shenwei granule group, benazepril group and model group were significantly higher than those in normal group (P <0.01) (P <0.05 or P <0.05), and SOD content was lower than that of the normal group (P <0.05). Compared with the model group, Shen-Di granule group and benazepril group could significantly reduce the contents of U-Pro / The levels of NF-κB p65, MCP-1 and FN in renal tissue were significantly increased (P <0.01 or P <0.05) . CONCLUSIONS: The process of Ms PGN induces oxidative stress-mediated activation of NF-κB signaling. SHEN Di particles play an active role in retarding the progression of glomerular sclerosis in Ms PGN rats. Its mechanism is related to the inhibition of oxidative stress Activation of NF-κB activation of the signal.