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参地颗粒对系膜增生性肾小球肾炎大鼠NF-κB信号通路的干预作用 被引量:10

Based on the NF-kappa B Signal Pathway to Explore the Mechanism of Shendi Granule with Mesangial Proliferative Glomerulonephritis
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摘要 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 explore oxidative stress-mediated activation of NF-κB signal pathway play a role in the development with mesangial proliferative glomerulonephritis and inflammatory reaction by Shendigranules. Methods:Used mesangial proliferative glomerulonephritis to model the rats,38 SD rats randomly divided it into Shendi granule group(n=8),benazepril group(n=9),model group(n=8)and normal group(n=13). Shendi granule group were given Shendi granule 0.4 g/(100 g·d)gavage,benazepril group were given benazepril 0.15 mg/(100 g·d)gavage,model group and the normal group was given the same amount of saline per day orally,for 12 weeks. The rats 24 h urinary protein(U-Pro/24 h)level was detected. Using ELISA method to detected ROS,MDA and SOD,the expression of NF-κB p65,MCP-1 and FN by immunohistochemistry. Results:The level of U-Pro/24 h,ROS,MDA and NF-κB p65,MCP-1,FN semi quantitative scores were higher compared with normal group in Shendi granule group,benazepril group and model group(P0.01 or P0.05),SOD was lower compared with normal group(P0.05). Compared with model group,Shendi granule group and benazepril group,the levels of U-Pro/24 h,ROS,MDA,NF-κB p65,MCP-1,FN were significantly lower(P0.01 or P0.05),the levels of SOD was significantly higher(P0.05),was better Shendi granule group than the benazepril group(P0.05). Conclusion:Oxidative stress-mediated NF-κB p65 signal activation take part in Ms PGN rat pathogenesis. Shendi granules can play a positive role in delaying the process of glomerulosclerosis in Ms PGN,and the mechanism is related with inhibiting oxidative stress-mediated NF-κB activation signals.
出处 《辽宁中医药大学学报》 CAS 2016年第2期8-10,共3页 Journal of Liaoning University of Traditional Chinese Medicine
基金 安徽省卫生厅中医药科研项目(2012ZY13)
关键词 系膜增生性肾炎 参地颗粒 氧化应激 核因子-ΚB mesangial proliferative glomerulonephritis Shendi granule oxidative stress nuclear factor-kappa B
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参考文献13

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