›› 2014, Vol. 35 ›› Issue (8): 877-877.

• 论文 • 上一篇    下一篇

阿托伐他汀对实验性肾间质纤维化大鼠细胞间黏附分子1、核因子-κB 表达的影响

张丽敏;林海英;刘占全;高燕;王咏梅;毕朝煜   

  1. 河北大学附属医院肾内科,河北 保定,071000%河北医科大学第三医院肾内科,河北 石家庄,050051
  • 发布日期:2014-08-25

WEN Ya;ZHU Chunhua;WANG Lina;JI Hui;LIU Ying

ZHANG Limin;LIN Haiying;LIU Zhanquan;GAO Yan;WANG Yongmei;BI Zhaoyu   

  • Published:2014-08-25

摘要: 目的:研究阿托伐他汀对肾间质纤维化大鼠的肾脏保护机制。方法54只 Wistar 大鼠随机分为假手术组(A 组,n =18)、单侧输尿管结扎(unilateral ureteral obstruction,UUO)模型组(B 组,n =18)、阿托伐他汀治疗组(C 组,n =18)。C 组于术前3天开始灌胃(阿托伐他汀10mg·kg -1·d -1,制成混悬液),A 组及 B 组给予等量生理盐水灌胃,分别于术后第3、7、14天处死。光镜观察肾脏病理改变,并采用免疫组织化学染色测定肾小管间质中细胞间黏附分子1(intercellular adhesion molecule 1,ICAM-1)、核因子-κB(nuclear factor-κB,NF-κB)的表达。结果 B组 ICAM-1、NF-кB 的表达随梗阻时间延长明显增加,C 组术后第3、7、14天 ICAM-1、NF-кB 的表达均显著低于同期B 组(P ﹤0.05)。相关分析结果显示,第3、7、14天 NF-кB 的表达与同期、同组 ICAM-1的表达呈正相关( P ﹤0.05)。结论阿托伐他汀能下调肾小管间质中 ICAM-1、NF-кB 的表达,抑制和延缓肾间质纤维化的进展。阿托伐他汀对 ICAM-1的下调作用至少部分是通过抑制 NF-кB 的表达而实现的。

关键词: 肾病, 阿托伐他汀, 胞间黏附分子 1, NK-κB

Abstract: Objective To observe the protective role of artorvastatin for kidney in rats with renal interstitial fibrosis. Methods Fifty-four male Wistar rats were randomly divided into three groups:sham-operated group(group A,n = 18),unilateral ureteral obstruction(UUO)group(group B,n = 18), UUO with artorvastatin treated group(group C,n = 18). Artorvastatin put to use 3 days before surgery. UUO and sham rats received equal volume physiological salif by daily gastric gavage. Rats were killed after 3,7,14 days of the surgery. The kidney pathological changes were observed under microscope. The expressions of intercellular adhesion molecule-1(ICAM-1)and nuclear factor-кB(NF-кB)were analyzed by routine immunohistochemical method. Results The levels of ICAM-1 and NF-кB in group B were various and significantly higher with the extension of obstruction time. The levels of ICAM-1 and NF-кB in group C were significantly lower than those of group B at the same period(P ﹤ 0. 05). The level of NF-кB was significantly associated with ICAM-1(P ﹤ 0. 05). Conclusion Artorvastatin reduces ICAM-1 and NF-кB expression,resulting in decreased tubular damage and interstitial fibrosis. The effect of artorvastatin in reducing ICAM-1 perhaps implements through the inhibition of NF-кB partly.

Key words: nephrosis, artorvastatin, intercellular adhesion molecule-1, NF-kappa B

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