中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (40): 7496-7502.doi: 10.3969/j.issn.2095-4344.2012.40.017

• 移植与中医药 transplantation and traditional Chinese medicine • 上一篇    下一篇

淫羊藿苷对大鼠肾脏缺血再灌注后炎性损伤的保护

丰贵文1，刘龙山2，尚文俊1   

  1. 1郑州大学第一附属医院，河南省郑州市 450052
    2中山大学附属第一医院器官移植科，广东省广州市510080
  • 收稿日期:2012-06-08 修回日期:2012-06-18 出版日期:2012-09-30 发布日期:2012-09-30
  • 通讯作者: 尚文俊，博士，副主任医师，郑州大学第一附属医院，河南省郑州市 450052 shangwj111@163.com
  • 作者简介:丰贵文☆，男，1963年生，河南省辉县人，汉族，博士，副主任医师，主要从事肾脏缺血再灌注损伤及临床器官移植药理学方面的研究。 fengguiwen@hotmail.com

Icariin alleviates renal ischemia-reperfusion injury in rats through inhibition of inflammation

Feng Gui-wen1, Liu Long-shan2, Shang Wen-jun1   

  1. 1The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
    2Department of Organ Transplantation, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China
  • Received:2012-06-08 Revised:2012-06-18 Online:2012-09-30 Published:2012-09-30
  • Contact: Shang Wen-jun, Doctor, Associate chief physician, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China shangwj111@163.com
  • About author:Feng Gui-wen☆, Doctor, Associate chief physician, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China fengguiwen@hotmail.com

PDF

480

被引次数

10

摘要：

背景：肾移植过程中移植肾缺血再灌注损伤不可避免，采用药物减轻该损伤有助于提高肾移植近远期疗效。淫羊藿苷对心肌和脑缺血的治疗效果较好，对肾脏缺血再灌注的作用尚不清楚。
目的：探索淫羊藿苷对肾脏的缺血再灌注损伤的保护机制。
方法：54只SD大鼠随机等分为假手术组、淫羊藿苷组和模型组，后2组大鼠建立单侧肾脏缺血再灌注损伤模型，假手术组大鼠仅游离肾蒂而不钳夹阻断肾血管。淫羊藿苷组和模型组在造模前2 d至造模后12 d分别给予100 mg/kg淫羊藿苷和1 mL/kg 0.3%羧甲基纤维素钠灌胃，1次/d。
结果与结论：相比于对照组，肾脏缺血再灌注损伤后大鼠血肌酐明显升高，肌酐清除率下降，肾组织出现病理性损伤，而给予淫羊藿苷的大鼠，大鼠肾组织诱生型一氧化氮合酶 mRNA和蛋白表达水平下降，肾组织内的促炎因子(肿瘤坏死因子α、白细胞介素1β，6)、趋化因子(干扰素诱导蛋白10、单核细胞趋化蛋白1、巨噬细胞炎性蛋白2)mRNA的表达水平降低，肾脏缺血再灌注损伤后6 h，大鼠血浆亚硝酸盐/硝酸盐和肾组织内髓过氧化物酶水平最高，而后逐渐下降；且淫羊藿苷组大鼠血浆亚硝酸盐/硝酸盐和肾组织内髓过氧化物酶水平低于模型组(P < 0.05)。提示淫羊藿苷可通过抑制诱生型一氧化氮合酶酶表达及其下游的炎症级联反应而减轻大鼠肾脏缺血再灌注损伤。

关键词: 肾脏, 缺血再灌注损伤, 促炎因子, 趋化因子, 一氧化氮, 淫羊藿苷, 中药, 组织工程

Abstract:

BACKGROUND: The renal ischemia-reperfusion injury is inevitable during renal transplantation, reducing the damage by drugs can help to improve the short- and long-term efficacy of renal transplantation. Icariin has a good effect on the treatment of myocardial and cerebral ischemia, but the effect on the renal ischemia reperfusion is not clear.
OBJECTIVE: To investigate the protection mechanism of icariin on renal ischemia-reperfusion injury.
METHODS: Fifty-four Sprague Dawley rats were randomly divided into sham-operation group, icariin group and model group, rats in the icariin group and model group were used to establish the unilateral renal ischemia reperfusion injury model, and rats in the sham-operation only received the renal pedicle freeing without blocking the renal vascular. In icariin group and model group, icariin (100 mg/kg) and 0.3% sodium carboxymethyl cellulose (1 mL/kg) were orally administrated by gavage daily from 2 days before modeling to 12 days after modeling.
RESULTS AND CONCLUSION: Compared with sham-operation group, the serum creatinine level was significantly increased and the creatinine clearance rate was decreased after renal ischemia-reperfusion injury in icariin group and model group, and the decreased creatinine clearance rate resulted in the pathological injury of renal tissue. In the icariin group, the expression level of inducible nitric oxide synthase mRNA and protein was decreased, and the expression levels of pro-inflammatory cytokines (tumor necrosis factor α, interleukin-1β, interleukin 6), chemokines (interferon-inducible protein 10, monocyte chemoattractant protein 1, macrophage cell inflammatory protein-2) mRNA in the renal tissue were decreased; at 6 hours after renal ischemia-reperfusion injury, the content of plasma nitrite/nitrate and myeloperoxidase in icariin group reached to peak and then decreased gradually; the content of plasma nitrite/nitrate and myeloperoxidase in icariin group was lower than that in the model group (P < 0.05). Icariin can attenuate renal ischemia-reperfusion injury through inhibiting inducible nitric oxide synthase expression and downstream inflammation cascades.

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