[1]李开龙,何娅妮,赵玲,等.甘草酸18α体上调p53的表达保护肾脏缺血再灌注损伤的实验研究[J].第三军医大学学报,2008,30(22):2078-2081.
 LI Kai-long,HE Ya-ni,ZHAO Ling,et al.Glycyrrhizin-18α protects against renal ischemia-reperfusion injury by upregulating p53 expression[J].J Third Mil Med Univ,2008,30(22):2078-2081.
点击复制

甘草酸18α体上调p53的表达保护肾脏缺血再灌注损伤的实验研究(/HTML )
分享到:

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
30卷
期数:
2008年第22期
页码:
2078-2081
栏目:
论著
出版日期:
2008-11-30

文章信息/Info

Title:
Glycyrrhizin-18α protects against renal ischemia-reperfusion injury by upregulating p53 expression
作者:
李开龙何娅妮赵玲王惠明陈林
第三军医大学大坪医院野战外科研究所:肾内科,全军创伤中心,创伤、烧伤与复合伤国家重点实验室
Author(s):
LI Kai-long HE Ya-ni ZHAO Ling WANG Hui-ming CHEN Lin
Department of Nephrology, Laboratory of Trauma Center, State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China
关键词:
甘草酸18α体 肾脏IRIp53核转录因子-κB
Keywords:
glycyrrhizin-18α kidney ischemia-reperfusion injury p53 NF-κB
分类号:
R285.5;R341;R692.02
文献标志码:
A
摘要:
目的    探讨甘草酸18α体对肾脏缺血再灌注损伤(ischemia reperfusion injury, IRI)后肾小管上皮细胞p53蛋白表达的影响及其意义。    方法    将成年(2月龄)野生型鼠[p53(+/+)]和p53基因敲除[p53(-/-)]鼠分成4组:p53(+/+)鼠生理盐水组、p53(+/+)鼠甘草酸治疗组、p53(-/-)鼠生理盐水组和p53(-/-)鼠甘草酸治疗组;建立左肾IRI模型,于再灌注后0、1和7 d处死动物,制作双肾(右肾作自身对照)标本。HE染色观察肾组织病理变化,免疫组化法检测NF-κB蛋白的表达,Western blot定量检测p53的表达,并用EIG综合图像分析系统对NF-κB的表达进行半定量分析。    结果    缺血再灌注损伤肾脏主要表现为肾小管坏死,半定量分析结果显示甘草酸治疗组比生理盐水组轻、p53(+/+)鼠组比p53(-/-)鼠组轻(P<0.01)。各组IRI肾NF-κB蛋白的表达在IRI后0 d即开始增加,1、7 d点,NF-κB蛋白的表达在p53(+/+)鼠比p53(-/-)鼠显著减少,甘草酸治疗组比生理盐水组显著减少(P<0.01);p53(+/+)鼠甘草酸治疗组p53蛋白的表达比生理盐水组显著增多(P<0.01)。p53的表达与肾小管坏死和NF-κB的表达呈显著负相关(P<0.01)。    结论    甘草酸可能主要通过对小鼠IRI肾脏p53表达的上调,抑制NF-κB的表达,减轻肾小管坏死,从而对IRI肾脏产生保护作用。
Abstract:
Objective    To investigate the effect of glycyrrhizin-18α on the expression of p53 in renal tubular epithelial cells after renal ischemia-reperfusion injury (IRI).     Methods    p53(+/+) and p53(-/-) male mice aged 2 months were used to make ischemic model by clamping left renal hila for 45 min, then immediately and on each following day, the animals were treated with glycyrrhizin-18α (20 mg·kg-1·d-1) or normal sodium (control) by subcutaneous injection. On day 0, 1 and 7 after reperfusion, renal tissues were processed for morphometric observation as well as NF-κB and p53 proteins analysis, using HE stain, immunohistochemistry and Western blot, respectively.     Results    In the IRI kidney, renal tubular necrosis was more severe in p53(-/-) mice and normal sodium treated mice than in p53(+/+) mice and glycyrrhizin-18α treated mice (P<0.01), respectively. The expressions of p53 and NF-κB proteins began to increase on day 0 after IRI, but the expression of NF-κB protein began to decrease on day 1 to 7, while the expression of p53 protein was still at a high level. The expression of p53 protein in p53(+/+) mice treated with glycyrrhizin-18α increased obviously compared with that in p53(+/+) mice treated with normal sodium (P<0.01), but the expression of NF-κB protein decreased obviously (P<0.01). The expression of p53 protein was negatively correlated with renal tubular necrosis and the expressions of NF-κB protein (P<0.01).     Conclusion    Glycyrrhizin-18α may inhibit the expression of NF-κB protein by upregulating the expression of p53 protein, resulting in relieving renal tubular necrosis.

参考文献/References:

李开龙,何娅妮,赵玲,等. 甘草酸18α体上调p53的表达保护肾脏缺血再灌注损伤的实验研究[J]. 第三军医大学学报,2008,30(22):2078-2081.

相似文献/References:

[1]李开龙,张建国,王慧民,等.甘草酸18α体调节梗阻性肾病大鼠肾间质中CTGF和TGF-β1表达的实验研究[J].第三军医大学学报,2005,27(04):323.

更新日期/Last Update: 2008-10-30