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[1]李剑瑜 刘鹏年 张霞等.三七皂甙Rg1、Rb1对肝纤维化大鼠线粒体DNA三磷酸腺苷酶6、8亚基的作用机制研究[J].环球中医药,2014,7(08):591-0.
　LI Jian-yu,LIU Peng-nian,ZHANG Xia,et al.Study on the mitochondrial mtDNA ATPase6、8 gene mutation and on the function mechanism of panax notoginseng saponins Rg1,Rb1 for hepatic fibrosis rats[J].,2014,7(08):591-0.
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三七皂甙Rg1、Rb1对肝纤维化大鼠线粒体DNA三磷酸腺苷酶6、8亚基的作用机制研究()
     
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《环球中医药》[ISSN:1006-6977/CN:61-1281/TN]

卷:
第7卷
期数:
2014年08期
页码:
591-0
栏目:
论著
出版日期:
2014-08-06

文章信息/Info

Title:
Study on the mitochondrial mtDNA ATPase6、8 gene mutation and on the function mechanism of panax notoginseng saponins Rg1,Rb1 for hepatic fibrosis rats
作者:
李剑瑜 刘鹏年 张霞等
Author(s):
LI Jian-yu;  LIU Peng-nian;  ZHANG Xia;  et al.
Blood Transfusion Department of Zhuozhou City Hospital, Zhuozhou 072750, China
关键词:
肝纤维化; 线粒体; 三磷酸腺苷酶6亚基; 三磷酸腺苷酶8亚基; 三七皂甙Rg1; 三七皂甙Rb1; Wistar大鼠
Keywords:
Hepatic fibrosis;  Mitochondria DNA;  Adenosine triphosphatase 6 gene;  Adenosine triphosphatase 8 gene;  Panax notoginseng saponins Rg1;  Panax notoginseng saponins Rb1;  Wistar rat
分类号:
-
DOI:
-
文献标志码:
A
摘要:
目的 探讨三七皂甙(panax notoginseng saponins,PnS)Rg1、PnS Rb1干预下,肝纤维化大鼠线粒体DNA三磷酸腺苷(adenine triphosphate,ATP)酶6亚基、ATP酶8亚基的基因突变和ATP含量变化。方法 96只Wistar大鼠分为对照组、四氯化碳(carbon tetrachloride,CCl4)肝纤维化大鼠模型组、PnS Rg1组、PnS Rb1组各24只。除对照组外,其余3组用5%CCl4橄榄油按5 ml/kg灌胃制作肝纤维化大鼠模型。PnS Rg1组在每次CCl4灌胃同时腹腔注射PnSRg1(5 mg/kg)。PnS Rb1组在每次C...
Abstract:
Objective To explore the changes of the mitochondrial DNA(mt DNA)adenine triphospholibase(ATPase)6 gene, ATPase 8 gene mutation under the intervention of panax notoginseng saponins(PnS)Rg1, PnS Rb1 for hepatic fibrosis rats which may have theoretical sense in the prevention and cure hepatic fibrosis. Methods 96 Wistar rats divided into contrast group,carbon tetrachloride(CCl4 )group, liver fibrosis rats model group, PnS Rg1 group and PnS Rb1group, with 24 rats in each group.Except contrast group, other three groups were reproduced by repeated injection 5% CCl4 solution in rats into liver fibrosis rats model. PnS Rg1 group were also injected 5 ml/kg, PnS Rb1 group were injected 5 ml/kg, and at the same time given 5% CCl4 solution. Extract RNA of hepatic mitochondrial and reverse transcription complementary DNA(cDNA). Gene-recommended and sequencing have been researched. Then further study the PnS Rg1 group, PnS Rb1 group ATPase 6 gene 7904-8584 region and ATPase 8 gene 7743-7946 region gene mutation after 6 weeks. Biological fluorescent method detect ATP content.Results(1)Compare with the contrast group, gene analysis of mtDNA ATPase 6 in hepatic fibrosis of model group rats showed that there were three mutation sites:C8294G, T8505G, C8584A. Using Fisher's exact test to analyze, mutations have increased significantly(P<0.01). Compare with the contrast group, PnS Rg1 group、PnS Rb1 group mutation increasing does not have marked sense(P>0.05).(2)Compare with the contrast group,the gene analysis of mtDNA ATPase 8 were two mutation sites: A7797non, T7863C. Using Fisher's exact test to analyze, mutations have increased significantly(P<0.01).(3)Liver fibrosis rats mitochondrial DNA ATP of each group with CCl4 manage time correlation analysis, undergoing pearson's test r=-0.935 negative correlation.(4)Liver fibrosis rats mitochondrial DNA ATP of each group with ATPase6 gene mutation has correlation analysis, undergoing pearson's test r=-0.943 negative correlation. Liver fibrosis rats mitochondrial DNA ATP of each group with ATPase8 gene mutation has correlation analysis, undergoing pearson's test r=-0.961 negative correlation.Conclusion The mutation of mtDNA ATPase 6 gene and ATPase 8 gene may be responsible for hepatic fibrosis development. PnS Rg1,PnS Rb1 were protective function remarkably for the mitochondrial of hepatic fibrosis rats through inhibition of mtDNA ATPase 6 gene, ATPase 8 gene mutation rate. Therefore delay hepatic fibrosis development.

参考文献/References:

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备注/Memo

备注/Memo:

作者单位:072750 河北省涿州市医院输血科(李剑瑜、刘鹏年、张霞、穆启梅、柳伟、刘强),检验科(武凡)
作者简介:李剑瑜(1973- ),女,本科,副主任技师。研究方向:临床检验。 E-mail:ljy1797@163.com 通讯作者:武凡(1949- ),女,博士,教授。研究方向:细胞损伤与抗损伤。E-mail:wufanfan49@163.com
更新日期/Last Update: 1900-01-01