| 普显宏 何媛 黄微 茹金 杨金伟.三七皂苷R1 对肝纤维化大鼠TGF-beta1/Smad3信号的影响[J].,2015,15(4):622-626 |
| 三七皂苷R1 对肝纤维化大鼠TGF-beta1/Smad3信号的影响 |
| The Effect of Notoginsenoside R1 on TGF-beta1/smad3 Signal Pathwayin Hepatic Fibrosis Rats |
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| DOI： |
| 中文关键词: 三七皂苷R1 肝纤维化 大鼠 转化生长因子-beta1 Smad3 |
| 英文关键词: Notoginsenoside R1 Hepatic fibrosis Rat TGF-beta1 Smad3 |
| 基金项目:国家自然科学基金项目（81260075，31260253）；云南省科技厅- 昆明医科大学应用基础研究联合专项（2012FB002，
2012FB092，2013FB114）；云南省肿瘤转化医学工程技术研究中心（2011DH011）；云南省教育厅科学研究基金重点项目（2012Z151C） |
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| 中文摘要: |
| 目的：探讨SD 大鼠肝纤维化后肝组织及血清中转化生长因子-beta1(Transforming Growth Factor-茁1, TGF-beta1)及Smad3 的表
达和变化，以及三七皂苷R1 对肝纤维化的保护作用。方法：72 只健康雄性SD 大鼠分为对照组、二甲基亚硝胺(NDMA)组和三七
皂苷R1 组，再按不同时间点分为1、2、4周，3 个亚组，每个亚组8 只动物。NDMA 组采用NDMA 2 mL/kg 腹腔注射，三七皂苷R1
组同时静脉注射三七皂苷R1，剂量为100 mg/kg体重，对照组注射等量的生理盐水。在各组的不同时间点采用RT-PCR及ELISA
技术检测肝组织及血清中TGF-beta1、Smad3 的表达及变化。结果：1、TGF-beta1、Smad3 mRNA及蛋白在各组中均有表达。2、对照组各
时间点比较均无统计学意义(P>0.05)。NDMA 组中，随着损伤时间的延长，TGF-茁1、Smad3 mRNA 及蛋白的表达逐渐上调，且各时
间点与对照组比较有统计学意义(P＜0.05)。而三七皂苷R1 组TGF-茁1、Smad3 mRNA 及蛋白在各时间点均较NDMA组表达下
调，有统计学意义(P＜0.05)。结论：1、TGF-茁1/Smad3 信号参与了肝纤维化的发生和发展过程，且随损伤的逐渐加重，表达越高。2、
三七皂苷R1 可降低肝组织中TGF-茁1/Smad3 信号的表达，减轻肝细胞的纤维化，发挥保护肝组织损伤的作用。 |
| 英文摘要: |
| Objective:To investigate the expression of transforming growth factor-beta1 (TGF-beta1) and Smad3 in liver and serum after
hepatic fibrosis, and the protective effect of Notoginsenoside R1 on hepatic fibrosis.Methods:72 healthy male SD rats were randomly
divided into control group, NDMA group and Notoginsenoside R1 group, according to the different time points of 1, 2, 4 weeks, 3 subgroups,
each subgroup 8 animals. For NMDA group, NMDA was administrated by intraperitoneal injection (2 mL/kg); and for Notoginsenoside
R1 group, Notoginsenoside R1 was administrated by intravenous injection with a dose of 100 mg/kg and the animals of control
group was injected with equal amount normal saline. The expression of TGF-beta1 and Smad3 in liver tissues and serum was detected at
different time points using ELISA and RT-PCR.Results:Expression of TGF-beta1 and Smad3 protein and mRNA was detectable in all
groups. In the control group, the expression of TGF-beta1 and Smad3 at different time points had no statistical significance (P>0.05). Compared
with that in the control group, the expression of TGF-beta1 and Smad3 protein and mRNA in NMDA group gradually increased at
each time point with the injury, and showed statistical significance (P<0.05). While in Notoginsenoside R1 group, expression of TGF-beta1
and Smad3 at each time point was down-regulated, with statistical significance (P<0.05) compared with that in the NDMA group.Conclusion:TGF-beta1/Smad3 signal was involved in the occurrence and development of liver fibrosis, and with the aggravation of injury, the
expression of TGF-beta1 and Smad3 gradually increased. Notoginsenoside R1 could reduce TGF-beta1/Smad3 signal in liver tissues, then reduce
liver fibrosis and protect the liver frominjury. |
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