三七总皂苷在肾间质纤维化中的药理作用

Pharmacological effect of panax notoginoside on tubulointerstitial fibrosis

目的:总结三七总皂苷对肾间质纤维化的药理学作用,探讨三七总皂苷在防治肾间质纤维化应关注的重要环节及其病理生理机制。资料来源:应用计算机检索Medline1990-01/2006-03关于三七总皂苷在肾间质纤维化中药理作用的文章,检索词“Panaxnotoginoside(PNS),tubu1ointerstitia1fibrosis(TIF),pharmacologicaction”并限定文章的语言种类为“English”。同时利用计算机检索中国期刊全文数据库1990-01/2006-03的相关文章,限定文章语言种类为中文,检索词“三七总皂苷,肾间质纤维化,药理作用”。资料选择:对资料进行初审,选择与三七总皂苷治疗肾间质纤维化的药理作用相关文章52篇,无论研究对象是人还是动物均纳入,排除综述类文献。资料提炼:对选择的文献进一步查找全文,排除不同程度重复的文章,选择近期发表在较权威杂志的18篇文章进行综述。资料综合:肾间质纤维化形成的机制主要是炎症细胞浸润,肾脏固有细胞在致纤维化性生长因子、各种细胞因子等作用下肾小管、肾间质细胞损伤和活化及细胞外基质成分的产生与降解过程的失调而致其过度积聚。临床和科研研究证实三七总皂苷可从细胞水平、分子水平及基因水平防治肾间质纤维化的形成。结论:三七总皂苷防治肾间质纤维化可能与减少胶原及转化生长因子β的表达、抑制肾小管上皮细胞转分化、抑制人肾间质成纤维细胞增殖及促进其凋亡等有关。

OBJECTIVE： To summarize the pharmacological effects of panax notoginoside （PNS） on tubulointerstitial fibrosis （TIF）, and probe into the key points of PNS in the prevention and treatment of TIF and the pathophysiological mechanism of patients. DATA SOURCES： A computer-based online search was conducted in Medline for articles related to the pharmacological action of PNS on TIF published between January 1990 and March 2006 with the key words of ＂panax notoginoside （PNS）, tubulointerstitial fibrosis （TIF）, pharmacologic action＂, and the language was limited to English. Meanwhile, CNKI was searched in full text for relevant Chinese articles between January 1990 and March 2006 with the key words of ＂Panax notoginoside （PNS）, tubulointerstitial fibrosis （TIF）, pharmacologic action＂. STUDY SELECTION： Data were checked in the first trial, and 52 literatures related to the pharmacological action of PNS on TIF were selected no matter the subjects were human or animals. Repetitive reviews were excluded. DATA EXTRACTION： Enrolled studids were looked for the full text, and repetitive articles were excluded. Eighteen studies published recently in authorized magazines were reviewed. DATA SYNTHESIS： The mechanisms of TIF were mainly inflammatory cell infiltration, the injuries and activation of renal tubule and interstitial cells under the action of growth factors and renal all kinds of cell factors as well as exceeding accumulation induced by the disproportion in the generation of extracellular matrix components and its degradation. It was proved by clinical researches that PNS could prevent the formation of TIF from cellular level, molecular level and gene level. CONCLUSION： PNS in the prevention and treatment of TIF may be related with the reduction of expressions of collagen and transforming growth factor β, inhibition of transdifferentiation of renal tubular epithelial cells, suppression of the proliferation of human renal interstitiual fibroblasts as well as the promotion of its apoptosis, etc.