中国中西医结合杂志
中國中西醫結閤雜誌
중국중서의결합잡지
CHINESE JOURNAL OF INTEGRATED TRADITIONAL AND WESTERN MEDICINE
2010年
1期
76-79
,共4页
袁继丽%张悦%姜哲浩%王清兰%陶艳艳%刘成%刘成海
袁繼麗%張悅%薑哲浩%王清蘭%陶豔豔%劉成%劉成海
원계려%장열%강철호%왕청란%도염염%류성%류성해
扶正化瘀方%肾间质纤维化%氯化汞
扶正化瘀方%腎間質纖維化%氯化汞
부정화어방%신간질섬유화%록화홍
Fuzheng Huayu Recipe%renal interstitial fibrosis%mercuric chloride
目的 观察扶正化瘀方抗氯化汞(HgCl_2)诱导的大鼠肾间质纤维化病变的作用,并初步探讨其作用机制.方法 将大鼠随机分为正常组、模型组、扶正化瘀方(FZHY)组及维生素E(VitE)组,模型组用HgCl_28 mg/kg灌胃9周,FZHY组(4.6 g/kg)和VitE组(100 mg/kg)分别给予相应的药物干预.检测肾功能情况(Cr和BUN),盐酸水解法检测肾组织羟脯氨酸(Hyp)含量,HE染色、Masson染色和六胺银(PASM)染色观察肾组织病理形态,Western blot观察Ⅰ型胶原(Col Ⅰ)、纤维连接蛋白(FN)、α-平滑肌肌动蛋白(α-SMA)的表达.结果 与模型组比较,FZHY组及VitE组大鼠肾体比(双肾质量/体重)明显下降(P<0.05)、肾组织Hyp含量明显下降(P<0.05),血清Cr和BUN含量明显下降(P<0.01),肾脏纤维化程度明显减轻.其中FZHY组比VitE组轻.FZHY组和VitE组肾组织Col Ⅰ和FN表达均较模型组减弱(Col Ⅰ,P<0.05;FN,P<0.01).FZHY组α-SMA表达较模型组减弱(P<0.01),VitE组则无明显变化(P>0.05).结论 FZHY可改善HgCl_2诱导模型大鼠的肾功能损伤,减少细胞外基质沉积,减轻肾间质纤维化病变,其作用机制与抑制肌成纤维细胞活化有关.
目的 觀察扶正化瘀方抗氯化汞(HgCl_2)誘導的大鼠腎間質纖維化病變的作用,併初步探討其作用機製.方法 將大鼠隨機分為正常組、模型組、扶正化瘀方(FZHY)組及維生素E(VitE)組,模型組用HgCl_28 mg/kg灌胃9週,FZHY組(4.6 g/kg)和VitE組(100 mg/kg)分彆給予相應的藥物榦預.檢測腎功能情況(Cr和BUN),鹽痠水解法檢測腎組織羥脯氨痠(Hyp)含量,HE染色、Masson染色和六胺銀(PASM)染色觀察腎組織病理形態,Western blot觀察Ⅰ型膠原(Col Ⅰ)、纖維連接蛋白(FN)、α-平滑肌肌動蛋白(α-SMA)的錶達.結果 與模型組比較,FZHY組及VitE組大鼠腎體比(雙腎質量/體重)明顯下降(P<0.05)、腎組織Hyp含量明顯下降(P<0.05),血清Cr和BUN含量明顯下降(P<0.01),腎髒纖維化程度明顯減輕.其中FZHY組比VitE組輕.FZHY組和VitE組腎組織Col Ⅰ和FN錶達均較模型組減弱(Col Ⅰ,P<0.05;FN,P<0.01).FZHY組α-SMA錶達較模型組減弱(P<0.01),VitE組則無明顯變化(P>0.05).結論 FZHY可改善HgCl_2誘導模型大鼠的腎功能損傷,減少細胞外基質沉積,減輕腎間質纖維化病變,其作用機製與抑製肌成纖維細胞活化有關.
목적 관찰부정화어방항록화홍(HgCl_2)유도적대서신간질섬유화병변적작용,병초보탐토기작용궤제.방법 장대서수궤분위정상조、모형조、부정화어방(FZHY)조급유생소E(VitE)조,모형조용HgCl_28 mg/kg관위9주,FZHY조(4.6 g/kg)화VitE조(100 mg/kg)분별급여상응적약물간예.검측신공능정황(Cr화BUN),염산수해법검측신조직간포안산(Hyp)함량,HE염색、Masson염색화륙알은(PASM)염색관찰신조직병리형태,Western blot관찰Ⅰ형효원(Col Ⅰ)、섬유련접단백(FN)、α-평활기기동단백(α-SMA)적표체.결과 여모형조비교,FZHY조급VitE조대서신체비(쌍신질량/체중)명현하강(P<0.05)、신조직Hyp함량명현하강(P<0.05),혈청Cr화BUN함량명현하강(P<0.01),신장섬유화정도명현감경.기중FZHY조비VitE조경.FZHY조화VitE조신조직Col Ⅰ화FN표체균교모형조감약(Col Ⅰ,P<0.05;FN,P<0.01).FZHY조α-SMA표체교모형조감약(P<0.01),VitE조칙무명현변화(P>0.05).결론 FZHY가개선HgCl_2유도모형대서적신공능손상,감소세포외기질침적,감경신간질섬유화병변,기작용궤제여억제기성섬유세포활화유관.
Objective To observe the effects of Fuzheng Huayu Recipe (FHR) on rat's renal interstitial fibrosis induced by mercuric chloride (HgCl_2), and to explore preliminarily its mechanism of action. Methods Rats were randomly divided into four groups: the normal group, the model group, the FHR group and the vitamine E group, the latter two were treated respectively by FHR 4.6 g/kg and vitamine E 100 mg/kg. Rats model was established by oral administration of 8 mg/kg HgCl_2 for 9 weeks. Serum creatinine (Cr) and urea nitrogen (BUN) content were tested with corresponding test kits; hydroxyproline (Hyp) content in kidney was assayed with hydrochloric acid hydrolysis; renal histologic change was observed with HE, Masson and methenamine silver (PASM) staining; and collagen type Ⅰ(ColⅠ), as well as protein expressions of fibronectin (FN) and α-smooth muscle actin (α-SMA) was determined with Western blot. Results Compared with the model group, the kidney/body weight ratio, serum levels of Cr and BUN, kidney Hyp content, and severity of renal interstitial fibrosis in the two treated groups were significantly lower (P<0.05 or P<0.01), and the improvements were more significant in the FHR group than those in the vitamine E group; ColⅠand FN protein expression was also weaker in the two treated group (Col, P<0.05; FN, P<0.01); while the expression of α-SMA was lower in the FHR group (P<0.01), but it wasn't in the vitamine E group (P>0.05). Conclusion FHR could improve the HgCl_2-induced renal function injury in rats, decrease extracellular matrix dEposition and restrain renal interstitial fibrosis, the mechanism of action might be related with its inhibitory effect on myofibroblast activation.