中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2009年
2期
185-187
,共3页
杨道坤%乔汉臣%孙屹峰%梁海军
楊道坤%喬漢臣%孫屹峰%樑海軍
양도곤%교한신%손흘봉%량해군
缬氨酸/类似物和衍生物/药理学%肝硬化/药物疗法
纈氨痠/類似物和衍生物/藥理學%肝硬化/藥物療法
힐안산/유사물화연생물/약이학%간경화/약물요법
Valine/AA/PD%Liver cirrhosis/DT
目的 观察缬沙坦预防、治疗大鼠肝纤维化的作用和机制.方法 雄性SD大鼠30只,随机分为3组:缬沙坦预防组(A组),模型组(B组),缬沙坦治疗组(C组).二甲基亚硝胺(DMN)腹腔注射,各组每周连续3 d,1次/d,共4周.A组造模同时给于缬沙坦10 mg/(kg·d)灌胃,共4周,第5周起停止腹腔注射DMN后仍按原剂量灌胃,再4周.C和B2组停止造模后,分别给予缬沙坦10 ms/(kg·d)或生理盐水灌胃,共4周.8周后留取肝标本,行HE染色和Masson染色,以免疫组化法检测a-平滑肌肌动蛋白(a-SMA)含量.结果 (1)A组:肝索排列基本整齐,有少量出血,汇管区稍扩大,未见胶原纤维增生.B组:肝组织大片出血坏死,有假小叶形成.C组:肝索排列紊乱,有出血坏死,汇管区扩大,有纤维间隔伸向肝小叶.(2)Masson染色胶原定量分析:B组明显高于A、C 2组(P<0.01),A组低于C组(P<0.05).(3)肝窦壁a-SMA观察:C组肝窦壁强阳性表达,A组肝窦壁基本不表达,仅见于汇管区,B组肝窦壁阳性表达,3组定量差异有统计学意义(P<0.05).结论 在DMN诱导的肝纤维化模型中,缬沙坦部分通过抑制肝星状细胞(HSC)的活化预防和治疗肝纤维化,且预防效果优于治疗.
目的 觀察纈沙坦預防、治療大鼠肝纖維化的作用和機製.方法 雄性SD大鼠30隻,隨機分為3組:纈沙坦預防組(A組),模型組(B組),纈沙坦治療組(C組).二甲基亞硝胺(DMN)腹腔註射,各組每週連續3 d,1次/d,共4週.A組造模同時給于纈沙坦10 mg/(kg·d)灌胃,共4週,第5週起停止腹腔註射DMN後仍按原劑量灌胃,再4週.C和B2組停止造模後,分彆給予纈沙坦10 ms/(kg·d)或生理鹽水灌胃,共4週.8週後留取肝標本,行HE染色和Masson染色,以免疫組化法檢測a-平滑肌肌動蛋白(a-SMA)含量.結果 (1)A組:肝索排列基本整齊,有少量齣血,彙管區稍擴大,未見膠原纖維增生.B組:肝組織大片齣血壞死,有假小葉形成.C組:肝索排列紊亂,有齣血壞死,彙管區擴大,有纖維間隔伸嚮肝小葉.(2)Masson染色膠原定量分析:B組明顯高于A、C 2組(P<0.01),A組低于C組(P<0.05).(3)肝竇壁a-SMA觀察:C組肝竇壁彊暘性錶達,A組肝竇壁基本不錶達,僅見于彙管區,B組肝竇壁暘性錶達,3組定量差異有統計學意義(P<0.05).結論 在DMN誘導的肝纖維化模型中,纈沙坦部分通過抑製肝星狀細胞(HSC)的活化預防和治療肝纖維化,且預防效果優于治療.
목적 관찰힐사탄예방、치료대서간섬유화적작용화궤제.방법 웅성SD대서30지,수궤분위3조:힐사탄예방조(A조),모형조(B조),힐사탄치료조(C조).이갑기아초알(DMN)복강주사,각조매주련속3 d,1차/d,공4주.A조조모동시급우힐사탄10 mg/(kg·d)관위,공4주,제5주기정지복강주사DMN후잉안원제량관위,재4주.C화B2조정지조모후,분별급여힐사탄10 ms/(kg·d)혹생리염수관위,공4주.8주후류취간표본,행HE염색화Masson염색,이면역조화법검측a-평활기기동단백(a-SMA)함량.결과 (1)A조:간색배렬기본정제,유소량출혈,회관구초확대,미견효원섬유증생.B조:간조직대편출혈배사,유가소협형성.C조:간색배렬문란,유출혈배사,회관구확대,유섬유간격신향간소협.(2)Masson염색효원정량분석:B조명현고우A、C 2조(P<0.01),A조저우C조(P<0.05).(3)간두벽a-SMA관찰:C조간두벽강양성표체,A조간두벽기본불표체,부견우회관구,B조간두벽양성표체,3조정량차이유통계학의의(P<0.05).결론 재DMN유도적간섬유화모형중,힐사탄부분통과억제간성상세포(HSC)적활화예방화치료간섬유화,차예방효과우우치료.
Objectives The purpose of this study is to observe the effects of valsartan on hepapetic fibrosis. Methods Thirty male Sprague-Dawley rats were randomly divided into three groups: valsartan -prevetive group (A), modle group of hepatic fibrosis (B)and valsar-tan-treating group (C). The model of hepatic fibrosis in rats was induced by intraperitoneai injection of dimethylnitrosamine (DMN) for 4 weeks(2ml/kg everyday, three times a week). Valsartan (10mg/kg everyday) was given together with injection of DMN per intrngastric (Ig) in group A for 8 weeks. After stop injection of DMN, the S valsartan(10mg/kg, everyday)was given per Ig in group C for 4 weeks. After modeling, normal saline were given per Ig everyday in group B. At the end of eighth week, the histomorphylogic structure of the liver was ob-served with light microscope. Immunohistoebemical staining was used to evaluate the expression of a-SMA. Results In group B, there was a large necrotic area and a number of pesudolobes appeared in the liver tissue. In group A, there were normal hepatic cords. In the group C, there was fibrosis interval formation and portal area expansion and fibrotie intervals extending to the lobule. The quantitative analysis of Mas-son staining showed that the collagen quantities in group B was higher than that of other group(P<0.01). The collagen quantities in group A was lower than that of group C(P<0.05). The results of immanohistochemical staining showed that the expression of a-SMA in group B was strong positive, middle positive in group C, and weak positive in group A (P<0.05). Conclusion The valsartan has preventive and treatment effects on hepatic fibrosis in rats of hepatic fibrosis model induced by DMN, and the preventive effect of valsartan is better than its treatment effect. The valsartan can ameliorate the hver cirrhosis by partly suppressing the activation of HSC.