国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
INTERNATIONAL JOURNAL OF TRIDITIONAL CHINESE MEDICINE
2011年
8期
686-688
,共3页
王礼凤%孙守才%李长秦%张宏勇%郑旭锐%曹宁
王禮鳳%孫守纔%李長秦%張宏勇%鄭旭銳%曹寧
왕례봉%손수재%리장진%장굉용%정욱예%조저
加味四逆散%肝纤维化%TβRⅠ%TβRⅡ
加味四逆散%肝纖維化%TβRⅠ%TβRⅡ
가미사역산%간섬유화%TβRⅠ%TβRⅡ
Jiawei-Sini Dection%Hepatic fibrosis%TβRⅠ,TβR Ⅱ
目的 观察加味四逆散对肝纤维化(hepatic fibrosis,HF)大鼠转化生长因子β1受体Ⅰ、Ⅱ(TβR Ⅰ,TβRⅡ)表达的影响,探讨加味四逆散抗HF的疗效和可能的作用机制.方法 采用四氯化碳(CCL4)皮下注射和自由饮用酒精的方法制各大鼠肝纤维化模型.将造模成功大鼠按照随机排列区组法分组,病理模型组(B组)、复方鳖甲软肝片组(C组)、加味四逆散组(D)各10只.A组与B组给予生理盐水2 ml/只,C组、D组分别给予复方鳖甲软肝片0.625 g/kg、加味四逆散药液15.625 g/kg 灌胃,1次/d,连续用药8周.为了防止肝脏自然修复对实验结果的影响,除A组外,其余各组于用药开始后仍每周注射40%CCL4植物油3 ml/kg(体重)1次.以复方鳖甲软肝片为阳性对照组,用免疫组织化学方法检测TβR Ⅰ,TβRⅡ的表达.观察大鼠血清谷丙转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)、肝纤维化TβR Ⅰ、TβRⅡ的变化.结果 大鼠TβR Ⅰ、TβRⅡ的表达,与病理组[(16.63±2.69)%、(14.57±1.09)%]比较,加味四逆散组均降低[分别为(8.09±0.71)%、(6.51±0.48)%],差异均有统计学意义(P均<0.05);加味四逆散组与复方鳖甲软肝片组的效果相当(P>0.05).结论 加味四逆散可抑制TβR Ⅰ、TβRⅡ的表达,并影响受体与TGFβ1的结合.
目的 觀察加味四逆散對肝纖維化(hepatic fibrosis,HF)大鼠轉化生長因子β1受體Ⅰ、Ⅱ(TβR Ⅰ,TβRⅡ)錶達的影響,探討加味四逆散抗HF的療效和可能的作用機製.方法 採用四氯化碳(CCL4)皮下註射和自由飲用酒精的方法製各大鼠肝纖維化模型.將造模成功大鼠按照隨機排列區組法分組,病理模型組(B組)、複方鱉甲軟肝片組(C組)、加味四逆散組(D)各10隻.A組與B組給予生理鹽水2 ml/隻,C組、D組分彆給予複方鱉甲軟肝片0.625 g/kg、加味四逆散藥液15.625 g/kg 灌胃,1次/d,連續用藥8週.為瞭防止肝髒自然脩複對實驗結果的影響,除A組外,其餘各組于用藥開始後仍每週註射40%CCL4植物油3 ml/kg(體重)1次.以複方鱉甲軟肝片為暘性對照組,用免疫組織化學方法檢測TβR Ⅰ,TβRⅡ的錶達.觀察大鼠血清穀丙轉氨酶(ALT)、天門鼕氨痠轉氨酶(AST)、堿性燐痠酶(ALP)、肝纖維化TβR Ⅰ、TβRⅡ的變化.結果 大鼠TβR Ⅰ、TβRⅡ的錶達,與病理組[(16.63±2.69)%、(14.57±1.09)%]比較,加味四逆散組均降低[分彆為(8.09±0.71)%、(6.51±0.48)%],差異均有統計學意義(P均<0.05);加味四逆散組與複方鱉甲軟肝片組的效果相噹(P>0.05).結論 加味四逆散可抑製TβR Ⅰ、TβRⅡ的錶達,併影響受體與TGFβ1的結閤.
목적 관찰가미사역산대간섬유화(hepatic fibrosis,HF)대서전화생장인자β1수체Ⅰ、Ⅱ(TβR Ⅰ,TβRⅡ)표체적영향,탐토가미사역산항HF적료효화가능적작용궤제.방법 채용사록화탄(CCL4)피하주사화자유음용주정적방법제각대서간섬유화모형.장조모성공대서안조수궤배렬구조법분조,병리모형조(B조)、복방별갑연간편조(C조)、가미사역산조(D)각10지.A조여B조급여생리염수2 ml/지,C조、D조분별급여복방별갑연간편0.625 g/kg、가미사역산약액15.625 g/kg 관위,1차/d,련속용약8주.위료방지간장자연수복대실험결과적영향,제A조외,기여각조우용약개시후잉매주주사40%CCL4식물유3 ml/kg(체중)1차.이복방별갑연간편위양성대조조,용면역조직화학방법검측TβR Ⅰ,TβRⅡ적표체.관찰대서혈청곡병전안매(ALT)、천문동안산전안매(AST)、감성린산매(ALP)、간섬유화TβR Ⅰ、TβRⅡ적변화.결과 대서TβR Ⅰ、TβRⅡ적표체,여병리조[(16.63±2.69)%、(14.57±1.09)%]비교,가미사역산조균강저[분별위(8.09±0.71)%、(6.51±0.48)%],차이균유통계학의의(P균<0.05);가미사역산조여복방별갑연간편조적효과상당(P>0.05).결론 가미사역산가억제TβR Ⅰ、TβRⅡ적표체,병영향수체여TGFβ1적결합.
Objective To investigate the role of Jiawei-sini Dection on expression of rat transforming growth factor-β1 receptor Ⅰ,Ⅱ(TβRⅠ,TβR Ⅱ), and study its treatment of anti-HF and the possible mechanisms. Methods The model of rat hepatic fibrosis was setup by subcutaneous injection of carbon tetrachloride and drinking alcohol freely;According to random block method, the successful model rats were divided into three groups:pathological model group (group B),Fufangbiejiarangan tablet group (group C), and Jiawei Sini Decoction group (group D), each group containing ten rats. Group A and group B were given two milliliters saline, group C was given Fufangbiejiarangan tablets 0.625 grams per kilogram of body weight, group D was given Jiawei Sini liquid 15.625 grams per kilogram of body weight.Each rat was fed once a day for 8 weeks.In order to avoid the natural repair of the hepatic affecting the experimental results, the rats,except group A, were still injected 40% CCl4 three milliliters per kilogram of body weight after feeding drug once a week. Fufang-Biejia-Ruangan Ttablet group was set as a positive control;The effects on expression of TβRⅠ,TβR Ⅱ were determined by immunohistochemical method. Changes of alanine aminotransferase (ALT), aspartate aminotransferase(AST),alkaline phosphatase(ALP) and TβRⅠ,TβR Ⅱ were observed in rats. Results The expression of TβRⅠ、Ⅱ, compared with the pathological model(16.63±2.69)%, (14.57±1.09)%, were significantly reduced in Jiawei-Sini Dection group[they are(8.09±0.71)%,(6.51±0.48)%, the difference was statistically significant(P<0.05).The effects of Jiawei-Sini Dection was equal to the effect of Fufang-Biejia-Ruangan Tablets on expression of TβRⅠ,TβR Ⅱ(P>0.05). Conclusion Jiawei-Sini Dection was able to inhibit the expression of TβRⅠ and TβR Ⅱ, thus affected the combination of TGFβ1, and their receptors.