中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2014年
7期
58-60,61
,共4页
刘绍能%杨清高%潘澎%陶夏平%刘慧敏
劉紹能%楊清高%潘澎%陶夏平%劉慧敏
류소능%양청고%반팽%도하평%류혜민
芪术颗粒%磷脂酰肌醇-3-激酶/丝氨酸蛋白激酶%信号传导通路%大鼠
芪術顆粒%燐脂酰肌醇-3-激酶/絲氨痠蛋白激酶%信號傳導通路%大鼠
기술과립%린지선기순-3-격매/사안산단백격매%신호전도통로%대서
Qishu granule%PI3K/Akt%signaling transduction pathway%rats
目的:观察芪术颗粒在肝纤维化形成过程中对磷脂酰肌醇-3-激酶/丝氨酸蛋白激酶(PI3K/Akt)信号传导通路的影响,进一步阐明其抗肝纤维化的作用机制。方法将Wistar大鼠随机分为正常组、模型组、实验对照组和芪术颗粒组,采用四氯化碳复制肝纤维化模型,造模同日即给予相应治疗,芪术颗粒组2 g/(kg?d)灌胃,体积为1.0 mL/100 g体质量,实验对照组、模型组给予等体积无菌水,正常组正常喂养。分别于造模后第1、2、4周处理、取材,Western blot免疫印迹法检测p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达。结果与正常组比较,模型组、芪术颗粒组各时间点p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达均升高(P<0.05)。与模型组比较,第1、2、4周时芪术颗粒组p-Akt(Ser473)表达显著降低,第1、4周Caspase9表达显著降低,差异有统计学意义(P<0.05,P<0.01);p-Akt(Thr308)、Bad(Ser136)表达低于模型组,但差异无统计学意义(P>0.05)。结论芪术颗粒对PI3K/Akt信号传导通路的激活有调控作用,从而抑制肝纤维化的发生和发展。
目的:觀察芪術顆粒在肝纖維化形成過程中對燐脂酰肌醇-3-激酶/絲氨痠蛋白激酶(PI3K/Akt)信號傳導通路的影響,進一步闡明其抗肝纖維化的作用機製。方法將Wistar大鼠隨機分為正常組、模型組、實驗對照組和芪術顆粒組,採用四氯化碳複製肝纖維化模型,造模同日即給予相應治療,芪術顆粒組2 g/(kg?d)灌胃,體積為1.0 mL/100 g體質量,實驗對照組、模型組給予等體積無菌水,正常組正常餵養。分彆于造模後第1、2、4週處理、取材,Western blot免疫印跡法檢測p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白錶達。結果與正常組比較,模型組、芪術顆粒組各時間點p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白錶達均升高(P<0.05)。與模型組比較,第1、2、4週時芪術顆粒組p-Akt(Ser473)錶達顯著降低,第1、4週Caspase9錶達顯著降低,差異有統計學意義(P<0.05,P<0.01);p-Akt(Thr308)、Bad(Ser136)錶達低于模型組,但差異無統計學意義(P>0.05)。結論芪術顆粒對PI3K/Akt信號傳導通路的激活有調控作用,從而抑製肝纖維化的髮生和髮展。
목적:관찰기술과립재간섬유화형성과정중대린지선기순-3-격매/사안산단백격매(PI3K/Akt)신호전도통로적영향,진일보천명기항간섬유화적작용궤제。방법장Wistar대서수궤분위정상조、모형조、실험대조조화기술과립조,채용사록화탄복제간섬유화모형,조모동일즉급여상응치료,기술과립조2 g/(kg?d)관위,체적위1.0 mL/100 g체질량,실험대조조、모형조급여등체적무균수,정상조정상위양。분별우조모후제1、2、4주처리、취재,Western blot면역인적법검측p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9단백표체。결과여정상조비교,모형조、기술과립조각시간점p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9단백표체균승고(P<0.05)。여모형조비교,제1、2、4주시기술과립조p-Akt(Ser473)표체현저강저,제1、4주Caspase9표체현저강저,차이유통계학의의(P<0.05,P<0.01);p-Akt(Thr308)、Bad(Ser136)표체저우모형조,단차이무통계학의의(P>0.05)。결론기술과립대PI3K/Akt신호전도통로적격활유조공작용,종이억제간섬유화적발생화발전。
Objective To observe the effects of Qishu granule on PI3K/Akt signaling transduction pathways in the process of hepatic fibrosis, and further explain the anti-hepatic fibrosis mechanism of Qishu granule.Methods Wistar rats were randomly divided into normal group, model group, experimental control group and Qishu granule group. Liver fibrosis was duplicated in rats by intraperitoneal injection of CCl4, and the rats were given appropriate treatment at the same day. Rats in Qishu granule group were given a gavage 2 g/(kg?d), 1.0 mL/100 g, while rats in experimental control group and normal group were given the same amount of aquae sterilisata. Rats in each group were taken liver tissue samples in the 1st, 2nd and 4th week, and were checked for the protein expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 by Western blot.Results Compared with the model group, expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 in model and Qishu granule groups increased in every time points (P<0.05). Compared with the model group, expression level of p-Akt (Ser473) in Qishu granule group decreased significantly in the 1st, 2nd, and 4th weeks, expression level of Caspase9 dropped in the 1st and the 4th weeks, with statistical significance (P<0.05,P<0.01);expressions of p-Akt (Thr308) and Bad (Ser136) were lower than those in model group, without statistical significance (P>0.05).Conclusion Qishu granule could regulate PI3K/Akt signaling transduction pathways, and inhibit the occurrence and development of liver fibrosis.