实用肝脏病杂志
實用肝髒病雜誌
실용간장병잡지
JOURNAL OF CLINICAL HEPATOLOGY
2013年
4期
323-326
,共4页
李骢%周情%姜妙娜%张彩华%贾玉杰
李驄%週情%薑妙娜%張綵華%賈玉傑
리총%주정%강묘나%장채화%가옥걸
肝纤维化%肝复康%磷脂酰肌醇-3激酶%血小板衍生生长因子受体-β
肝纖維化%肝複康%燐脂酰肌醇-3激酶%血小闆衍生生長因子受體-β
간섬유화%간복강%린지선기순-3격매%혈소판연생생장인자수체-β
Liver fibrosis%Gan-fu-kang%PI3K%Platelet-derived growth factor-β
目的探讨中药肝复康对大鼠肝纤维化组织PI3K/PKB信号通路和血小板衍生生长因子受体-β(PDGFR-β)表达的影响。方法制备大鼠四氯化碳诱导的肝纤维化模型,给予肝复康干预。采用免疫组织化学法检测肝组织PDGFR-β蛋白的表达,采用半定量RT-PCR法测定肝组织PI3K和PKB1mRNA水平的变化。结果与对照组比,模型组肝组织PDGFR-β蛋白的表达上调,而肝复康治疗组其表达被显著抑制;模型组肝组织PI3K和PKB1 mRNA水平的相对光密度值分别为2.08±0.09和2.54±0.10,较对照组均显著上升(0.86±0.04和0.36±0.03, P<0.01),但肝复康治疗组其水平均被显著抑制(分别为0.88±0.05和0.41±0.03,与模型组比,P<0.01)。结论肝复康对肝纤维化的治疗作用可能与其作用于PI3K/PKB信号转导途径和抑制PDGFR-β表达有关。
目的探討中藥肝複康對大鼠肝纖維化組織PI3K/PKB信號通路和血小闆衍生生長因子受體-β(PDGFR-β)錶達的影響。方法製備大鼠四氯化碳誘導的肝纖維化模型,給予肝複康榦預。採用免疫組織化學法檢測肝組織PDGFR-β蛋白的錶達,採用半定量RT-PCR法測定肝組織PI3K和PKB1mRNA水平的變化。結果與對照組比,模型組肝組織PDGFR-β蛋白的錶達上調,而肝複康治療組其錶達被顯著抑製;模型組肝組織PI3K和PKB1 mRNA水平的相對光密度值分彆為2.08±0.09和2.54±0.10,較對照組均顯著上升(0.86±0.04和0.36±0.03, P<0.01),但肝複康治療組其水平均被顯著抑製(分彆為0.88±0.05和0.41±0.03,與模型組比,P<0.01)。結論肝複康對肝纖維化的治療作用可能與其作用于PI3K/PKB信號轉導途徑和抑製PDGFR-β錶達有關。
목적탐토중약간복강대대서간섬유화조직PI3K/PKB신호통로화혈소판연생생장인자수체-β(PDGFR-β)표체적영향。방법제비대서사록화탄유도적간섬유화모형,급여간복강간예。채용면역조직화학법검측간조직PDGFR-β단백적표체,채용반정량RT-PCR법측정간조직PI3K화PKB1mRNA수평적변화。결과여대조조비,모형조간조직PDGFR-β단백적표체상조,이간복강치료조기표체피현저억제;모형조간조직PI3K화PKB1 mRNA수평적상대광밀도치분별위2.08±0.09화2.54±0.10,교대조조균현저상승(0.86±0.04화0.36±0.03, P<0.01),단간복강치료조기수평균피현저억제(분별위0.88±0.05화0.41±0.03,여모형조비,P<0.01)。결론간복강대간섬유화적치료작용가능여기작용우PI3K/PKB신호전도도경화억제PDGFR-β표체유관。
Objective To investigate the effects of traditional Chinese herbal medicine Gan-fu-kang on hepatic PI3K/PKB signaling pathway and platelet-derived growth factor-β(PDGFR-β) in fibrotic liver in rats. Methods A rat model of liver fibrosis were induced by injection of 10%carbon tetrachloride (CCl4) subcuta-neously and was treated with Gan-fu-kang. The PDGFR-β protein in livers was detected by immunohistochem-istry and the PI3K and PKB1 mRNA were detected by semi-quantitive RT-PCR. Results The hepatic PDGFR-β protein in model animals was markedly increased than in the controls and was suppressed by Gan-fu-kang treatment;In the controls,the relative quantification value of PI3K and PKB1 mRNA were 0.86±0.04 and 0.36±0.03, respectively,which were significantly lower than that in the model animals (2.08±0.09 and 2.54±0.10,respectively,P<0.01); However,Gan-fu-kang treatment significantly inhibited the increased PI3K and PKB1 mRNA levels(0.88±0.05 and 0.41 ±0.03,respectively,P<0.01) as compared to that in the models. Conclusion Gan-fu-kang may inhibit liver fibrosis by through inhibition of PI3K/PKB signaling pathway and PDGFR-β expression.