• 華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院普外科(武漢430030);

目的 探討阻塞性黃疸肝損害的調(diào)控機(jī)理。方法①采用膠原酶原位肝灌注法獲取大鼠肝細(xì)胞,行原代培養(yǎng),用蛋白激酶C(PKC) 激動(dòng)劑帕斯酶埃(PMA)、拮抗劑切勒斯埃(chelerythrine)作用于肝細(xì)胞,再用50 μmol/L甘氨鵝脫氧膽酸鈉(GCDC)作用后行流式細(xì)胞術(shù)(FCM)及用末端脫氧核苷酸轉(zhuǎn)移酶(TdT)介導(dǎo)的脫氧核苷酸(dUTP)缺口末端標(biāo)記技術(shù)(TUNEL)檢測(cè)肝細(xì)胞凋亡情況。②分別于結(jié)扎大鼠膽總管后3 d、7 d、14 d及21 d處死大鼠, 用TUNEL技術(shù)及免疫組織化學(xué)方法檢測(cè)阻塞性黃疸大鼠肝臟組織細(xì)胞凋亡狀態(tài)及PKC蛋白的表達(dá)。 結(jié)果①隨PMA濃度的增加,肝細(xì)胞的凋亡明顯增加,隨Chelerythrine的增加,肝細(xì)胞的凋亡明顯減少。②大鼠膽總管結(jié)扎后隨結(jié)扎時(shí)間的延長(zhǎng)細(xì)胞凋亡指數(shù)(AI)增加,結(jié)扎14 d后AI達(dá)高峰。PKC蛋白表達(dá)越強(qiáng), AI就越高。結(jié)論蛋白激酶C信號(hào)通道參與了阻塞性黃疸肝細(xì)胞凋亡的調(diào)節(jié),并在阻塞性黃疸肝損害的發(fā)生和發(fā)展中起重要作用。

引用本文: 王劍明,鄒聲泉. 蛋白激酶 C信號(hào)通道在阻塞性黃疸肝損害發(fā)生發(fā)展中的作用. 中國(guó)普外基礎(chǔ)與臨床雜志, 2002, 9(2): 76-79. doi: 復(fù)制

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