本文選題：卡維地洛 + 人肝星狀細胞��； 參考：《中國藥房》2017年19期

【摘要】：目的:研究卡維地洛對瘦素誘導(dǎo)的LX2人肝星狀細胞(HSC-LX2)活化增殖的影響及機制。方法:取對數(shù)生長期的HSC-LX2細胞分為空白對照組、瘦素刺激組和卡維地洛低、中、高濃度組(5、10、20μmol/L),除空白對照組外,其余各組均加入0.1 g/L的瘦素及相應(yīng)濃度的卡維地洛作用24 h。采用MTT法檢測細胞的光密度(OD)值,計算細胞增殖抑制率;流式細胞術(shù)檢測細胞周期和凋亡情況;實時熒光定量聚合酶鏈式反應(yīng)法檢測細胞中α-平滑肌肌動蛋白(α-SMA)、基質(zhì)金屬蛋白酶抑制因子1(TIMP-1)、瘦素及瘦素受體m RNA表達;Western blot法檢測磷酸化Janus激酶2(p-JAK2)、磷酸化信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子3(p-STAT3)蛋白表達。結(jié)果:與空白對照組比較,瘦素刺激組細胞的OD值增加、凋亡率降低、G_0/G_1期細胞減少(P0.05);α-SMA、TIMP-1、瘦素、瘦素受體m RNA表達和p-JAK2、p-STAT3蛋白表達均增強(P0.05)。與瘦素刺激組比較,卡維地洛各濃度組細胞的OD值減小、凋亡率升高、細胞主要阻滯在G_0/G_1期(P0.05);α-SMA、TIMP-1、瘦素、瘦素受體m RNA表達和p-JAK2、p-STAT3蛋白表達均減弱(P0.05),且呈濃度依賴性(P0.05)。結(jié)論:卡維地洛能夠抑制瘦素誘導(dǎo)的HSC-LX2細胞的活化增殖,促進HSC-LX2細胞凋亡;其機制可能與下調(diào)瘦素、瘦素受體基因表達并阻斷瘦素誘導(dǎo)的細胞內(nèi)JAK2/STAT3信號通路激活有關(guān)。
[Abstract]:Objective: To study the effect and mechanism of carvedilol on the activation and proliferation of LX2 human hepatic stellate cells (HSC-LX2) induced by leptin. Methods: the HSC-LX2 cells from the logarithmic growth period were divided into blank control group, leptin stimulation group and carvedilol low, medium and high concentration group (5,10,20 mu mol/L), except for the blank control group, all the other groups were added to 0.1 g/L leptin and phase. The concentration of carvedilol at 24 h. was used to detect cell light density (OD) and cell proliferation inhibition rate; cell cycle and apoptosis were measured by flow cytometry; alpha smooth muscle actin (alpha -SMA), matrix metalloproteinase inhibitor 1 (TIMP-1), leptin and leptin were detected by real-time fluorescence quantitative polymerase chain reaction. The expression of leptin receptor m RNA; Western blot method to detect the phosphorylated Janus kinase 2 (p-JAK2), phosphorylation signal transduction and transcription activator 3 (p-STAT3) protein expression. Results: compared with the blank control group, the OD value of the cells in the leptin stimulation group increased, the apoptosis rate decreased and the G_0/G_1 phase cell decreased (P0.05); alpha -SMA, TIMP-1, leptin, leptin receptor M And p-JAK2, the expression of p-STAT3 protein increased (P0.05). Compared with the leptin stimulation group, the OD value of cells in the concentration group of carvilol decreased, the apoptosis rate increased, and the cells mainly blocked in the G_0/G_1 phase (P0.05); alpha -SMA, TIMP-1, leptin, m RNA expression of M, p-JAK2, p-STAT3 protein decreased (P0.05), and showed concentration dependence. Carvedilol can inhibit the activation and proliferation of leptin induced HSC-LX2 cells and promote apoptosis of HSC-LX2 cells. The mechanism may be related to the downregulation of leptin, leptin receptor gene expression and blocking the activation of JAK2/STAT3 signaling pathway induced by leptin.
【作者單位】： 河北省人民醫(yī)院門診辦公室;河北省人民醫(yī)院代謝病重點實驗點;河北省人民醫(yī)院神經(jīng)外二科;河北省人民醫(yī)院消化內(nèi)二科;
【基金】：河北省醫(yī)學(xué)科學(xué)研究重點課題計劃項目(No.ZL20140250)
【分類號】：R96

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本文編號：1980964