| PAX6通过MEK/ERK信号通路抑制肝星状细胞活化和增殖实验研究 |
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| 引用本文： | 白亮,王宝太,高志峰,蒋安,梁金强. PAX6通过MEK/ERK信号通路抑制肝星状细胞活化和增殖实验研究[J]. 实用肝脏病杂志, 2022, 25(3): 318-322. DOI: 10.3969/j.issn.1672-5069.2022.03.004 |
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| 作者姓名： | 白亮 王宝太 高志峰 蒋安 梁金强 |
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| 作者单位： | 710000 西安市 西安交通大学第二附属医院普外科 |
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| 摘 要： | 目的 探讨PAX6通过丝裂原活化蛋白激酶(MEK)/细胞外调节蛋白激酶(ERK)信号通路抑制肝星状细胞活化和增殖的效果。方法 取LX2肝星状细胞，分为对照组、PAX6 inhibitor组和PAX6 mimics组。采用CCK-8试剂盒测定细胞增殖，采用油红O染色测定细胞分化水平，使用流式细胞仪分析细胞凋亡，采用RT-PCR法和蛋白印迹法测定细胞PAX6、MEK和ERK mRNA和蛋白表达水平。结果 PAX6 inhibitor组细胞PAX6 mRNA水平、凋亡率和G1期分别为(1.49±0.23)、(2.70±0.85)%和(59.02±1.25)%,显著低于LX2肝星状细胞组【分别为(1.85±0.19)、(3.40±0.47)%和(64.66±1.41)%,P<0.05】,而细胞增殖、存活率、分化率、MEK和ERK mRNA和蛋白水平分别为(0.79±0.03)、(73.35±9.74)%、(49.37±4.24)%、(2.55±0.43)、(3.90±0.49)、(0.89±0.15)和(1.17±0.17),显著高于LX2肝星状细胞组【分别为(0.58±0.05)、(6...
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| 关 键 词： | 肝星状细胞 PAX6 MEK/ERK信号通路 细胞活化 细胞增殖 体外 |
| 收稿时间： | 2021-12-10 |
PAX6 inhibiting activation and proliferation of hepatic stellate cells through MEK/ERK signaling pathway in vitro |
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| Bai Liang,Wang Baotai,Gao Zhifeng,et al. PAX6 inhibiting activation and proliferation of hepatic stellate cells through MEK/ERK signaling pathway in vitro[J]. Journal of Clinical Hepatology, 2022, 25(3): 318-322. DOI: 10.3969/j.issn.1672-5069.2022.03.004 |
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| Authors: | Bai Liang Wang Baotai Gao Zhifeng et al |
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| Affiliation: | Department of General Surgery, Second Affiliated Hospital, Jiaotong University, Xi’an 710000, Shaanxi Province, China |
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| Abstract: | Objective The purpose of this experiment was to investigate the effect of PAX6 on inhibition of activation and proliferation of hepatic stellate cells (HSCs) by through MEK/ERK signaling pathway. Methods The LX2 HSCs were divided into control, PAX6 inhibitor and PAX6 mimics group and managed accordingly. The cell proliferation was determined by CCK-8 kit, the cell differentiation was detected by oil red O staining, the cell apoptosis was analyzed by flow cytometry, and PAX6, MEK and ERK mRNA and their protein expression were assayed by RT-PCR and Western blotting, respectively. Results The PAX6 mRNA level, apoptosis rate and G1 stage in PAX6 inhibitor-intervened group were (1.49±0.23), (2.70±0.85)% and (59.02±1.25)%, significantly lower than [(1.85± 0.19), (3.40±0.47)% and (64.66±1.41)%, respectively, P<0.05] in LX2 HSCs, and the cell proliferation, survival rate, differentiation rate, MEK and ERK mRNA and their protein expression in PAX6 inhibitor-intervened group were (0.79±0.03), (73.35±9.74)%, (49.37±4.24)%, (2.55±0.43), (3.90±0.49), (0.89±0.15) and (1.17±0.17), significantly higher than [(0.58±0.05), (60.74±9.24)%, (29.35±4.47)%, (2.67±0.47), (4.55±0.50), (0.74±0.14) and (1.35±0.16), respectively, P<0.05] in the control; the PAX6 mRNA level, apoptosis rate and G1 stages in PAX6 mimics-intervened group were (2.67±0.20), (6.70±1.04)% and (66.38±1.35)%, significantly higher than [(1.85± 0.19), (3.40±0.47)% and (64.66±1.41)%, respectively, P<0.05] in the control, and the cell proliferation, survival rate, differentiation rate, MEK and ERK mRNA and their protein expression in PAX6 mimics group were (0.40±0.04), (52.24±5.57)%, (13.85±3.35)%, (1.94±0.53), (1.45±0.42), (0.53±0.15) and (0.53±0.16), significantly lower than [(0.58 ±0.05), (60.74±9.24)%, (29.35±4.47)%, (2.67±0.47), (4.55±0.50), (0.74±0.14) and (1.35±0.16), respectively, P<0.05] in the control. Conclusion The PAX6 overexpression could inhibit the activation and proliferation of hepatic stellate cells, and promote cell apoptosis. The mechanism involved might be related to the inhibition of MEK and ERK expression and MEK/ERK pathway in hepatic stellate cells. |
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| Keywords: | Hepatic stellate cells PAX6 MEK/ERK signaling pathway Cell activation Cell proliferation In vitro |
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