| 罗晓旭,肖蕾,艾尼瓦尔·艾木都拉,吴戈,王云莲,张华,包永星.PI3K/Akt信号通路与肝星状细胞活化的关系及其在放射性肝纤维化中的作用[J].中华放射医学与防护杂志,2015,35(9):652-656 |
| PI3K/Akt信号通路与肝星状细胞活化的关系及其在放射性肝纤维化中的作用 |
| Relationship of PI3K/Akt signaling pathway and the activation of hepatic stellate cells and its role in radiation-induced hepatic fibrosis |
| 投稿时间：2015-03-25 |
| DOI：10.3760/cma.j.issn.0254-5098.2015.09.003 |
| 中文关键词: X射线 肝星状细胞 放射性肝纤维化 PI3K/Akt信号通路 |
| 英文关键词:X-rays Hepatic stellate cells Radiation-induced hepatic fibrosis PI3K/Akt signaling pathway |
| 基金项目:新疆维吾尔自治区自然科学基金(2014211C075) |
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| 中文摘要: |
| 目的 探讨磷脂酰肌醇3激酶-蛋白激酶B(PI3K/Akt)信号通路与肝星状细胞(HSC)活化的关系及其在放射性肝纤维化中的作用。方法 6 MV X射线照射,联合PI3K/Akt信号通路特异性抑制剂处理HSC,分为空白对照组、抑制剂组、10 Gy照射组、10 Gy+抑制剂组、20 Gy照射组和20 Gy+抑制剂组。检测各组的细胞凋亡率、细胞上清液转化生长因子β1(TGF-β1)浓度、平滑肌肌动蛋白(α-SMA)的mRNA表达量和磷酸化蛋白激酶B(p-Akt)的表达量。结果 与空白对照组相比,10 和20 Gy照射组细胞的凋亡率随照射剂量的增加而增加(t=8.43、11.63,P<0.05);与10 和20 Gy照射组比较,分别加抑制剂后细胞的凋亡率降低(t=8.09、4.88,P<0.05)。与10 Gy照射组比较,20 Gy照射组TGF-β1、α-SMA、p-Akt的量增加(t=6.91、7.80、9.28,P<0.05),10 Gy+抑制剂组TGF-β1、α-SMA、p-Akt的量降低(t=6.17、15.11、10.34,P<0.05)。与20 Gy照射组比较,20 Gy+抑制剂组TGF-β1、α-SMA、p-Akt的量同样降低(t=10.04、6.85、23.84,P<0.05)。结论 X射线通过激活PI3K/Akt信号通路使HSC活化,导致放射性肝纤维化的发生。 |
| 英文摘要: |
| Objective To investigate the relationship of PI3K/Akt signaling pathway with the activation of hepatic stellate cells (HSC) and its role in radiation-induced hepatic fibrosis. Methods HSC was treated with 6 MV X-ray irradiation (IR) together with the inhibitor of PI3K/Akt signaling pathway. The cells were divided into inhibitor group, 10 Gy IR group, 10 Gy+inhibitor group, 20 Gy IR group, an 20 Gy+inhibitor group and blank control group. Then cell apoptosis rate was detected, the expression of transforming growth factor β1 (TGF-β1) in cell supernatant and the mRNA expressions of α-smooth muscle actin (α-SMA) and phosphorylation protein kinase B (p-Akt) were measured. Results Compared with the control group, the apoptosis rate of 10 and 20 Gy IR group increased with irradiation dose (t=8.43, 11.63, P<0.05) but they were reduced by the inhibitor of PI3K/Akt (t=8.09, 4.88, P<0.05). The expressions of TGF-β1, α-SMA, and p-Akt also increased with irradiation dose (t=6.91, 7.80, 9.28, P<0.05) but they were declined by this inhibitor for both 10 Gy IR (t=6.17, 15.11, 10.34, P<0.05) and 20 Gy IR (t=10.04, 6.85, 23.84, P<0.05). Conclusions X-ray irradiation could activate HSC through PI3K/Akt signaling pathway, which may further result in hepatic fibrosis. |
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