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目的探讨磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号通路在虾青素调节人肝星状细胞(LX-2细胞)活化中的作用。方法实验设对照组、低、中、高剂量虾青素组(5、10、20μmol/L)、抑制剂组(25μmol/L LY294002)、抑制剂+虾青素组(25μmol/L LY294002+20μmol/L虾青素),作用48 h后检测LX-2细胞中α-平滑肌肌动蛋白(α-SMA)和Ⅰ型胶原(col1a1)mRNA表达水平、各组细胞Akt及其磷酸化水平。结果与对照组比较,虾青素组LX-2细胞中α-SMA和col1a1 mRNA表达明显降低,并呈剂量依赖关系(P<0.05);与对照组比较,抑制剂组LX-2细胞中磷酸化Akt水平(0.42±0.05)、α-SMA和col1a1 mRNA表达水平[分别为(0.23±0.05)、(0.35±0.06)]均明显降低(P<0.05);与对照组比较,虾青素组LX-2细胞中磷酸化Akt水平(0.60±0.07)、α-SM A和col1a1 mRNA表达水平[分别为(0.48±0.07)、(0.61±0.04)]均明显降低(P<0.05);与抑制剂组比较,抑制剂+虾青素组LX-2细胞中磷酸化Akt水平(0.18±0.04)、α-SMA和col1a1 mRNA表达水平[分别为(0.11±0.05)、(0.20±0.03)]均明显降低(P<0.05)。结论虾青素可通过PI3K/Akt信号通路抑制肝星状细胞活化,发挥抗非酒精性脂肪肝纤维化作用。
Objective To investigate the role of phosphatidylinositol 3-kinase / protein kinase B (PI3K / Akt) signaling pathway in astaxanthin-mediated activation of human hepatic stellate cells (LX-2). Methods In the control group, low, medium and high doses of astaxanthin (5,10,20μmol / L), inhibitor group (25μmol / L LY294002) and inhibitor of astaxanthin group (25μmol / L LY294002 + / L astaxanthin), the expression of α-smooth muscle actin (α-SMA) and type Ⅰ collagen (col1a1) mRNA and the phosphorylation of Akt in LX-2 cells were detected 48 h after treatment. Results Compared with the control group, the expressions of α-SMA and col1a1 mRNA in astaxanthin-treated LX-2 cells were significantly decreased (P <0.05). Compared with the control group, (0.23 ± 0.05) and (0.35 ± 0.06), respectively (all P <0.05). Compared with the control group, the levels of astaxanthin The levels of phosphorylated Akt in LX-2 cells (0.60 ± 0.07), α-SM A and col1a1 mRNA levels (0.48 ± 0.07 and 0.61 ± 0.04, respectively) were significantly decreased The levels of phosphorylated Akt (0.18 ± 0.04), α-SMA and col1a1 mRNA in LX-2 cells treated with inhibitor + astaxanthin were Significantly lower (P <0.05). Conclusion Astaxanthin inhibits the activation of hepatic stellate cells through the PI3K / Akt signaling pathway and plays an important role in anti-non-alcoholic fatty liver fibrosis.