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    巯基丙酮酸硫基转移酶介导PI3K/AKT信号对急性胰腺炎细胞模型凋亡和自噬的影响

    Effects of PI3K/AKT signaling mediated by mercaptopyruvate sulfurtransferase on apoptosis and autophagy in acute pancreatitis cell model

      摘要
    • 摘要:
      目的 研究巯基丙酮酸硫基转移酶(MPST)介导PI3K/AKT信号对急性胰腺炎(AP)细胞模型凋亡和自噬的影响。
      方法 构建AP体外细胞模型，分组为CON组、AP组、AP+siMPST组和AP+oeMPST组。采用CCK-8法检测细胞活力；采用ELISA法检测细胞上清炎症因子TNF-α、IL-1和IL-6水平；采用流式细胞仪检测细胞凋亡水平；采用Western blotting检测腺泡细胞LC3 Ⅱ/Ⅰ、beclin1、ATG5、MPST、PI3K、p-PI3K、AKT、p-AKT的表达水平。
      结果 AP组、AP+siMPST组和AP+oeMPST组的细胞存活率均低于CON组(P < 0.01)，而细胞凋亡率则均高于CON组(P < 0.01)；AP+siMPST组细胞存活率、AP+oeMPST组细胞凋亡率均高于AP组(P < 0.01)，而AP+siMPST组细胞凋亡率、AP+oeMPST组细胞存活率均低于AP组(P < 0.01)。AP组、AP+oeMPST组的腺泡细胞TNF-α、IL-1和IL-6、LC3 Ⅱ/Ⅰ、beclin1、ATG5、MPST、p-PI3K/PI3K、p-AKT/AKT水平明显高于CON组(P < 0.01)；上述指标水平AP+siMPST组均低于AP组(P < 0.01)，而AP+oeMPST组则均高于AP组(P < 0.01)。
      结论 MPST可通过PI3K/AKT信号诱导胰腺腺泡细胞凋亡、自噬和炎症反应；抑制MPST可能对AP具有治疗意义。

       

      Abstract:
      Objective To investigate the effect of mercaptopyruvate thiotransferase (MPST) mediated PI3K/AKT signaling on apoptosis and autophagy in acute pancreatitis (AP) cell model.
      Methods An AP in vitro cell model was constructed.Cells were divided into CON group, AP group, AP+siMPST group, and AP+oeMPST group.CCK-8 method was used to detect cell viability.The levels of inflammatory cytokines TNF-α, IL-1 and IL-6 were detected by ELISA.Flow cytometry was used to detect the level of apoptosis.Western blotting was used to detect the expression levels of LC3 Ⅱ/Ⅰ, beclin1, ATG5, MPST, PI3K, p-PI3K, AKT, and p-AKT in acinar cells.
      Results The cell survival rates of the AP group, AP+siMPST group, and AP+oeMPST group were all lower than those of the CON group (P < 0.01), while the apoptosis rate was higher than that of the CON group (P < 0.01);The cell survival rate of the AP+siMPST group and the apoptosis rate of the AP+oeMPST group were higher than those of the AP group (P < 0.01), while the apoptosis rate of the AP+siMPST group and the cell survival rate of the AP+oeMPST group were lower than those of the AP group (P < 0.01).The levels of TNF-α, IL-1, IL-6, LC3 Ⅱ/Ⅰ, beclin1, ATG5, MPST, p-PI3K/PI3K, and p-AKT/AKT in acinar cells of AP group and AP+oeMPST group were significantly higher than in the CON group (P < 0.01).The above indicators were lower in the AP+siMPST group than in the AP group (P < 0.01), while the AP+oeMPST group was higher than in the AP group (P < 0.01).
      Conclusions MPST can induce pancreatic acinar cell apoptosis, autophagy, and inflammatory response through PI3K/AKT signaling.Inhibiting MPST may have therapeutic significance for AP.

       

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