Insulin-like growth factor-1 inhibits the apoptosis of rat gastric smooth muscle cells cultured under high glucose condition through PI3K-Akt-PKC-Ca2 pathway
Insulin-like growth factor-1 inhibits the apoptosis of rat gastric smooth muscle cells cultured under high glucose condition through PI3K-Akt-PKC-Ca2 pathway
复制标题
胰岛素样生长因子1通过PI3K-Akt-PKC-Ca2通路抑制高糖条件下培养的大鼠胃平滑肌细胞凋亡
DOI：
10.1080/13102818.2019.1585206
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发表时间：
2019
影响因子：
1.4
通讯作者：
Jin Zheng
中科院分区：
文献类型：
--
作者：
Fang Xue Sen;Zhang Mo Han;Zhang Xiang Zi;Guo Jun Yu;Jin Zheng
本研究探讨胰岛素样生长因子1（IGF-1）对高糖条件下大鼠胃平滑肌细胞凋亡的影响，并探讨PI 3 K-Akt-PKC-Ca 2+通路的参与机制。在正常和高糖条件下体外培养大鼠胃平滑肌细胞，并用IGF-1处理。分别于24 h和48 h采用Western blot、酶联免疫吸附试验、激光共聚焦显微镜和流式细胞术检测相关蛋白表达、PKC活性、细胞内Ca 2+浓度变化和细胞凋亡。与未处理组相比，IGF-1处理24 h和高糖条件下PKCβ1、p-PKCβ1、PI 3 K和p-Akt表达均增加，PKCα表达在高糖+ IGF-1 24 h组增加，在高糖+IGF-1 48 h组减少;正常葡萄糖24 h + IGF-1组p-PKCα表达降低，高糖24 h和48 h + IGF-1组p-PKCα表达升高。正常葡萄糖24 h + IGF-1组、高糖24 h + IGF-1组和高糖48 h + IGF-1组的PKC活性均高于对照组。IGF-1处理24和48 h后，正常葡萄糖组Ca 2+浓度较未处理组显著升高，高糖组Ca 2+浓度较未处理组显著降低。48 h高糖+ IGF-1组细胞凋亡率明显低于48 h常糖+ IGF-1组和24 h高糖+ IGF-1组。在高糖条件下，IGF-1可通过激活PI 3 K-Akt-PKC通路，降低细胞内Ca 2+浓度，抑制大鼠胃平滑肌细胞凋亡。
This study investigated the effect of insulin-like growth factor 1 (IGF-1) on rat gastric smooth muscle cell apoptosis under high glucose conditions, and explored the involvement of the PI3K-Akt-PKC-Ca2+pathway. Rat gastric smooth muscle cells were cultured in vitro under normal and high glucose conditions and treated with IGF-1. Related protein expression, PKC activity, changes of intracellular Ca2+concentration and cell apoptosis were detected at 24 and 48 h by western blotting, enzyme-linked immunosorbent assay, confocal laser-scanning microscopy and flow cytometry, respectively. Compared with the non-treated group, PKCβ1, p-PKCβ1, PI3K and p-Akt expression in IGF-1-treated cells in normal and high glucose conditions at 24 and 48 h were increased; PKCα expression was increased in the 24-h high glucose + IGF-1 group, and decreased in the 48-h normal glucose + IGF-1 group; p-PKCα expression was decreased in the 24-h normal glucose + IGF-1 group, and increased in the 24-h and 48-h high glucose + IGF-1 group. PKC activity was increased in the 24-h normal glucose + IGF-1, 24-h and 48-h high glucose + IGF-1 groups compared with the non-treated group. After 24 and 48 h of IGF-1 treatment, the Ca2+concentration was significantly increased in the normal glucose group, and decreased in the high glucose group compared with the non-treated group. The apoptosis rate in the 48-high glucose + IGF-1 group was significantly lower than that in the 48-h normal glucose + IGF-1 and 24-h high glucose + IGF-1 groups. Under high glucose conditions, IGF-1 can inhibit apoptosis in rat gastric smooth muscle cells through activating the PI3K-Akt-PKC pathway, and decreasing intracellular Ca2+concentration.