Insulin-like growth factor-1 inhibits the apoptosis of rat gastric smooth muscle cells cultured under high glucose condition through PI3K-Akt-PKC-Casup2+/sup pathway

摘要

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-Ca 2+ 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 Ca 2+ 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 Ca 2+ 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 Ca 2+ concentration.