Inhibitory Effects of Astragalus Polysaccharide on Proliferation of Human Lung Adenocarcinoma H1299 Cells via the Toll-Like Receptor 4/Myeloid Differentiation Factor 88/Nuclear Factor-Kappa B Signaling Pathway

Abstract

To assess the inhibitory effects of Astragalus polysaccharide on the proliferation of human lung adenocarcinoma H1299 cells via the toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway. H1299 cells were treated with different concentrations of Astragalus polysaccharide. After 24 h and 48 h, cell counting kit-8 assay was employed to measure the cell proliferation. The effects of Astragalus polysaccharide (25 μg/ml) on the invasion ability, migration ability and apoptosis of H1299 cells were determined by transwell assay, wound healing and apoptosis assays, respectively. The changes in expressions of toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway-related proteins in H1299 cells after 48 h of treatment with 25 μg/ml Astragalus polysaccharide were detected by western blotting. Astragalus polysaccharide inhibited the proliferation of H1299 cells in a dose-dependent manner (p<0.05). The migration rate of H1299 cells treated with 25 μg/ml Astragalus polysaccharide was significantly lower than that of blank control group. After treatment with 25 μg/ml Astragalus polysaccharide, the number of H1299 cells invading through Matrigel into the lower chamber significantly reduced. The apoptosis rate of H1299 cells treated with 25 μg/ml Astragalus polysaccharide was significantly higher than that of blank control group. Toll-like receptor 4, myeloid differentiation factor 88 and nuclear factor-kappa B protein expression levels in H1299 cells treated with Astragalus polysaccharide (25 μg/ml) for 48 h were significantly lower than those of blank control group. Astragalus polysaccharide can inhibit the proliferation, migration and invasion of H1299 cells and induce apoptosis, possibly being related to the reduction of toll-like receptor 4, myeloid differentiation factor 88 and nuclear factor-kappa B protein expressions in cells.