Astragalus saponins inhibit cell growth, aerobic glycolysis and attenuate the inflammatory response in a DSS-induced colitis model.

Abstract

Recent studies have reported that Astragalus saponins (AST), extracted from the medicinal plant Astragalus membranaceus, possess anti‑tumor and apoptosis‑inducing abilities on various types of human cancer in vitro and in vivo. However, limited studies have explored how AST impacts glucose metabolism and growth conditions in vitro. The present study aimed to explore cell growth, proliferation, apoptosis and a series of glycolysis metabolic alterations associated with AST treatment in colorectal cancer (CRC) cells. MTT, a colony formation assay and flow cytometry demonstrated that AST dose‑dependently inhibited cell viability and induced apoptosis. Glucose uptake and lactate production measurements revealed that AST could inhibit glycolysis metabolism and lactate production. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis identified that the expression levels of glycolytic enzymes were decreased by AST treatment in CRC cells. To uncover the possible impact of AST on inflammation and glucose metabolism in vivo, a dextran sulfate sodium (DSS)‑induced colitis mouse model was established. Notably, AST could inhibit growth and glycolysis metabolism in CRC cells in vitro, and attenuate the inflammatory response and tumor‑like aerobic glycolysis in the DSS‑induced mouse model. The findings indicated that AST may have the capacity to resist tumor‑associated inflammation and maintain normal glucose homeostasis, suggesting that AST could be a novel therapeutic strategy in CRC treatment.