Role of autophagy in LPS‑induced inflammation in INS‑1 cells.

Abstract

Inflammation has been implicated in the pathogenesis of type 2 diabetes (T2D), which is a progressive disease characterized by pancreatic β‑cell dysfunction and apoptosis with consequential insufficient insulin secretion. Autophagy is necessary to maintain the structure, mass and function of pancreatic β‑cells. The present study investigated the crosstalk between autophagy and inflammasome activation in T2D. INS‑1 cells were stimulated with lipopolysaccharide. Apoptosis and reactive oxygen species (ROS) formation were measured using flow cytometry, and cell proliferation was measured using Cell Counting Kit‑8 solution. Autophagy was assayed using western blotting and transmission electron microscopy. The expression levels of interleukin‑1β (IL‑1β) and caspase‑1 were detected by western blotting. The results demonstrated that inhibiting autophagy using 3‑methyladenine (3‑MA) promoted INS‑1 cell apoptosis. This response was correlated with an increase in ROS production and the inflammatory response, including IL‑1β maturation and caspase‑1 activation. Furthermore, when ROS were inhibited using N‑acetyl‑L‑cysteine, inflammation was decreased. These results demonstrated that inhibition of autophagy enhanced inflammatory injury via the ROS‑mediated activation of the Nod‑like receptor pyrin domain‑containing protein 3 inflammasome. Autophagy may have a protective effect by mitigating inflammation in T2D, which may provide a novel approach for T2D treatment.