Chloroquine inhibiting the activation of primary hepatic stellate cells induced by lipopolysaccharide

Lipopolysaccharide (LPS) leakage from bacteria causes liver inflammation and directly activates hepatic stellate cells (HSCs), contributing to liver fibrosis development. The current study investigated the effect of an autophagy inhibitor (Chloroquine, CQ) on in vitro HSC activation induced by LPS. Primary HSCs were isolated and cultured from BALB/c mice. Cells were cultured for 24 hours in a medium containing LPS 200 ng/ml, CQ 5 ,uM, or LPS 200 ng/ml + CQ 5 ,uM. All treated cells were evaluated by immunocytochemistry for morphology, proliferation, expression of activation markers & alpha;-sma and collagen 1, storage of lipid droplets and autophagy markers lc3/p62 at days 1 (D1), 3 (D3) and 7 (D7) after treatment. Proliferation of primary HSCs and expression of activation markers (& alpha;-sma and collagen 1) caused by LPS induction were significantly inhibited by CQ treatment until D7 of culture (p<0.01). Additionally, CQ treatment preserves cell function in lipid droplet storage. This effect of CQ on LPS-induced HSC activation was consistent with the late-stage inhibition of autophagy demonstrated by the decrease in lc3 and increase in p62 at D1 (p<0.01). CQ inhibits primary HSC activation in vitro when induced by LPS.