Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells

<div>LPS inhibits autophagy via p38 MAPK in HSCs. (a, b) LX-2 cells in the logarithmic growth phase were treated with different concentrations of LPS (0-10 μg/mL) for 4 h. (c, d) LX-2 cells in the logarithmic growth phase were treated with 1 μg/mL LPS in a time-dependent manner (0-12 h). (e, f) LX-2 cells in the logarithmic growth phase were treated with 1 μg/mL LPS together with or without 50 nM rapamycin or 20 μM SB203580 for 4 h for the detection of autophagy. (g, h) LX-2 cells in the logarithmic growth phase were treated with 1 μg/mL LPS together with or without 200 nM Bafilomycin A in a time-dependent manner (0-8 h) for the detection of autophagy.</div>

Mediators of Inflammation

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Figure 4: Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 

Figure 4 | Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 