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

<div>LPS promotes inflammation via p38 MAPK in HSCs. (a–c) THP-1 cells in the logarithmic growth phase were treated with 1 μg/mL LPS for 15 min for the detection of p38 MAPK or for 4 h for the detection of inflammation. (d) LX-2 cells in the logarithmic growth phase were treated with 1 μg/mL LPS in a time-dependent manner (0-8 h). (e–g) LX-2 cells in the logarithmic growth phase were treated with or without 20 μM SB203580 for 30 min, then cells were treated with 1 μg/mL LPS for 15 min for the detection of p38 MAPK or in a time-dependent manner (0-8 h) for the detection of inflammation.</div>

Mediators of Inflammation

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Figure 3: Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 

Figure 3 | Lipopolysaccharide Inhibits Autophagy and Promotes Inflammatory Responses via p38 MAPK-Induced Proteasomal Degradation of Atg13 in Hepatic Stellate Cells 