Objective To explore the mechanism of thymic stromal lymphopoietin (TSLP) in regulating lipopolysaccharide (LPS) -induced inflammation in mouse hepatocytes.

Methods Ten male C57BL/6J wild-type (WT) mice and 10 male TSLP receptor-deficient (TSLPR-/-) mice were each randomly divided into a blank control group and a LPS intervention group (n=5 per group). Primary hepatocytes were isolated from mice in each group using a modified in situ perfusion method. The blank control group was cultured normally, while the intervention group was treated with LPS. The cell viability at different time points was assessed via MTS assay. The levels of aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH) in the cell culture supernatant were measured using detection kits. The mRNA expression of inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in hepatocytes was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and the TSLP and LC3 protein expression was detected by western blotting. The LC3 expression in hepatocytes was evaluated by immunofluorescence.

Results MTS assays revealed a significant decrease in hepatocyte viability 8 hours after 10 μg/mL LPS intervention (P < 0.05). No significant differences were observed in the relative expression level of TSLP protein, the levels of AST, ALT, LDH, inflammatory cytokine, and the relative expression level of LC3Ⅱ protein between the blank control groups of primary hepatocytes from the two types of mice (P > 0.05). Compared to the WT+LPS group, the TSLPR-/- +LPS group exhibited significantly higher relative expression level of TSLP protein, levels of AST, ALT, LDH, and inflammatory cytokine (P < 0.05), but significantly lower relative expression level of LC3Ⅱ protein (P < 0.05).

Conclusion The TSLP protein alleviates LPS-induced hepatocyte injury by regulating autophagy, thereby reducing hepatic enzyme and inflammatory cytokine levels.