IL‑22 alleviates the fibrosis of hepatic stellate cells via the inactivation of NLRP3 inflammasome signaling
- Zhuyun Xing
- Yayun Wu
- Na Liu
Affiliations: Department of Infectious Diseases, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China, Department of Hepatology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- Published online on: July 30, 2021 https://doi.org/10.3892/etm.2021.10522
Copyright: © Xing
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Persistent and progressive liver injury causes liver fibrosis due to the inability of the liver to regenerate. Interleukin (IL)‑22 serves an important role in liver fibrosis. However, the underlying mechanism by which IL‑22 exerts its effects on liver fibrosis has not been fully elucidated. The aim of the present study was to investigate the underlying mechanism by which IL‑22 affects the development of liver fibrosis. Following activation of the hepatic stellate cells (HSCs) using transforming growth factor β (TGF‑β), HSC proliferation was measured using the Cell Counting Kit‑8 assay. The indicators of oxidative stress were detected using specific kits. In addition, the mRNA and protein expression levels of fibrosis‑associated genes were determined using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. Subsequently, the protein expression levels of the NOD‑like receptor protein 3 (NLRP3), caspase-1 and IL‑1β were examined using western blotting. Following addition of Nigericin, a NLRP3 activator, the levels of oxidative stress and fibrosis were measured. IL‑22 increased the viability of HSCs, which were activated by TGF‑β. The malondialdehyde content was significantly decreased, whereas superoxide dismutase and glutathione levels were increased following IL‑22 treatment. Moreover, IL‑22 markedly downregulated the expression levels of fibrosis‑associated genes, including α‑smooth muscle actin, type I collagen and TIMP metallopeptidase inhibitor 1. Furthermore, the expression levels of NLRP3, caspase-1 and IL‑1β were decreased in the IL‑22‑treated groups. However, the NLRP3 activator Nigericin reversed the inhibitory effects of IL‑22 on the induction of oxidative stress and fibrosis of HSCs induced by TGF‑β. In conclusion, the present study indicated that IL‑22 alleviated the fibrosis of HSCs by inactivation of NLRP3 inflammasome signaling, which may provide further insight on the underlying mechanism by which IL‑22 exerts protective effects on liver fibrosis.