Protective Effects of Interleukin-37 Expression against Acetaminophen-Induced Hepatotoxicity in Mice

Zhiwei Xu; Kan Li; Xiuhe Pan; Jun Tan; Yan Li; Mingcai Li

doi:10.1155/2022/6468299

Protective Effects of Interleukin-37 Expression against Acetaminophen-Induced Hepatotoxicity in Mice

Evid Based Complement Alternat Med. 2022 Apr 4:2022:6468299. doi: 10.1155/2022/6468299. eCollection 2022.

Authors

Zhiwei Xu^{1

2}, Kan Li², Xiuhe Pan², Jun Tan³, Yan Li², Mingcai Li²

Affiliations

¹ The Affiliated Lihuili Hospital of Ningbo University, Ningbo Medical Center Lihuili Hospital, Ningbo, China.
² School of Medicine, Ningbo University, Ningbo, China.
³ HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, China.

Abstract

Aim: Interleukin (IL)-37 is a new anti-inflammatory cytokine of the IL-1 family. This study aimed to determine the effects of IL-37 on acetaminophen (APAP)-induced liver injury.

Materials and methods: IL-37 plasmids were injected into mice via a tail vein hydrodynamics-based gene delivery.

Results: Our results showed that IL-37 pretreatment significantly decreased serum alanine aminotransferase and aspartate aminotransferase levels, hepatic myeloperoxidase activity, and attenuated the histological liver damage. Compared to the APAP group, IL-37 administration decreased Kupffer cells numbers in the liver of APAP-induced hepatotoxicity in mice. Furthermore, IL-37 pretreatment reduced the expression of proinflammatory cytokines including tumor necrosis factor-α, IL-6, IL-17, and nuclear factor-κB (NF-κB) in APAP-induced mice.

Conclusion: These results demonstrate that delivery of IL-37 plasmid can ameliorate APAP-induced liver injury by reducing proinflammatory cytokines production and preventing the activation of the NF-κB signaling pathway. IL-37 may be a promising candidate against APAP-induced liver injury.