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. 2020 Jul:84:106529.
doi: 10.1016/j.intimp.2020.106529. Epub 2020 Apr 27.

Cafestol preconditioning attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting ERK/PPARγ pathway

Jie Ji  1 , Liwei Wu  1 , Jiao Feng  1 , Wenhui Mo  2 , Jianye Wu  3 , Qiang Yu  1 , Sainan Li  1 , Jie Zhang  4 , Weiqi Dai  5 , Xuanfu Xu  2 , Yuqing Mao  6 , Shizan Xu  7 , Kan Chen  1 , Jingjing Li  8 , Chuanyong Guo  9
Affiliations

Cafestol preconditioning attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting ERK/PPARγ pathway

Jie Ji et al. Int Immunopharmacol. 2020 Jul.

Abstract

Objective: The study was aimed to explore the hepatocellular protective functions of cafestol during hepatic ischemia-reperfusion injury and the possible mechanisms.

Methods: Ninety male Balb/c mice were randomly divided into seven groups, including normal control group, L-cafestol(20mg/kg) group, H-cafestol(40mg/kg) group, sham group, IR group, L-cafestol(20mg/kg) + IR group, H-cafestol(40mg/kg) + IR group. Serum liver enzymes (ALT, AST), inflammation mediators, proteins associated with apoptosis and autophagy, indicators linked with ERK/PPARγ pathway, and liver histopathology were measured using ELISA, qRT-PCR, immunohistochemical staining, and western blotting at 2, 8, and 24 hours after reperfusion.

Results: Our findings confirmed that cafestol preconditioning groups could reduce the levels of ALT and AST, alleviate liver pathological damage, suppress the release of inflammation mediators, inhibit the production of pro-apoptosis protein including caspase-3, caspase-9 and Bax, decrease the expression of autophagy-linked protein including Beclin-1 and LC3, increase anti-apoptosis protein Bcl-2, and restrain the activation of ERK and PPARγ.

Conclusion: Cafestol preconditioning could attenuate inflammatory response, apoptosis and autophagy on hepatic ischemia reperfusion injury by suppressing ERK/PPARγ pathway.

Keywords: Apoptosis; Autophagy; Cafestol; ERK; HIRI; PPARγ.

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