Jolkinolide B Ameliorates Liver Inflammation and Lipogenesis by Regulating JAK/STAT3 Pathway
10.4062/biomolther.2024.033
- Author:
Hye-Rin NOH
1
;
Guoyan SUI
;
Jin Woo LEE
;
Feng WANG
;
Jeong-Su PARK
;
Yuanqiang MA
;
Hwan MA
;
Ji-Won JEONG
;
Dong-Su SHIN
;
Xuefeng WU
;
Bang-Yeon HWANG
;
Yoon Seok ROH
Author Information
1. College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju 28160, Republic of Korea
- Publication Type:Original Article
- From:Biomolecules & Therapeutics
2024;32(6):793-800
- CountryRepublic of Korea
- Language:English
-
Abstract:
Hepatic dysregulation of lipid metabolism exacerbates inflammation and enhances the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). STAT3 has been linked to lipid metabolism and inflammation. Jolkinolide B (JB), derived from Euphorbia fischeriana, is known for its pharmacological anti-inflammatory and anti-tumor properties. Therefore, this study investigated whether JB affects MASLD prevention by regulating STAT3 signaling. JB attenuated steatosis and inflammatory responses in palmitic acid (PA)-treated hepatocytes. Additionally, JB treatment reduced the mRNA expression of de-novo lipogenic genes, such as acetyl-CoA carboxylase and stearoyl-CoA desaturase 1. Interestingly, JB-mediated reduction in inflammation and lipogenesis was dependent on STAT3 signaling. JB consistently modulated mitochondrial dysfunction and the mRNA expression of inflammatory cytokines by inhibiting PA-induced JAK/STAT3 activation. This study suggests that JB is a potential therapeutic agent to prevent major stages of MASLD through inhibition of JAK/STAT3 signaling in hepatocytes.
