Open AccessTGF‐β/Smad and JAK/STAT pathways are involved in the anti‐fibrotic effects of propylene glycol alginate sodium sulphate on hepatic fibrosis
Author(s) -
Xu Shizan,
Mao Yuqing,
Wu Jianye,
Feng Jiao,
Li Jingjing,
Wu Liwei,
Yu Qiang,
Zhou Yuting,
Zhang Jie,
Chen Jiaojiao,
Ji Jie,
Chen Kan,
Wang Fan,
Dai Weiqi,
Fan Xiaoming,
Guo Chuanyong
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15175
Subject(s) - hepatic stellate cell , smad , hepatic fibrosis , fibrosis , stat protein , stat3 , janus kinase , chemistry , transforming growth factor , salidroside , cancer research , extracellular matrix , signal transduction , microbiology and biotechnology , medicine , biology , pathology , pharmacology , biochemistry
Liver fibrosis, a consequence of unhealthy modern lifestyles, has a growing impact on human health, particularly in developed countries. Here, we have explored the anti‐fibrotic effects of propylene glycol alginate sodium sulphate (PSS), a natural extract from brown algae, in fibrotic mice and cell models. Thus, we established bile duct ligature and carbon tetrachloride mouse models and LX‐2 cell models with or without PSS treatment. Liver pathological sections and the relevant indicators in serum and liver tissues were examined. PSS prevented hepatic injury and fibrosis to a significant extent, and induced up‐regulation of matrix metalloproteinase‐2 and down‐regulation of tissue inhibitor of metalloproteinase‐1 through suppressing the transforming growth factor β1 (TGF‐β1)/Smad pathway. PSS additionally exerted an anti‐autophagy effect through suppressing the Janus kinase (JAK) 2/transducer and activator of transcription 3 (STAT3) pathway. In conclusion, PSS prevents hepatic fibrosis by suppressing inflammation, promoting extracellular matrix (ECM) decomposition and inactivating hepatic stellate cells through mechanisms involving the TGF‐β1/Smad2/3 and JAK2/STAT3 pathways in vivo and in vitro.