Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 24, Issue 9, Pages 5224-5237Publisher
WILEY
DOI: 10.1111/jcmm.15175
Keywords
autophagy; JAK2/STAT3; liver fibrosis; propylene glycol alginate sodium sulphate; TGF-beta 1/Smad2/3
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Funding
- Health System Innovation Project of Shanghai Putuo Science and Technology Commission [ptkwws201901]
- National Natural Science Foundation of China [81800538]
- Natural Science Foundation of Shanghai [19ZR1447700]
- Yangfan Project of Shanghai Science and Technology Commission [18YF1420000]
- WBN liver disease research fund of Chinese Foundation for Hepatitis Prevention and Control [2019031]
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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 beta 1 (TGF-beta 1)/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-beta 1/Smad2/3 and JAK2/STAT3 pathways in vivo and in vitro.
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