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TGF-β/Smad 和 JAK/STAT 通路参与了藻酸丙二醇酯钠硫酸酯对肝纤维化的抗纤维化作用。

TGF-β/Smad and JAK/STAT pathways are involved in the anti-fibrotic effects of propylene glycol alginate sodium sulphate on hepatic fibrosis.

机构信息

Department of Gastroenterology, Putuo People's Hospital, Tongji University School of Medicine, Shanghai, China.

Department of Gastroenterology, Jinshan Hospital of Fudan University, Shanghai, China.

出版信息

J Cell Mol Med. 2020 May;24(9):5224-5237. doi: 10.1111/jcmm.15175. Epub 2020 Mar 31.

DOI:10.1111/jcmm.15175
PMID:32233073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7205790/
Abstract

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.

摘要

肝纤维化是不健康现代生活方式的后果，对人类健康的影响越来越大，尤其是在发达国家。在这里，我们研究了褐藻来源的天然提取物藻酸丙二醇酯钠（PSS）在纤维化小鼠和细胞模型中的抗纤维化作用。因此，我们建立了胆管结扎和四氯化碳小鼠模型以及用或不用 PSS 处理的 LX-2 细胞模型。检查了肝病理切片以及血清和肝组织中的相关指标。PSS 显著预防了肝损伤和纤维化，并通过抑制转化生长因子 β1（TGF-β1）/Smad 通路，诱导基质金属蛋白酶-2 的上调和组织抑制剂金属蛋白酶-1 的下调。PSS 还通过抑制 Janus 激酶（JAK）2/信号转导子和转录激活子 3（STAT3）通路发挥抗自噬作用。总之，PSS 通过抑制炎症、促进细胞外基质（ECM）分解和使肝星状细胞失活来预防肝纤维化，其机制涉及体内和体外的 TGF-β1/Smad2/3 和 JAK2/STAT3 通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/e09a0c7a8e74/JCMM-24-5224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/98e9c6837448/JCMM-24-5224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/899429562c5b/JCMM-24-5224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/3efcdf5fbb17/JCMM-24-5224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/d80eefe2de54/JCMM-24-5224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/685a762bfd9b/JCMM-24-5224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/869ff2252c81/JCMM-24-5224-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/e09a0c7a8e74/JCMM-24-5224-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/98e9c6837448/JCMM-24-5224-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/899429562c5b/JCMM-24-5224-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/3efcdf5fbb17/JCMM-24-5224-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/d80eefe2de54/JCMM-24-5224-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/685a762bfd9b/JCMM-24-5224-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/869ff2252c81/JCMM-24-5224-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31da/7205790/e09a0c7a8e74/JCMM-24-5224-g007.jpg

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