• 我的賬戶 7×24小時客服熱線:400-829-7929 語言:
    熱門產品: 人參皂苷Rh2,人參皂苷Rg3,雷公藤甲素,蟲草素,金絲桃素
    產品分類
    在線咨詢
    聯系電話:
    銷售:
    400-829-7929(7*24小時)
    028-82633860
    028-82633397 
    028-
    82633165
    技術服務和產品定制:
    028-82633987
    在線服務:  
    沈帥 點擊這里給我發消息 
    文靜  點擊這里給我發消息
    文獻信息

    A TMT-based shotgun proteomics uncovers overexpression of thrombospondin 1 as a contributor in pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome

    期刊名:Springer
    文獻編號:
    文獻地址: https://link.springer.com/article/10.1007/s00204-022-03281-7
    發表日期:31 March 2022
    Hepatic sinusoidal obstruction disease (HSOS) is a rare but life-threatening vascular liver disease. However, its underlying mechanism and molecular changes in HSOS are largely unknown, thus greatly hindering the development of its effective treatment. Hepatic sinusoidal endothelial cells (HSECs) are the primary and essential target for HSOS. A tandem mass tag-based shotgun proteomics study was performed using primary cultured HSECs from mice with HSOS induced by senecionine, a representative toxic pyrrolizidine alkaloid (PA). Dynamic changes in proteome were found at the initial period of damage and the essential role of thrombospondin 1 (TSP1) was highlighted in PA-induced HSOS. TSP1 over-expression was further confirmed in human HSECs and liver samples from patients with PA-induced HSOS. LSKL peptide, a known TSP1 inhibitor, protected mice from senecionine-induced HSOS. In addition, TSP1 was found to be covalently modified by dehydropyrrolizidine alkaloids in human HSECs and mouse livers upon senecionine treatment, thus to form the pyrrole-protein adduct. These findings provide useful information on early changes in HSECs upon PA treatment and uncover TSP1 overexpression as a contributor in PA-induced HSOS.
    相關產品
    在線客服系統
    97色色_日本免费最新高清不卡视频_色欲天天天综合网_欧美综合区自拍亚洲综合图