RT Journal Article
SR Electronic
T1 Corilagin controls post-parasiticide schistosome egg-induced liver fibrosis by inhibiting Stat6 signalling pathway
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 340299
DO 10.1101/340299
A1 Peng Du
A1 Qian Ma
A1 Jun Xiong
A1 Yao Wang
A1 Fan Yang
A1 Feng Jin
A1 Yun-Fei Chen
A1 Zhen-Zhong Shang
A1 Zhi-Lin Chen
A1 Xuan Zhou
A1 Hua-Rong Li
A1 Lei Zhao
YR 2018
UL http://biorxiv.org/content/early/2018/06/07/340299.abstract
AB This study aims to explore the effect of Corilagin (Cor) on post-parasiticide schistosome egg-induced hepatic fibrosis through the Stat6 signalling pathway in vitro and in vivo. Cellular and animal models were established and treated by Corilagin. The inhibitory effect of Corilagin was also confirmed in RAW264.7 cells in which Stat6 was overexpressed based on the GV367-Stat6-EGFP lentiviral vector system and in which Stat6 was knock-downed by gene specific siRNAs. As a result, Corilagin prevented increases in the protein level of Phospho-Stat6 (P-Stat6). Both the mRNA and protein levels of the downstream mediators SOCS1, KLF4, and PPARγ/δ were markedly suppressed after Corilagin treatment. Expression of ARG1 and FIZZ1/Retnla, Ym1, TGF-β and PDGF in serum were also inhibited by Corilagin. The pathological changes, area of granulomas of liver sections, and degree of hepatic fibrosis were significantly alleviated in the Corilagin group. The areas of CD68- and CD206-positive cells stained by immunofluorescence were significantly decreased by Corilagin. In conclusion, Corilagin can suppress post-parasiticide schistosome egg-induced hepatic fibrosis by inhibiting the Stat6 signalling pathway and provide a new therapeutic strategy for schistosomiasis liver fibrosis.