Role and mechanism of DPP4-nestin axis in liver fibrosis induced by Echinococcus alveolar infection
10.16303/j.cnki.1005-4545.2025.02.17
- VernacularTitle:DPP4-Nestin轴在泡球蚴感染所致肝纤维化的促进作用及机制
- Author:
Jin GAO
1
;
Tao SUN
;
Mulati MUKEXINA
;
Xiaolong HE
;
Jing SHI
;
Liang LI
;
Ning YANG
;
Jin CHU
;
Xue ZHANG
;
Hui LIU
;
Guodong LYU
;
Renyong LIN
;
Xiaojuan BI
;
Qingyong GUO
Author Information
1. 新疆农业大学动物医学学院新疆草食动物新药研究与创制重点实验室,新疆乌鲁木齐 830052
- Publication Type:Journal Article
- Keywords:
Echinococcus alveolar;
Nestin;
DPP4;
mice
- From:
Chinese Journal of Veterinary Science
2025;45(2):298-304
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the role of the DPP4-nestin axis in liver fibrosis induced by alveolar cyst infection,a murine model was established using C57BL/6 mice via hepatic portal vein injection.Liver histopathological changes were assessed using HE staining,while immunohistochemistry and immunofluorescence were employed to evaluate the expression levels of nestin and DPP4 in infected mouse livers.In vitro,J S1 cell line was stimulated with recombinant DPP4 protein to es-tablish a cellular model,and qPCR,Western blot,and shRNA lentivirus interference techniques were utilized to examine the involvement of the DPP4-nestin axis in hepatic stellate cell activation.The findings demonstrated that compared to the Sham group,liver tissue structure disruption and collagen deposition were evident along with significantly increased expressions of nestin and DPP4(P＜0.050 0),which colocalized with nesin and α-SMA.Furthermore,stimulation with recombi-nant DPP4 protein significantly enhanced JS1 cell activation(P＜0.050 0)as well as upregulated nestin expression(P＜0.050 0)when compared to control group cells.Notably,shRNA lentivirus-mediated inhibition of nestin expression effectively suppressed the activating effects exerted by re-combinant DPP4 protein on JS1 cells(P＜0.050 0).Collectively,these results highlight the crucial regulatory role played by the DPP4-nestin axis in hepatic stellate cell activation triggered by alveo-lar infection;thus,targeting this axis may represent a novel therapeutic strategy for treating alveo-lar infection-induced liver fibrosis.
