Role of TGF-β1 in hepatic fibrosis induced by echinococcus multilocular infection
10.16571/j.cnki.1008-8199.2020.02.004
- VernacularTitle: 转化生长因子β1在泡状棘球蚴感染所致肝纤维化中的作用机制
- Author:
Maimaitinijiati YUSUFUKADIER
1
;
Yasen AIMAITI
1
;
Rui-qing ZHANG
2
;
Aji TUERGANAILI
2
;
Ying-mei SHAO
2
;
Hao WEN
1
Author Information
1. State Key Laboratory on "Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia" Xinjiang Medical University, Urumqi 830011, Xinjiang, China
2. Department of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang, China
- Publication Type:Journal Article
- Keywords:
echinococcus multilocular;
hepatic fibrosis;
transforming growth factor β1
- From:
Journal of Medical Postgraduates
2020;33(2):127-132
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the role of transforming growth factor (TGF-β1) in hepatic fibrosis induced by echinococcus multilocular infection and its possible mechanisms in this process.Methods Forty-five C57BL/6 mice were randomly divided into the model group（30）and the control group (15). Protoscolece suspension of echinococcus multilocular was infused through portal vein in the model group (4000/each). Mice in the control group was injected the same volume of normal saline solution. Six mice in the model group and 3 mice in the control group were sacrificed at 1, 2, 4, 8 and 12 weeks after infection. The liver tissues were observed the histopathological changes by using hematoxylin-eosin (H&E) staining. The fibrosis degree and glycogen synthesis function of liver tissue were observed by Sirius-red staining and Periodic acid schiff (PAS), respectively. The expression levels of TGF-β1 and a-smooth muscle actin (α-SMA) were measured by immunohistochemical staining.ResultsThe obvious abnormal changes were not observed in 1 week after model setup. The diffuse distribution of multiple white spots began to appear at 2 weeks, but the amount of white plaques decreased after 8 weeks. Meanwhile, forming small lesions were not obviously observed the boundary with the surrounding normal liver tissue. Clear echinococcal vesicles were seen at week 12. H&E staining showed that hepatic tissue structure of control group was normal. In the model group, the number of lesions with worms decreased gradually and amount of granulomas were increased. The inflammatory lesions did not change significantly. Sirius-red staining demonstrated that collagen deposition in the control group was mainly around the bile duct and blood vessels. However, the deposition in the model group was mainly around the lesion and the degree of fibrosis became more serious with time. PAS staining displayed that the content of glycogen in the liver tissues of the control group was rich, evenly distributed and stained uniformly. However, the glycogen staining positive area decreased with the time of infection and the staining became lighter in the model group. Immunohistochemical staining indicated that the positive expression of α-SMA and TGF- β1 in the control group were mainly found in the bile ducts and perivascular areas. The positive areas in the model group were mostly granulomatous areas around the metacercariae and fibroblasts. Expression of α-SMA and TGF- β1 increased over time after infection with the expression peak at 12 weeks(16.80±2.09、4.10±2.14).ConclusionThe degree of fibrosis in liver tissues at different time points was consistent with the expression trend of TGF- β1 and α-SMA. TGF-β1 may promote collagen deposition and lead to fibrosis by activating hepatic stellate cells.
