Splenic tyrosine kinase promotes pulmonary angiogenesis in rats with hepatopulmonary syndrome.
- Author:
Wei-Zhong GAO
1
;
Yi-Hui YANG
1
;
Ling DAN
2
;
Xi-Wen ZHU
3
Author Information
1. Department of Anesthesiology, the First People's Hospital of Zunyi, Zunyi 563000, China.
2. Department of Anesthesiology, Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
3. Department of Anesthesiology, Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China. 125625844@qq.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Disease Models, Animal;
Hepatopulmonary Syndrome;
Lung;
Rats;
Rats, Sprague-Dawley;
Syk Kinase
- From:
Acta Physiologica Sinica
2020;72(6):785-792
- CountryChina
- Language:Chinese
-
Abstract:
The present paper was aimed to study the role of spleen tyrosine kinase (Syk) in angiogenesis in hepatopulmonary syndrome (HPS) and the underlying mechanism. Sprague Dawley (SD) rats were randomly divided into three groups: sham operation group (sham group), common bile duct ligation (CBDL) 5-week group (5W group) and R788 intervention group (R788 group). HPS model was established by CBDL. Rats in R788 group were intraperitoneally injected with R788 (20 mg/kg) once daily to week 5 after CBDL operation. The protein expression levels and distribution of Syk, p-Erk1/2, and p-Akt in lung tissue were detected by Western blot and immunohistochemistry. Immunofluorescence staining was used to observe the location of Syk expression and the number of angiogenesis in lung tissue. The results showed that, compared with sham group, 5W group exhibited up-regulated protein expression level of Syk, increased phosphorylation levels of Erk1/2 and Akt, and increased number of pulmonary microvessels. Compared with 5W group, R788 group exhibited down-regulated protein expression level of Syk, decreased phosphorylation levels of Erk1/2 and Akt, and decreased number of pulmonary microvessels. These results suggest that Syk may promote pulmonary angiogenesis in HPS model rats by activating downstream Erk1/2 and Akt signaling pathways, which provides a theoretical basis and potential drug therapeutic targets for the clinical treatment of HPS.
