Effect of leech on VSMCs in early atherosclerosis rats via p38MAPK signaling pathway.
10.19540/j.cnki.cjcmm.2017.0128
- Author:
Jing-Kui WU
1
;
Qiao YANG
1
;
Yang-Yang LI
2
;
Dong-Jie XIE
1
Author Information
1. Tianjin Medical University General Hospital, Tianjin 300052, China.
2. The First Affiliated Hospital of Henan University of Science and Technology, Luoyang 471003, China.
- Publication Type:Journal Article
- Keywords:
atherosclerosis;
leech;
p38MAPK signaling pathway;
proliferation and apoptosis;
vascular smooth muscle cells
- From:
China Journal of Chinese Materia Medica
2017;42(16):3191-3197
- CountryChina
- Language:Chinese
-
Abstract:
To explore the effect of leech on proliferation and apoptosis of vascular smooth muscle cells(VSMCs) in early atherosclerosis rats via p38MAPK signaling pathway and investigate its possible mechanism. Biochemical analyzer was used to examine the regulation of leech on levels of triglycerides(TG), total cholesterol(TC), low-density lipoprotein(LDL-C), and high-density lipoprotein(HDL-C) in blood lipid of rats. The expression of transforming growth factor-beta 1(TGF-β1) in serum was detected by ELISA. Immunological histological chemistry (IHC) was taken to measure the expression levels of proliferating cell nucleus antigen(PCNA) and cell apoptosis proteinase-3(Caspase-3), while the protein expression levels of MKK3, p38 and C-myc were detected by Western blot. In addition, hematoxylin and eosin(HE) staining was used to observe the morphological change of thoracic aortas. The results showed that leech decreased the levels of TC, LDL-C obviously and increased HDL-C, suppressed the expression levels of TGF-β1 and PCNA, up-regulated Caspase-3, down-regulated the expression levels of MKK3, p38, and C-myc protein. HE staining indicated that it could inhibit intimal thickening and reduce plaque formation. The above results indicated that leech may affect the protein expression of the p38MAPK signaling pathway to inhibit proliferation and promote the apoptosis of VSMCs via reducing blood lipid levels and suppressing TGF-β1, aiming at inhibiting intimal thickening and reducing plaque formation, tand then slowing down the process of early atherosclerosis.
