Ulinastatin Inhibits the Proliferation, Invasion and Phenotypic Switching of PDGF-BB-Induced VSMCs via Akt/eNOS/NO/cGMP Signaling Pathway
| Autor: | Weihui Huang, Rui Wang, Cheng Cheng Huang, Yongli He |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Pharmacology Vascular smooth muscle biology medicine.diagnostic_test Chemistry Cell growth Phenotypic switching Pharmaceutical Science Inflammation biology.organism_classification 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Western blot Enos 030220 oncology & carcinogenesis Drug Discovery Cancer research medicine biology.protein medicine.symptom Protein kinase B Platelet-derived growth factor receptor |
| Zdroj: | Drug Design, Development and Therapy. 14:5505-5514 |
| ISSN: | 1177-8881 |
| DOI: | 10.2147/dddt.s275488 |
| Popis: | Background Atherosclerosis is a chronic inflammatory disease responsible for thrombosis, blood supply disorders, myocardial infarction and strokes, eventually leading to increased deaths and reduced quality of life. As inflammation plays a vital role in the development of this disease, the present study aims to investigate whether urinary trypsin inhibitor (UTI) with anti-inflammatory property can inhibit the proliferation, invasion and phenotypic switching of PDGF-BB-induced vascular smooth muscle cells (VSMCs) and probe its potential mechanism. Methods Western blot was used to detect the expressions of the proteins related to the Akt/eNOS/NO/cGMP signaling pathway, phenotypic switching and proliferation. CCK-8 assay and EdU staining were used to detect cell proliferation of VSMCs. Transwell and wound healing assays were respectively conducted to measure the invasion and migration of VSMCs. The concentration of NO was evaluated by NO detection kit. ELISA assay analyzed the expression of cyclic GMP (cGMP). Results The expressions of p-Akt and p-eNOS were elevated by UTI treatment. Furthermore, UTI inhibited the proliferation, migration and invasion of VSMCs. UTI also increased the expressions of proteins related to phenotypic switching. The amount of NO and expression of cGMP were both elevated under UTI treatment. Conclusion UTI inhibits the proliferation, invasion and phenotypic switching of PDGF-BB-induced VSMCs via Akt/eNOS/NO/cGMP signaling pathway, which might provide a theoretical basis for the UTI treatment of atherosclerosis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|