Effect of Au NanoStars/collagen matrix material on oxidative stress damage in ventricular myocytes of newborn rats
10.7644/j.issn.1674-9960.2018.02.010
- VernacularTitle:金纳米星/胶原复合基质材料对新生大鼠心室肌细胞氧化应激损伤的影响
- Author:
Hui-Hui XIN
1
;
Yi LI
;
Rui BAI
;
Yu-Jie WEI
;
Hui-Liang LIU
Author Information
1. 锦州医科大学武警总医院研究生培养基地
- Keywords:
Au NanoStars(AuNSs);
collagen(Col);
newborn rat ventricular myocyte (NRVM);
oxidative stress;
hydrogen peroxide;
apoptosis;
nanostructures
- From:Military Medical Sciences
2018;42(2):124-129
- CountryChina
- Language:Chinese
-
Abstract:
Objective To verify antioxidation of Au NanoStars/collagen ( AuNSs/Col ) for ventricular myocytes of newborn rats(NRVMs) by in vitro studies.Methods (1)Different concentrations of AuNSs/Col composite materials were created.The optimum concentration of the material was selected by Live /dead staining and Cell Counting Kit-8 (CCK-8) and Col was used for subsequent experiments .( 2 ) NRVMs were randomly divided into Col group , AuNSs/Col group, H2O2-induced Col group, and H2O2-induced AuNSs/Col group.After 6 h treatment, apoptotic cell morphology and early cell apoptosis rate were observed with Annexin Ⅴ-FITC/propidium iodide ( PI)/4′,6-diamidino-2-phenylindole ( DAPI) and the expressions of apoptosis related proteins-B-cell lymphoma-2 ( Bcl-2 ) and Bcl-2 associated x protein ( Bax ) were detected by Western blotting .Results ( 1 ) Both Live/dead and CCK-8 experiments indicated that the AuNSs/Col composite material with 0.1 mg/ml was nontoxicity to NRVMs and could further promote their proliferation .(2) Compared with the uninduced group , the early apoptosis rate of the Col group and the AuNSs /Col group after H2O2 induction was significantly increased , while the Bcl-2/Bax ratio was decreased , indicating that the oxidative stress damage model was established.After H2O2 induction, compared with the Col group , the early apoptosis rate of the AuNSs/Col group was decreased , but the Bcl-2/Bax ratio was increased .Conclusion AuNSs/Col composite material has protective effect on the oxidative damage of cardiomyocytes cultured in vitro.