Exogenous cardiotrophin-1:The possibility to protect PC12 cells and Schwann cells
10.3969/j.issn.2095-4344.2013.41.012
- VernacularTitle:外源性心脏营养素1：保护PC12细胞和许旺细胞的可能性
- Author:
Zetuan XIN
;
Xiangze LIU
;
Mingjin ZHANG
;
Wei LI
;
Bohua CHEN
;
Xuexiao MA
- Publication Type:Journal Article
- Keywords:
nervous system;
cell survival;
culture media,serum-free;
Schwann cells;
tissue engineering
- From:
Chinese Journal of Tissue Engineering Research
2013;(41):7265-7271
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Restoration of neurological functions after the damaged peripheral nerve is reconstructed is a hot topic in existing research. Within a short term fol owing peripheral nerve injury, nerve and muscle begin to develop irreversible degeneration. Restoration of the damaged nerve requires delayed degeneration and basic microenvironment. OBJECTIVE:To investigate the protective effect of cardiotrophin-1 on PC12 cells and Schwann cells. METHODS:Schwann cells and PC12 cells were obtained and cultured in complete medium, serum-free medium and 50 ℃ medium, respectively. cells in cardiotrophin-1 group were treated with exogenous cardiotrophin-1 solvent, while those in the control group were treated with equivalent Dulbecco’s modified Eagle’s medium, for 24 hours. The survival rate for PC12 cells and Schwann cells was determined using cellCounting Kit-8 colorimetric method. The lactate dehydrogenase activity in supernatant was detected by lactate dehydrogenase kit, and the malondialdehyde content and superoxide dismutase activity were measured by thiobarbituricaicd and xanthine oxidese method respectively. RESULTS AND CONCLUSION:The survival rate of PC12 cells and Schwann cells in cardiotrophin-1 group was obviously increased, lactate dehydrogenase releasing and malondialdehyde content were obviously decreased, superoxide dismutase activity was dramatical y improved compared with control group. Exogenous cardiotrophin-1 reduces the injury caused by ischemia and heat stress stimulation for PC12 cells and Schwann cells. The mechanism of protection may be related to the expression of anti-apoptosis protein activated by the combination of cardiotrophin-1 and its receptors.
