Preliminary mechanism of senegenin against H/R-induced apoptosis of primary cortical neurons
10.3969/j.issn.1000-4718.2014.07.003
- VernacularTitle:远志皂苷元抗 H／R 诱导皮层神经元凋亡的机制初探
- Author:
Yandong ZHAO
;
Panhong LIU
;
Xuemin LI
;
Fan LU
;
Huadong WANG
;
Daxiang LU
;
Renbin QI
- Publication Type:Journal Article
- Keywords:
Senegenin;
Neurons;
Hypoxia/reoxygenation;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2014;(7):1166-1171
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the preliminary mechanism of senegenin ( Sen) on inhibiting hypoxia/reoxygenation ( H/R)-induced apoptosis of primary cortical neurons .METHODS:The cultured cortical neurons were randomly divided in-to normal group (control group), model group (H/R group), Sen+H/R group and Sen group.Flow cytometry was used to evaluate the effect of Sen on H/R-induced cell apoptosis .The protein levels of JNK , p-JNK, c-Jun, p-c-Jun, Bcl-2 and Bax were assessed by Western blotting .RESULTS:The apoptotic rate in H/R group was obviously higher than that in control group (P<0.05), while the apoptotic rate in Sen +H/R group was obviously lower than that in H/R group (P<0.05), suggesting that the model of apoptosis was established successfully .The results of Western blotting showed that Sen increased the expression of JNK and c-Jun, inhibited the phosphorylation of JNK and c-Jun (P<0.05), increased the protein level of Bcl-2 and inhibited the protein level of Bax in H/R treated primary cortical neurons (P<0.05).CONCLUSION:Sen has a protective effect against H/R-induced neuronal apoptosis by increasing the expression of JNK and c-Jun, inhibiting the phosphorylation of JNK and c-Jun, increasing the protein level of Bcl-2 and decreasing the protein level of Bax .
