Effects of Zuogui Jiangtang Jieyu Formula on Hippocampal Neuronal Apoptosis in Diabetic ;Rats with Depression
10.3969/j.issn.1005-5304.2016.09.019
- VernacularTitle:左归降糖解郁方对糖尿病并发抑郁症大鼠海马神经元凋亡的影响
- Author:
Pan MENG
;
Hongqing ZHAO
;
Qing DU
;
Yuhong WANG
;
Hui YANG
;
Xuli ZHANG
;
Yalan XU
- Publication Type:Journal Article
- Keywords:
Zuogui Jiangtang Jieyu Formula;
diabetes with depression;
neuronal apoptosis;
JNK;
Bcl-2;
Bax;
rats
- From:
Chinese Journal of Information on Traditional Chinese Medicine
2016;23(9):78-81
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of Zuogui Jiangtang Jieyu Formula (ZJJF) on the ability of learning and memory and the expressions of JNK, Bcl-2 and Bax in hippocampus in diabetic rats with depression; To explore the protective mechanism of hippocampal damage in diabetic rats with depression. Methods High-fat gavage combined with intravenous injection of STZ was used to establish the model of diabetic rats. 28 days of chronic stress was given continuously and diabetic rats complicated with depression were built successfully. Then rats were randomly divided into 6 groups, including normal, model, positive medicine, high-, medium-, and low-dose of ZJJF groups. After the last administration, Morris water maze was used to detect escape latency time;Western blot was used to disclose the protein expressions of JNK, Bcl-2 and Bax in rat hippocampaus;RT-PCR was used to test the gene expressions of JNK and Bcl-2 and Bax. Results Compared with the normal group, escape latency time in model rats was significant longer (P<0.01), the protein and gene expression of JNK and Bax in rat hippocampaus significantly increased, Bcl-2 was markedly decreased (P<0.05, P<0.01);Compared with the model group, escape latency time in positive medicine group and high-dose of ZJJF group was significant shorter (P<0.01), the protein and gene expressions of JNK and Bax significantly decreased, and Bcl-2 markedly increased (P<0.05, P<0.01). Conclusion ZJJF can significantly improve the ability of learning and memory in diabetic rats with depression, which might be associated with preventing neuronal apoptosis in hippocampus.
