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Chinese Journal of Behavioral Medicine and Brain Science ; (12): 684-688, 2017.
Article in Chinese | WPRIM | ID: wpr-613085

ABSTRACT

Objective To investigate the effects of dizocilpine(MK801) on depressive-like behaviors and damaged hippocampus in rats with diabetes-related depression.MethodsThe animal models of diabetes-related depression were established and they were randomly divided into two groups based on random number table: model group and MK801 group,while 6 rats were included in each group.And another six health rats were regarded as control group.The Open-field test was used to detect the activities.The damage of hippocampus was valued by HE staining,Nissl staining,and Tunel staining.The protein expressions of Bax,Bcl-2 in hippocampus were detected by Western blot.ResultsThe number of activities was significant decreased in Open-field test in model group when compared with control.Hippocampal neurons vacuoles,Nissl bodies were decreased and apoptotic cells were increased in hippocampus in model group as well.Furthermore,the expression of Bax was significant up-regulated(94.57±7.97,P<0.01),while the Bcl-2 was declined(24.65±5.26,P<0.01).Compared with the model group,the animals in MK801 group exhibited increased activities(12.50±4.42,P<0.01),which accompany with an increased Nissl body(133.55±16.74,P<0.01) and a decreased apoptosis(22.50±6.35,P<0.01).Moreover,the expression of Bax was decreased and the Bcl-2 was increased in MK801 group when they were contrasted to model(33.00±4.57,P<0.01).Conclusion MK801 is a significant element to regulate the expression of apoptosis protein including Bax,Bcl-2,and to protecte the hippocampal neuron in rats with diabetes-related depression effectively.

2.
Chinese Journal of Information on Traditional Chinese Medicine ; (12): 78-81, 2016.
Article in Chinese | WPRIM | ID: wpr-498245

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.

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