[Effect of moxibustion on cognitive function and proteins related with apoptosis of hippocampal neurons in rats with vascular dementia].

OBJECTIVE: To observe the effect of moxibustion on proteins related with apoptosis of hippocampal neurons in rats with vascular dementia (VD), and to explore the possible mechanism of moxibustion on improving VD.

METHODS: Thirty SD rats were selected from 100 rats (3 rats were excluded) and randomly divided into a normal group and a sham operation group, 15 rats in each group. The remaining 67 rats were treated with ischemia-reperfusion method at bilateral common carotid artery to establish VD model. The 45 rats with successful VD model were randomly divided into a model group, a moxibustion group and a medication group, 15 rats in each group. On the 7th day after successful modeling, the rats in the moxibustion group were treated with suspended moxibustion at "Guanyuan" (CV 4), "Mingmen" (GV 4) and "Dazhui" (GV 14), 15 min per acupoint, once a day; there was 1 d of rest after 6 d of moxibustion, and the treatment was given for 4 weeks. The rats in the medication group was treated with nimodipine tablets by gavage, 2 mg/kg per day, 3 times a day for 4 weeks. Before and after intervention, the Morris water maze test was used to detect the escape latency of rats in each group; after the intervention, the TUNEL method was used to detect the apoptosis rate of neurons in hippocampal CA1 area; the immunofluorescence double labeling method was used to detect the number of co-expression positive cells of B-cell lymphoma-2 (Bcl-2)/neuronal nuclear antigen (NeuN) and Bcl-2-associated X protein (Bax)/NeuN in hippocampal CA1 area; the immunofluorescence single labeling method was used to detect cytochrome C (cytC) and outer mitochondrial membrane receptor Tom20 (Tom20) in hippocampal CA1 area; the Western blot method was used to detect the p53 upregulated modulator of apoptosis (PUMA) in hippocampus.

RESULTS: Before intervention, compared with the normal group and the sham operation group, the escape latency in the model group, the moxibustion group and the medication group was prolonged (P<0.01). After intervention, the escape latency in the moxibustion group and the medication group was shorter than that before intervention (P<0.01). Compared with the model group, the escape latency in the moxibustion group and the medication group was shortened (P<0.05); compared with the medication group, the escape latency in the moxibustion group was shortened (P<0.05). Compared with the normal group and the sham operation group, the apoptosis rate of neurons in hippocampal CA1 area was increased, the number of Bcl-2/NeuN co-expression positive cells was decreased, and the number of Bax/NeuN co-expression positive cells was increased in the model group (P<0.01); compared with the model group, the apoptosis rates of hippocampal CA1 neurons were decreased, the number of Bcl-2/NeuN co-expression positive cells was increased, and the number of Bax/NeuN co-expression positive cells was decreased in the moxibustion group and the medication group (P<0.01); compared with the medication group, the apoptosis rate of neurons in hippocampal CA1 area was decreased, the number of Bcl-2/NeuN co-expression positive cells was increased, and the number of Bax/NeuN co-expression positive cells was decreased in the moxibustion group (P<0.01, P<0.05). Compared with the normal group and the sham operation group, the expressions of cytC, Tom20 protein in hippocampal CA1 area and PUMA protein in hippocampal tissue in the model group were increased (P<0.01); compared with the model group, the expressions of cytC, Tom20 protein in hippocampal CA1 area and PUMA protein in hippocampal tissue in the moxibustion group and the medication group were decreased (P<0.01); compared with the medication group, the expressions of cytC, Tom20 protein in hippocampal CA1 area and PUMA protein in hippocampal tissue in the moxibustion group were decreased (P<0.05, P<0.01).

CONCLUSION: Moxibustion could improve the cognitive function of VD rats, which may be related to reducing the expression of Bax, cytC, Tom20 and PUMA protein in hippocampal CA1 area, promoting the release of Bcl-2 and inhibiting the apoptosis of hippocampal neurons.