OBJECTIVE: To investigate the effect of Valsartan and Ligustrazine on hippocampal neuronal loss and the ability of learning and memory of rats with vascular dementia. METHODS: Vascular dementia was induced in rats by blocking bilateral carotid artery repeatedly and intraperitoneal injection of sodium nitroprusside. The vacuity learning and memory of the rats were measured with Morris water maze. The plasma AVP and ANGII were determined by radio-immunity methods. The activities of SOD, GSH-Px and MDA in hippocampal tissues were detected by chemistry colorimetry. The hippocampal neuronal loss was observe with light microscope. RESULTS: Both valsartan and ligustrazine shortened escape latency (P < 0.05), and increased the numbers of rats crossing platform and the time spent in target quadrant (P < 0.01). Valsartan decreased plasma AVP, whereas ligustrazine increased plasma AVP. Both valsartan and ligustrazine increased plasma ANGII (P < 0.01), increased the activities of SOD and GSH-PX in hippocampal tissues, and decreased MDA activities in hippocampal tissues (P < 0.05). The damages in structure, number and volume of hippocampal neuron cells were reduced by Valsartan and Ligustrazine. The combined use of Valsartan and Ligustrazine produced greater effects than either of the drugs alone in all of the indicators except for plasma AVP. CONCLUSION: Valsartan or/and Ligustrazine have protective effect on hippocampal neuronal loss in rats with vascular dementia, possibly through inhibiting RAS activation and free radical formation induced by cerebral ischemia-reperfusion.
OBJECTIVE: To investigate the effect of Valsartan and Ligustrazine on hippocampal neuronal loss and the ability of learning and memory of rats with vascular dementia. METHODS:Vascular dementia was induced in rats by blocking bilateral carotid artery repeatedly and intraperitoneal injection of sodium nitroprusside. The vacuity learning and memory of the rats were measured with Morris water maze. The plasma AVP and ANGII were determined by radio-immunity methods. The activities of SOD, GSH-Px and MDA in hippocampal tissues were detected by chemistry colorimetry. The hippocampal neuronal loss was observe with light microscope. RESULTS: Both valsartan and ligustrazine shortened escape latency (P < 0.05), and increased the numbers of rats crossing platform and the time spent in target quadrant (P < 0.01). Valsartan decreased plasma AVP, whereas ligustrazine increased plasma AVP. Both valsartan and ligustrazine increased plasma ANGII (P < 0.01), increased the activities of SOD and GSH-PX in hippocampal tissues, and decreased MDA activities in hippocampal tissues (P < 0.05). The damages in structure, number and volume of hippocampal neuron cells were reduced by Valsartan and Ligustrazine. The combined use of Valsartan and Ligustrazine produced greater effects than either of the drugs alone in all of the indicators except for plasma AVP. CONCLUSION:Valsartan or/and Ligustrazine have protective effect on hippocampal neuronal loss in rats with vascular dementia, possibly through inhibiting RAS activation and free radical formation induced by cerebral ischemia-reperfusion.