Protective effects of angelica polysaccharide on hippocampal neuron of rats with cerebral ischemia-reperfusion injury / 中草药

ABSTRACT

Objective: To investigate the protection of angelica polysaccharide (APS) on hippocampal neuron in rats with cerebral ischemia-reperfusion (I/R) injury. Methods: The model of cerebral I/R injury was established by suture method in rats. A total of 50 rats were randomly divided into five groups: Sham-operation, cerebral I/R injury, high-dose APS (200 mg/kg), mid-dose APS (100 mg/kg), and low-dose APS (50 mg/kg) groups. APS was ig administrated 3 d before operation. At 24 h after reperfusion, learning and memory function was detected by step down test, the apoptosis of hippocampal neuron was observed by terminal deoxylnucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and the expression of cleaved caspase-3, bcl-2, and bax in the hippocampus of rats was measured by enzyme-linked immunosorbent assay (ELISA). Results: Compared with those in the Sham-operation group, the learning and memory function was notably impaired in the I/R injury group, the number of errors increased. The apoptosis of hippocampal neuron increased and the expression of cleaved caspase-3, bcl-2, and bax in the hippocampus remarkably increased in the I/R injury group. The APS could significantly improve the learning and memory function of rats with the cerebral I/R injury and remarkably delay the decrease of the number of errors and the decrease of the apoptosis rate in the hippocampus of rats with the cerebral I/R injury. And the APS could also cause a significant down-regulation of cleaved caspase-3 and bax expression, while up-regulation of bcl-2 expression in hippocampus of rats with the cerebral I/R injury. Conclusion: APS has a neuroprotection on rats with the cerebral I/R injury. The neuroprotective mechanism of APS may involve in the inhibition of the neuronal apoptosis.