| Background and objective:Cerebrovascular disease is a clinical common, frequently encountered disease in the elderly. The rates of morbility, deformity and mortality are very high. It is one of the important diseases that lead significant harm to human health. Among them, the incidence of ischemic cerebrovascular disease is more accounted in the clinic. Recently, with further research, the relationship between mediator of inflammation and cell apoptosis is increasingly emphasized.Paeonol, a major phenolic component of Moutan Cortex, as Chinese traditional medicine, has been described to possess analgesic, sedative, anti-inflammatory, anti-allergic and antimicrobial properties. Many previous studies have shown that paeonol, as Chinese traditional medicine, could exhibit its protective effects against brain ischemia injury, resulting in reducing the infarct size, decreasing the content of inflammatory effects and inhibiting cell apoptosis in ischemia area in vivo.In our present study, the injury model was established to investigate the protective effects against ischemia-reperfusion of paeonol and the potential neuroprotective mechanism of paeonol. We suggest that paeonol can lighten cerebral ischemia-reperfusion injury in multiple ways and provide proof for clinic to facilitate work.Methods:Middle cerebral artery occlusion (MCAO) was used to establish the focal cerebral ischemia-reperfusion model. The rats were divided into 6 groups in random:sham group, ischemia-reperfusion group, paeonol groups (30 mg-kg-1,20 mg-kg-1,15 mg-kg-1),nimodipine group(0.4 mg-kg-1).0.9%NaCl of the same capacity was given to the sham group and ischemia-reperfusion group. All these rats were given corresponding drug 8 days continuously. MCAO models were made after anaesthesia and fixation after the last drug was given 2 hours. The blood was deprived 2 hours and was reperfused 22 hours. Scores of neurological deficit were observed and the cerebral infarction size was measured by 2,3,5—triphenytetrazolium chloride (TTC) staining technique. The morphological changes of cerebral cortical neurons through HE staining were observed. The expression of Toll like receptor 4 (TLR4) and Bcl-2 in brain was determined by immunohistochemistry. The content of Tumor necrosis factor-a(TNF-α) and interleukin-1β(IL-1β),interleukin-6 (IL-6) in serum was measured by ELISA. The apoptosis was detected by flow cytometry.Result: After 2 hours of cerebral ischemia and 22 hours of reperfusion, scores of neurological deficit were lower significantly in the groups treated with paeonol and nimodipine. The content of TLR4 in brain was decreased. And the levels of TNF-α,IL-1βand IL-6 in serum were obviously decreased (p<0.01, p<0.05), neuronal apoptosis of cortex is obviously reduced. The content of Bcl-2 in brain was increased.Conclusion:1. Paeonol had a neuro-protective effect against neuronal damage following focal ischemic in the Wistar rats.2. One of the neuro-protective mechanisms of paeonol is that it can inhibit the formation of mediator of inflammation.3. Another one of the neuro-protective mechanisms of paeonol is that it can reduce the neuronal apoptosis after the ischemia and the reperfusion in the focal models of Wistar rats.4. Paeonol reduced neuronal damage induced by focal ischemic of Wistar rats in a dose-dependent manner, large dose of paeonol administration could significantly suppressed these neuronal cell damages. |
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