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目的观察二氢杨梅素(dihydromyricetin,DMY)对小鼠局灶性脑缺血再灌注(ischemia/reperfusion,I/R)损伤的保护作用。方法雄性昆明种小鼠随机分为4组,即假手术组,I/R模型组,DMY高(500 mg·kg-1)、低剂量(250 mg·kg-1)组。改良线栓法制备小鼠大脑中动脉阻塞/再灌注(middle cerebral artery occlusion/reperfusion,MCAO/R)模型,缺血3 h再灌注24 h;术前10 d开始灌胃给药,每天1次,并在缺血前1 h及再灌注后12 h各给药1次。再灌注24h后观察小鼠神经功能缺损评分,取脑测定脑梗死比(%)及脑含水量(%),HE染色观察脑组织病理学改变并计数皮层半暗带区神经元数目,同时测定脑组织MDA含量及SOD、GSH-Px活性。结果与模型组比较,DMY 500 mg·kg-1可减轻脑I/R损伤后神经功能缺损评分,降低脑梗死比和脑含水量,改善脑组织病理学变化及增加皮层半暗带区神经元数量(P<0.05,P<0.01);DMY 500 mg·kg-1还能明显降低脑组织MDA含量及提高SOD、GSH-Px活性(与模型组比较,P<0.05,P<0.01)。DMY 250 mg·kg-1可降低脑I/R损伤后脑梗死比(与模型组比较,P<0.05)。结论 DMY对局灶性脑I/R损伤有一定的保护作用,保护机制与其抗氧化作用有关。
Objective To observe the protective effect of dihydromyricetin (DMY) on focal cerebral ischemia-reperfusion (I / R) injury in mice. Methods Male Kunming mice were randomly divided into 4 groups: sham operation group, I / R model group, DMY high (500 mg · kg -1) and low dose (250 mg · kg -1) groups. The middle cerebral artery occlusion / reperfusion (MCAO / R) model was induced by modified suture method in mice. The ischemia reperfusion was performed at 3 h after reperfusion for 24 h. The intragastric administration was started 10 days before the operation, once a day , And administered 1 h before ischemia and 12 h after reperfusion. After 24h of reperfusion, the neurological deficit scores of mice were observed. The cerebral infarction ratio (%) and brain water content (%) were measured by brain. The pathological changes of brain tissue were observed by HE staining and the number of neurons in cortex penumbra was counted. Brain tissue MDA content and SOD, GSH-Px activity. Results Compared with model group, DMY 500 mg · kg -1 could reduce neurological deficit score, decrease cerebral infarction ratio and brain water content, improve brain histopathological changes and increase cortical neurons in penumbra zone (P <0.05, P <0.01). DMY 500 mg · kg-1 also significantly decreased the content of MDA and increased the activity of SOD and GSH-Px in brain tissue (P <0.05, P <0.01). DMY 250 mg · kg-1 can reduce cerebral infarction ratio after cerebral I / R injury (compared with the model group, P <0.05). Conclusion DMY has a certain protective effect on focal cerebral I / R injury, and its protective mechanism is related to its antioxidative effect.