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芍药苷通过激活大麻素受体2对脑缺血再灌注大鼠海马的保护作用

[Protective effect of paeoniflorin on the hippocampus in rats with cerebral ischemia-reperfusion through activating cannabinoid receptor 2].

作者信息

Cai Jianghui, Rao Menglin, Tang Mi, Xiang Li, Feng Sha, Xiao Chengyan, Liu Yingju

机构信息

Teaching and Research Section of Biochemical and Molecular Pharmacology, College of Pharmacy, Chongqing Medical University, Chongqing 400016, China.

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Apr;31(4):443-7.

Abstract

OBJECTIVE

To investigate the protective effect of paeoniflorin on hippocampal neurons in rats subjected to cerebral ischemia and reperfusion through activating cannabinoid receptor 2 (CBR2).

METHODS

A total of 144 male SD rats were randomly divided into sham-operation group, cerebral ischemia-reperfusion model group, menstruum group, 10 and 40 mg/kg paeoniflorin groups, 3 mg/kg CBR2 selective antagonist AM630 group, 40 mg/kg paeoniflorin combined with 3 mg/kg AM630 group, and 3 mg/kg CBR2 selective agonist HU308 treatment group. Focal cerebral ischemia-reperfusion models were made by inserting a monofilament suture into internal carotid artery. The neurological scores, infarction volume and cerebral edema were detected carefully to find out the effect of paeoniflorin on neurons. Pathological changes were observed by HE staining. The expressions of caspase-3 and cyclooxygenase 2 (COX-2) in hippocampal CA1 region were determined by immunohistochemistry.

RESULTS

Paeoniflorin significantly decreased the neurological scores, infarction volume and cerebral edema. In addition, paeoniflorin relieved the pathological changes and inhibited the expressions of caspase-3 and COX-2 in hippocampus CA1 area. But injecting AM630 in advance obviously counteracted the neuroprotective effect of paeoniflorin.

CONCLUSION

CBR2 may participate in the protective effect of paeoniflorin on hippocampal neurons of cerebral ischemia-reperfusion rat models.

摘要

目的

通过激活大麻素受体2(CBR2)研究芍药苷对脑缺血再灌注大鼠海马神经元的保护作用。

方法

将144只雄性SD大鼠随机分为假手术组、脑缺血再灌注模型组、溶剂组、10和40mg/kg芍药苷组、3mg/kg CBR2选择性拮抗剂AM630组、40mg/kg芍药苷联合3mg/kg AM630组以及3mg/kg CBR2选择性激动剂HU308治疗组。通过将单丝缝合线插入颈内动脉制作局灶性脑缺血再灌注模型。仔细检测神经功能评分、梗死体积和脑水肿,以了解芍药苷对神经元的影响。通过苏木精-伊红(HE)染色观察病理变化。采用免疫组织化学法测定海马CA1区半胱天冬酶-3(caspase-3)和环氧化酶2(COX-2)的表达。

结果

芍药苷显著降低神经功能评分、梗死体积和脑水肿。此外,芍药苷减轻了病理变化,并抑制了海马CA1区caspase-3和COX-2的表达。但预先注射AM630明显抵消了芍药苷的神经保护作用。

结论

CBR2可能参与芍药苷对脑缺血再灌注大鼠模型海马神经元的保护作用。

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