Miao Mingsan, Cao Lihua, Li Ruiqi, Fang Xiaoyan, Miao Yanyan
Department of Pharmacology, Henan University of TCM, Zhengzhou 450046, China.
Saudi Pharm J. 2017 May;25(4):556-563. doi: 10.1016/j.jsps.2017.04.023. Epub 2017 Apr 28.
The aim of the study was to investigate the protective characteristic of chlorogenic acid, a natural glucosyl xanthone found in Lonicera Japonica on the cerebral ischemia reperfusion injury and the underlying mechanism.
Focal cerebral ischemia reperfusion model was built by blocking the left middle cerebral artery in rats by using the suture-occluded method. Before operation, the corresponding drugs were given for each group once a day for 7 days. After 1 h of final administration, the model was built, after operation, reperfusion was conducted for 22 h, Before the reperfusion 10 min tail vein injection of large, medium and small dose of chlorogenic acid and then mortality was calculated, and Neurological deficit score (NDS) was conducted, and serum was collected to measure the NSE level; a 2 mm thick brain slice located at the intersection of optic nerves was collected for TTC staining, and the percentage of cerebral infarction area was calculated; brain homogenate was collected to measure the ICAM-1, VCAM-1, EPO and HIF-1α levels in brain tissue of cerebral ischemia reperfusion rat models; NGF was detected using immunohistochemical method; the morphological changes in brain tissue was observed with HE staining.
All focal cerebral ischemia reperfusion rat models were duplicated successfully. Every chlorogenic acid group with different dosage can significantly reduce the mortality, NDS and cerebral infarction area of rats, and significantly increase the EPO, HIF-1α and NGF levels in brain tissue; significantly improve the pathological lesions of hippocampus and cortex in brain tissue.
The results showed that chlorogenic acid could protect the focal cerebral ischemia reperfusion injury rat models by adjusting the inflammatory factor, hypoxia factor and nerve growth factor.
本研究旨在探讨金银花中发现的天然葡糖基黄酮绿原酸对脑缺血再灌注损伤的保护特性及其潜在机制。
采用线栓法阻断大鼠左侧大脑中动脉建立局灶性脑缺血再灌注模型。术前,每组每天给药一次,连续给药7天。末次给药1小时后建立模型,术后再灌注22小时,再灌注前10分钟尾静脉注射大、中、小剂量绿原酸,然后计算死亡率,进行神经功能缺损评分(NDS),并采集血清检测NSE水平;取位于视神经交叉处的2mm厚脑片进行TTC染色,计算脑梗死面积百分比;采集脑匀浆检测脑缺血再灌注大鼠模型脑组织中ICAM-1、VCAM-1、EPO和HIF-1α水平;采用免疫组化法检测NGF;用HE染色观察脑组织形态学变化。
所有局灶性脑缺血再灌注大鼠模型均成功复制。不同剂量绿原酸组均可显著降低大鼠死亡率、NDS和脑梗死面积,显著提高脑组织中EPO、HIF-1α和NGF水平;显著改善脑组织海马和皮质的病理损伤。
结果表明,绿原酸可通过调节炎症因子、缺氧因子和神经生长因子对局灶性脑缺血再灌注损伤大鼠模型起到保护作用。