复方归苓片提取物对反复缺血再灌注诱导脑损伤的保护作用

Neuroprotective Effects of Extracts of Guiling Pill on Ischemic-Reperfusion Induced Brain Injury

目的：考察中药复方归苓片（茯苓、白术、当归,FDB）提取物对缺血再灌注诱导小鼠脑损伤的保护作用。方法：小鼠预先ig给予FBD CO2超临界萃取物（FBD-CO2,37.5 mg.kg-1）、水提物（FBD-H2O,150 mg.kg-1）与总提物（FBD,187.5 mg.kg-1）,bid×3.5 d,应用双侧颈总动脉反复夹闭10 min与再灌注24 h诱导小鼠神经炎症与脑损伤,2,3,5-三苯基氯化四氮唑（TTC）染色法检测脑梗死,伊文思蓝法检查血脑屏障（BBB）通透性,分类计数血液白细胞,比色法测定脑组织髓过氧化物酶（MPO）活性、前列腺素E2（PGE2）与一氧化氮（NO）水平。结果：FBD与FBD-CO2/H2O均可显著抑制BBB通透性升高（P〈0.05）,并显著保持血液白细胞数量（P〈0.05-0.001）,抑制脑组织MPO活性（P〈0.01-0.001）,防止中性粒细胞中枢浸润;其中,FBD与FBD-CO2可显著减少脑梗死面积（P〈0.05）,降低脑组织PGE2与NO水平（P〈0.05-0.001）。结论：FBD具有抗炎与神经保护作用,其抗炎与神经保护机制可能与FBD-CO2抑制中性粒白细胞中枢浸润,减少炎症介质PGE2与NO生成有关。

Objective： To investigate the anti-inflammatory and neuroprotective action of Guiling Pill （Fuling, Baizhu and Danggui, FBD） on ischemic-reperfusion induced brain injury. Methods： Mice were orally administered 37.5 mg·kg^- 1 supercritieal fluid extract of FBD （ FBD- CO2 ）, 150 mg· kg^- 1 aqueous extract （ FBD- H2 O）, and 187.5 mg· kg^-1 both （FBD） beforehand, twice daily for 3.5 d, and subjected to repetitive 10 min isehemia and 24 h reperfusion, then brain infarction was observed by 2, 3,5-triphenyhertrazolium chloride （TTC） staining, the permeability of BBB was examined by Evans Blue dyeing, the total blood leukoeytes and its three subpopulations were counted while cerebral myeloperoxidase （MPO） activity was detected, and levels in prostaglandin E2 （PGE2） and nitric oxide （NO） were assayed by speetrophotometry. Results： Compared with the saline-pretreated mice, oral pretreatment with FBD or FBD-CO2 had not only obviously less Evans Blue influx, and brain infarction, but also recruitment of leukoeytes, evidenced with maintained circulating neutrophils counts and low cerebral MPO activity; excessive cerebral prostaglandin E2 （PGE2 ）, and nitric oxide （NO） production were markedly also restrained by FBD-CO2, rather than FBD-H2O. Conclusion： FBD exerted an anti-inflammatory and neuroprotective action on cerebral I/R, partially via inhibition of neutrophils recruitment and generation of NO and PGE2 . Its anti-inflammatory effect was mainly related with FBD-CO2.