Tao Xiao-Qian, Cao Ze-Yu, Cao Liang, Xiao Wei
State Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Jiangsu Kanion Parmaceutical Co., Ltd., Lianyungang 222001, China.
Zhongguo Zhong Yao Za Zhi. 2017 Dec;42(24):4727-4732. doi: 10.19540/j.cnki.cjcmm.2017.0208.
To investigate the antagonism effects of different concentrations of ginkgolide K(GK) on platelet activating factor (PAF)-induced platelet aggregation and neuroprotective effect on cells and animal models of ischemia-reperfusion injury. GK-containing serum in rabbit was prepared, and the effects of GK-containing serum on PAF-induced platelet aggregation was observed by platelet aggregation assay. The effect of different concentrations of GK on apoptosis of SH-SY5Y cells injured by oxygen-glucose deprivation/reoxygenation (OGD/R) was investigated by Hoechst 33342/PI double staining in OGD/R cell model. The focal cerebral ischemia-reperfusion model (I/R)was established in rats to detect the effects of GK on neurobehavioral scores and cerebral infarction volume. GK could inhibit PAF-induced platelet aggregation, reverse the apoptosis induced by OGD/R injury and improve the neurobehavioral score and cerebral infarction volume after cerebral ischemia-reperfusion injury in rats in a dose-dependent manner. GK can inhibit PAF-induced platelet aggregation and improve nerve injury after cerebral ischemia-reperfusion.
研究不同浓度银杏内酯K（GK）对血小板活化因子（PAF）诱导的血小板聚集的拮抗作用以及对缺血再灌注损伤细胞和动物模型的神经保护作用。制备兔含GK血清，采用血小板聚集试验观察含GK血清对PAF诱导的血小板聚集的影响。在氧糖剥夺/复氧（OGD/R）细胞模型中，通过Hoechst 33342/PI双染法研究不同浓度GK对OGD/R损伤的SH-SY5Y细胞凋亡的影响。建立大鼠局灶性脑缺血再灌注模型（I/R），检测GK对神经行为评分和脑梗死体积的影响。GK可抑制PAF诱导的血小板聚集，逆转OGD/R损伤诱导的细胞凋亡，并以剂量依赖方式改善大鼠脑缺血再灌注损伤后的神经行为评分和脑梗死体积。GK可抑制PAF诱导的血小板聚集并改善脑缺血再灌注后的神经损伤。
