以小鼠大脑皮质血管内皮细胞研究EGb761舒张血管机制

Mechanisms of EGb761 in vasodilatation in cultured mouse cerebral cortex endothelial cells

目的探讨银杏叶提取物EGb761对小鼠大脑皮质血管内皮细胞(bEnd3)一氧化氮合酶、前列腺素I_2、血栓素A_2活性和细胞内钙离子浓度等水平的影响。方法在体外培养的bEnd3系细胞培养液中加入EGb761(质量浓度分别为25、50、100、200 mg·L^(-1)),比较各用药组及空白对照组的一氧化氮合酶、6-酮-前列腺素Fla、血栓素B_2活性和细胞内钙离子浓度等水平的变化。结果与空白对照组比较,用药组细胞悬液中一氧化氮合酶的活性和细胞内钙离子浓度均有明显升高,并呈剂量依赖性;细胞培养液上清中的6-酮-前列腺素Fla水平略有升高,但无统计学意义;血栓素B_2水平略有下降,也无统计学意义。结论EGb761舒张血管机制与其增加血管内皮细胞一氧化氮合酶的活性,进而增加一氧化氮的生成有关;其进一步机制与其升高血管内皮细胞内钙离子浓度,进而增加内皮型一氧化氮合酶的活性有关。

AIM To investigate the effects of Ginkgo biloba extracts （EGb761） on the levels of nitrogen monoxide synthase （NOS）,PGI2,TXA2 and [Ca^2＋ ]i in cultured mouse cerebral cortex endothelial cells （bEnd3）. METHODS The levels of the NOS, 6-Keto-PGFla, TXB2 and [ Ca^2 ＋ ]i were examined to evaluate the effects of EGb761 in cultured bEnd3. RESULTS Compared with control group, the activity of NOS and the concentration of calcium in cells were increased in a concentration-dependent manner in administration groups. The changes of the levels of 6-Keto-PGFla and TXB2 showed no statistical significance compared with control group. CONCLUSION The mechanism of the EGb761 in vasodilatation is partly due to its enhancement of the activity of NOS in vascular endothelial cells, and which increased the level of NO. The further mechanism is due to the increase of [ Ca^2＋ ] induced by EGb761, resulting in the increase of activity of endothelial NOS.