CAJ | 학술논문

目的：体外观察银杏叶提取物各主要单体成分对血小板聚集及血小板磷酸二酯酶（phosphodiesterase，PDE）3活性的影响，明确银杏叶提取物抑制血小板PDE3的确切成分。方法收集分离2周内未服任何药物的健康志愿者的血小板，观察各种浓度的银杏黄酮单体成分槲皮素、山柰酚、异鼠李素和银杏内酯单体成分银杏内酯 A、B、C、J 对血小板聚集抑制率及血小板 PDE3亚型活性的影响，设不加药物、加同等体积药物溶剂为空白对照。结果1μmol/L、10μmol/L、100μmol/L的槲皮素对ADP诱导的血小板聚集抑制率分别为（47.30±13.80）%、（49.00±11.00）%、（45.90±9.88）%，对 PAF 诱导的血小板聚集抑制率分别为（45.00±15.41）%、（52.10±14.24）%、（50.00±14.38）%，与溶剂对照组相比，差异有统计学意义。同样浓度的山柰酚、异鼠李素、银杏内酯A、B、C、J对ADP、PAF诱导的血小板聚集也均有抑制作用。1、10、100μmol/L的槲皮素作用后血小板PDE3活性分别为（1163.02±523.52） pmol·（mg protein）-1·min-1、（930.98±324.09）pmol·（mg protein）-1·min-1、（820.70±283.14）pmol·（mg protein）-1·min-1，与溶剂对照组相比，差异有统计学意义，同样浓度的山柰酚、异鼠李素、银杏内酯A、B、C、J组的PDE3活性与对照组相比，差异无统计学意义。在槲皮素、山柰酚、异鼠李素、银杏内酯A、B、C、J各药物组内分别对两种诱聚剂ADP、PAF诱导的血小板聚集抑制率进行比较，差别均无统计学意义。对槲皮素作用后的血小板聚集抑制率及PDE3活性进行相关性分析，显示ADP、PAF诱导的血小板聚集抑制率与PDE3活性均无相关性（r＝0.263，r＝-0.013，P均>0.05）。结论银杏叶提取物中各单体成分均有抑制血小板聚集作用。槲皮素具抑制血小板PDE3活性作用，其他单体对血小板PDE3活性无影响。目的：體外觀察銀杏葉提取物各主要單體成分對血小闆聚集及血小闆燐痠二酯酶（phosphodiesterase，PDE）3活性的影響，明確銀杏葉提取物抑製血小闆PDE3的確切成分。方法收集分離2週內未服任何藥物的健康誌願者的血小闆，觀察各種濃度的銀杏黃酮單體成分槲皮素、山柰酚、異鼠李素和銀杏內酯單體成分銀杏內酯 A、B、C、J 對血小闆聚集抑製率及血小闆 PDE3亞型活性的影響，設不加藥物、加同等體積藥物溶劑為空白對照。結果1μmol/L、10μmol/L、100μmol/L的槲皮素對ADP誘導的血小闆聚集抑製率分彆為（47.30±13.80）%、（49.00±11.00）%、（45.90±9.88）%，對 PAF 誘導的血小闆聚集抑製率分彆為（45.00±15.41）%、（52.10±14.24）%、（50.00±14.38）%，與溶劑對照組相比，差異有統計學意義。同樣濃度的山柰酚、異鼠李素、銀杏內酯A、B、C、J對ADP、PAF誘導的血小闆聚集也均有抑製作用。1、10、100μmol/L的槲皮素作用後血小闆PDE3活性分彆為（1163.02±523.52） pmol·（mg protein）-1·min-1、（930.98±324.09）pmol·（mg protein）-1·min-1、（820.70±283.14）pmol·（mg protein）-1·min-1，與溶劑對照組相比，差異有統計學意義，同樣濃度的山柰酚、異鼠李素、銀杏內酯A、B、C、J組的PDE3活性與對照組相比，差異無統計學意義。在槲皮素、山柰酚、異鼠李素、銀杏內酯A、B、C、J各藥物組內分彆對兩種誘聚劑ADP、PAF誘導的血小闆聚集抑製率進行比較，差彆均無統計學意義。對槲皮素作用後的血小闆聚集抑製率及PDE3活性進行相關性分析，顯示ADP、PAF誘導的血小闆聚集抑製率與PDE3活性均無相關性（r＝0.263，r＝-0.013，P均>0.05）。結論銀杏葉提取物中各單體成分均有抑製血小闆聚集作用。槲皮素具抑製血小闆PDE3活性作用，其他單體對血小闆PDE3活性無影響。
목적：체외관찰은행협제취물각주요단체성분대혈소판취집급혈소판린산이지매（phosphodiesterase，PDE）3활성적영향，명학은행협제취물억제혈소판PDE3적학절성분。방법수집분리2주내미복임하약물적건강지원자적혈소판，관찰각충농도적은행황동단체성분곡피소、산내분、이서리소화은행내지단체성분은행내지 A、B、C、J 대혈소판취집억제솔급혈소판 PDE3아형활성적영향，설불가약물、가동등체적약물용제위공백대조。결과1μmol/L、10μmol/L、100μmol/L적곡피소대ADP유도적혈소판취집억제솔분별위（47.30±13.80）%、（49.00±11.00）%、（45.90±9.88）%，대 PAF 유도적혈소판취집억제솔분별위（45.00±15.41）%、（52.10±14.24）%、（50.00±14.38）%，여용제대조조상비，차이유통계학의의。동양농도적산내분、이서리소、은행내지A、B、C、J대ADP、PAF유도적혈소판취집야균유억제작용。1、10、100μmol/L적곡피소작용후혈소판PDE3활성분별위（1163.02±523.52） pmol·（mg protein）-1·min-1、（930.98±324.09）pmol·（mg protein）-1·min-1、（820.70±283.14）pmol·（mg protein）-1·min-1，여용제대조조상비，차이유통계학의의，동양농도적산내분、이서리소、은행내지A、B、C、J조적PDE3활성여대조조상비，차이무통계학의의。재곡피소、산내분、이서리소、은행내지A、B、C、J각약물조내분별대량충유취제ADP、PAF유도적혈소판취집억제솔진행비교，차별균무통계학의의。대곡피소작용후적혈소판취집억제솔급PDE3활성진행상관성분석，현시ADP、PAF유도적혈소판취집억제솔여PDE3활성균무상관성（r＝0.263，r＝-0.013，P균>0.05）。결론은행협제취물중각단체성분균유억제혈소판취집작용。곡피소구억제혈소판PDE3활성작용，기타단체대혈소판PDE3활성무영향。
Objective To observe the effect of the main monomer ingredients of EGB on platelet aggregation and platelet PDE3 activity in vitro, and to find out which ingredients can inhibit PDE3 activity. Methods Platelets were collected and purified from healthy volunteers who have not taken any medicines two weeks before collections. Then to observe the effect of each ingredient on the inhibition of platelet aggregation and platelet PDE3 activity. Various concentrations of quercetin, kaempferol, isorhamnetin, ginkgolide A, ginkgolide B, ginkgolide C and ginkgolide J were applied in experiment respectively. Blank control was set. Results After treated by 1μmol/L, 10μmol/L, and 100μmol/L quercetin respectively, inhibition of platelet aggregation induced by ADP were (47.30±13.80)%, (49.00±11.00)%, (45.90±9.88)%, induced by PAF were (47.30±13.80)%, (49.00±11.00)%, and (45.90±9.88)%, and had notable differences with blank control. The same concentration of Kaempferol, isorhamnetin, ginkgolide A, ginkgolide B, ginkgolide C and ginkgolide J all inhibited platelet aggregation induced by ADP or PAF, Treated by the same concentration of quercetin, platelet PDE3 activity were (1163.02±523.52) pmol·(mg protein)-1·min-1, (930.98±324.09) pmol·(mg protein)-1·min-1, (820.70± 283.14) pmol·(mg protein)-1·min-1 respectively, and had notable differences with blank control. However, treated by Kaempferol, isorhamnetin, ginkgolide A, ginkgolide B, ginkgolide C and ginkgolide J respectively, the PDE3 activity had no statistically significant difference with that of blank controls. No statistical difference was found between the results induced by ADP and by PAF in each ingredient groups. In quercetin group, correlation analysis showed that there were no correlation between inhibition of platelet aggregation and PDE3 activity(r=0.263, r=-0.013). Conclusion All the monomer ingredients of EGB inhibit platelet aggregation, but only quercetin inhibits PDE3 activity, and the other ingredients have no effect on PDE3 activity.