第四军医大学学报
第四軍醫大學學報
제사군의대학학보
JOURNAL OF THE FOURTH MILITARY MEDICAL UNIVERSITY
2001年
2期
128-130
,共3页
杨俊旺%刘莉%鲁润华%汪汉卿
楊俊旺%劉莉%魯潤華%汪漢卿
양준왕%류리%로윤화%왕한경
吡啶-2,6(1H,3H)二酮生物碱%腺苷二磷酸%花生四烯酸%血小板聚集%血栓素B2%6-酮-前列腺素F1α
吡啶-2,6(1H,3H)二酮生物堿%腺苷二燐痠%花生四烯痠%血小闆聚集%血栓素B2%6-酮-前列腺素F1α
필정-2,6(1H,3H)이동생물감%선감이린산%화생사희산%혈소판취집%혈전소B2%6-동-전렬선소F1α
目的 研究吡啶-2,6(1H,3H)二酮生物碱(SH1)对二磷酸腺苷(ADP),花生四烯酸(AA)和胶原(COL)诱导兔血小板聚集和TXB2和6-keto-PGF1α生成的影响. 方法 用比浊法和放射 免疫法. 结果 SH1 0.8~3.0 mmol.L-1能显著地抑制2.0 μmol.L -1 ADP, 33.3 μmol.L-1 AA和20.0 g.L-1 COL诱导的兔血小板聚集并有良好的量效关系. SH1 3.0 mmol.L-1抑制TXB2产生,而增加6-keto-PGF1α 产生,并因此6-keto-PGF1α和TXB2的比值增加. 结论 SH 1显著抑制血小板聚集和TXB2产生,同时增加6-keto-PGF1α产生.
目的 研究吡啶-2,6(1H,3H)二酮生物堿(SH1)對二燐痠腺苷(ADP),花生四烯痠(AA)和膠原(COL)誘導兔血小闆聚集和TXB2和6-keto-PGF1α生成的影響. 方法 用比濁法和放射 免疫法. 結果 SH1 0.8~3.0 mmol.L-1能顯著地抑製2.0 μmol.L -1 ADP, 33.3 μmol.L-1 AA和20.0 g.L-1 COL誘導的兔血小闆聚集併有良好的量效關繫. SH1 3.0 mmol.L-1抑製TXB2產生,而增加6-keto-PGF1α 產生,併因此6-keto-PGF1α和TXB2的比值增加. 結論 SH 1顯著抑製血小闆聚集和TXB2產生,同時增加6-keto-PGF1α產生.
목적 연구필정-2,6(1H,3H)이동생물감(SH1)대이린산선감(ADP),화생사희산(AA)화효원(COL)유도토혈소판취집화TXB2화6-keto-PGF1α생성적영향. 방법 용비탁법화방사 면역법. 결과 SH1 0.8~3.0 mmol.L-1능현저지억제2.0 μmol.L -1 ADP, 33.3 μmol.L-1 AA화20.0 g.L-1 COL유도적토혈소판취집병유량호적량효관계. SH1 3.0 mmol.L-1억제TXB2산생,이증가6-keto-PGF1α 산생,병인차6-keto-PGF1α화TXB2적비치증가. 결론 SH 1현저억제혈소판취집화TXB2산생,동시증가6-keto-PGF1α산생.
AIM To investigate the effect of pyridine-2,6(1H,3H)-dion e alkaloids (SH1) on rabbit platelet aggrega-tion induced by adenosine diphosphate (ADP), arachidonic acid (AA) and collagen (COL), as well as thromboxone B2 (TXB2) and 6-keto-PGF1α production. METHODS Turbidimetry and radioimmunoassay were used in rabbits. RESULTS SH2 0.8~3.0 mmol.L-1 could inhibit significantly th e rabbit platelet aggregation induced by ADP 2 μmol.L-1, AA 33.3 μmol.L-1, COL 20. 0 mg.mL-1, which showed good dose-dependence. The inhibition by SH1 0. 8~3.0 mmol.L-1was 23.3%~53.2% (ADP-induced), 13.3~44.4 (AA-induced), 5.1%~49.3% (COL-induced), respectively. SH2 0.8~3.0 mmol.L-1 inhibited TXB2 production, whereas increased 6-keto-PGF1α to TXB2 was enhanced. CONCLUSION SH1 inhibits significantly platelet aggregation and TXB2 production, and simultane ously increases 6-keto-PGF1α.