摘要
目的:探讨一氧化氮(NO)信号转导通路在脂联素抑制高脂血症血小板聚集机制中的作用。方法:采用成年大鼠饲以高脂饲料14周,分离其血小板并以重组脂联素(rAPN)孵育。采用免疫荧光、Western blot-ting等方法观察检测血小板聚集、NO含量、超氧化物含量、内皮型一氧化氮合酶(eNOS)/诱导型一氧化氮合酶(iN-OS)的表达和抗氧化物活性。结果:采用rAPN处理能抑制高脂血症诱导的血小板聚集(P<0.05),并导致血小板NO的生成显著减少。同时,在高脂血症血小板中,采用rAPN处理还能显著减少超氧化物的生成(降低62%,P<0.05)并增强其抗氧化能力(增加38%,P<0.05)。此外,高脂血症诱导的eNOS磷酸化的降低和iNOS表达的增加在rAPN处理后被显著逆转(P<0.05,P<0.01)。结论:脂联素是一种抑制高脂血症血小板聚集的脂肪细胞因子,其机制与减少超氧化物水平、增加抗氧化物活性和阻断iNOS的表达有关。
AIM： To investigate the mechanism that adiponeetin inhibits platelet aggregation via nitric oxide （NO） signaling pathway. METHODS： Adult rats were fed with normal or highfat diet for 14 weeks. Their platelets were immediately isolated and treated with or without recombinant full - length adiponectin （rAPN）. The platelet aggregation, NO and superoxide production, endothelial nitric oxide synthase （eNOS）/inducible NOS （iNOS） expression, and antioxidant capacity were determined. RESULTS： Treatment with rAPN inhibited platelet aggregation induced by hyperlipidemia （P 〈 0. 05 ）. Interestingly, total NO, a crucial molecule depressing platelet aggregate and thrombus formation, was significantly reduced, rather than increased in rAPN - treated platelets. Treatment with rAPN significantly decreased superoxide production by 62% （P 〈0. 05） and increased antioxidant capacity by 38% （P 〈0. 05） in hyperlipidemic platelets. Importantly, hyperlipidemia - induced reduction of eNOS phosphorylation and increase in iNOS expression were markedly reversed by rAPN treatment （P 〈 0. 05 and P 〈 0. 01, respectively）. CONCLUSION： Adiponectin is an adipokine that inhibits platelet aggregation by enhancing eNOS activation and attenuating oxidative/uitrative stress including blockage of iNOS expression and superoxide production.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2012年第10期1761-1765,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81270401)
关键词
脂联素
血小板
高脂血症
Adiponectin
Blood platelets
Hyperlipidemia
