The leaf extract of Ginkgo Biloba L. suppresses oxidized LDL‐stimulated fibronectin production through an antioxidant action in rat mesangial cells
The leaf extract of Ginkgo Biloba L. suppresses oxidized LDL‐stimulated fibronectin production through an antioxidant action in rat mesangial cells
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DOI：
10.1038/sj.bjp.0705805
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发表时间：
2004-06
影响因子：
7.3
通讯作者：
S. Akiba;M. Chiba;Y. Mukaida;A. Tamura;Takashi Sato
中科院分区：
文献类型：
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作者：
S. Akiba;M. Chiba;Y. Mukaida;A. Tamura;Takashi Sato
银杏叶提取物。通过抗氧化作用表现出多种药理作用。我们研究了银杏叶提取物（Ginkgolon-24）对氧化低密度脂蛋白（oxLDL）诱导的大鼠系膜细胞纤连蛋白产生的影响。oxLDL刺激促进了前代活性氧（ROS）产生的纤连蛋白的产生。用银杏酮-24预处理可抑制oxLDL诱导的纤连蛋白生成以及ROS生成。oxLDL还可激活参与纤连蛋白生成的转录因子SP-1、核因子-κB和cAMP反应元件结合蛋白。在这些激活的转录因子中，Ginkgolon-24仅抑制SP-1的激活，而oxLDL颗粒中的氧化脂质7-酮基胆固醇诱导纤连蛋白的产生和SP-1的激活，Ginkgolon-24也抑制了这些活性。抑制oxLDL诱导的纤连蛋白的产生，可能是通过抑制大鼠肾小球系膜细胞中ROS的产生和SP-1的活化。British Journal of Pharmacology（2004）142，419-424。doi：10.1038/sj.bjp.0705805
The leaf extract ofGinkgo Biloba L. exhibits a variety of pharmacological effects through an antioxidant action. We examined the effects of the leaf extract (Ginkgolon‐24) on the production of fibronectin induced by oxidized low‐density lipoprotein (oxLDL) in rat mesangial cells.Stimulation with oxLDL accelerated the production of fibronectin with the preceding generation of reactive oxygen species (ROS). Pretreatment with Ginkgolon‐24 inhibited the oxLDL‐induced fibronectin production as well as ROS generation.oxLDL also elicited the activation of SP‐1, nuclear factor‐κB, and cAMP response element‐binding protein, which are transcription factors involved in the fibronectin production. Among these activated transcription factors, Ginkgolon‐24 inhibited the activation of SP‐1 only.Furthermore, 7‐ketocholesterol, an oxidized lipid in oxLDL particles, induced the production of fibronectin and the activation of SP‐1, which were also suppressed by Ginkgolon‐24.These results suggest that the leaf extract ofGinkgo Biloba L. inhibits the oxLDL‐induced production of fibronectin probably through inhibitory effects on ROS generation and SP‐1 activation in rat mesangial cells.British Journal of Pharmacology(2004)142, 419–424. doi:10.1038/sj.bjp.0705805