Anti-injury effect of ginkgolide B on vascular endothelial cells induced by hypoxia/reoxygenation[J]. Chinese Heart Journal, 2011, 23(3): 318-321.
    Citation: Anti-injury effect of ginkgolide B on vascular endothelial cells induced by hypoxia/reoxygenation[J]. Chinese Heart Journal, 2011, 23(3): 318-321.
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    Anti-injury effect of ginkgolide B on vascular endothelial cells induced by hypoxia/reoxygenation

      摘要
    • 摘要: 目的:探讨银杏内酯B(GB)减轻缺氧/复氧(H/R)所致血管内皮细胞损伤的作用和机制。方法： 将体外培养的人脐静脉内皮细胞分为5个组，即空白对照组（不加任何处理）、GB组（100 μmol/L）、H/R组（缺氧2 h/复氧24 h）、GB+H/R组及GB+H/R+ N-硝基-L-精氨酸甲酯（L-NAME，NOS抑制剂）组。用3-(4，5-二甲基噻唑-2)-2，5-二苯基四氮唑溴盐（MTT）比色法测定内皮细胞的存活率(%)。用乳酸脱氢酶（LDH）测试盒和一氧化氮（NO）测试盒分别检测细胞培养上清液中LDH和NO的含量。用Western blot法检测培养的人脐静脉内皮细胞中内皮型一氧化氮合成酶（eNOS）表达的水平。结果： MTT比色法的结果显示，H/R可显著降低内皮细胞的存活率(%)，增加LDH的含量，降低NO的生成量（与空白对照组比较，P<0.01）；而GB则可逆转上述效应，但GB的作用又可被L-NAME所抑制（与GB+H/R组比较，P<0.01）。GB可以显著提高H/R作用后血管内皮细胞中eNOS表达的水平（与H/R组比较，P<0.01），但是该效应不被L-NAME阻断。结论： GB可显著减轻H/R对内皮细胞的损伤，其作用是通过eNOS-NO途径实现的。

       

      Abstract: AIM:To investigate the protective effects of ginkgolide B (GB) on human umbilical vein endothelial cells (HUVECs) induced by hypoxia/reoxygenation (H/R) injury and the underlying mechanisms. METHODS: Cultured HUVECs were divided into five groups: control group, GB group (100 mol/L), H/R group (hypoxia 2 h/reoxygenation 24 h), GB+H/R group and GB+H/R+NG-nitro-L-arginine methyl ester (L-NAME) group. Cell viability was measured by 3-［4,5-dimethylthiazol-2-yl］-2,5-diphenyltetrazolium bromide (MTT) colorimetric method and lactate dehydrogenase (LDH), nitric oxide (NO) in the supernatant fluid of cultured cells was detected by spectrophotometer. Endothelial nitric oxide synthase (eNOS) protein was detected by Western blot. RESULTS: H/R reduced the MTT OD value, increased LDH content and decreased NO level significantly (P<0.01 vs. control group), but GB reversed these effects on HUVECs. These GB effects were inhibited by L-NAME (P<0.01 vs. GB+H/R group). GB increased H/R-reduced content of eNOS (P<0.01 vs. H/R group), but this effect was not inhibited by L-NAME. CONCLUSION: GB has some anti-injury effects on HUVECs induced by H/R via enhancing the levels of eNOS and NO.

       

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