摘要
本文用离体豚鼠心乳头肌和离体兔主动脉自由基损伤模型,探讨了绞股蓝总皂甙对自由基损伤心血管功能的保护作用。结果发现绞股蓝皂甙(50mg·L^(-1))能对抗自由基所致的心肌收缩力降低、不应期缩短和自律性增加;并能降低心肌组织MDA含量,保护SOD活动和血管内皮释放EDRF的能力。
Using oxygen free radicals(OEF)produced by xanthine-xanthine oxidaseCX-XOD)we investigated the protective effect of gypenosides(GPS) on oxidative damage of guinea pig myocardium and rabbit arterial endothelium. In the isolated guinea pig papillary muscles,X(0. 42 mmol·L^(-1))-XOD (5. 3 nmol· L^(-1)) induced a quick positive inotropism at first and then a continuous negative one, shortened the functional refractory period(FRD) (206. 6±44. 9 vs 262. 8±49. 0 ms,P<C0. 01),increased the automaticity induced by adrenaline (threshold concentration:1. 4±0. 9 vs 5. 9±3. 4 fimol·L^(-1),P<0. 01),reduced the activity of SOD(0. 61± 0. 27 vs 1. 06±0. 40 U·mg^(-1) wet wt,P<0. 05)and increased the content of MDA(137. 2± 29. 3 vs 84. l±10. 6 nmol·g^(-1) wet wt,P<0. 01). GPS 50 mg·L^(-1) inhibited OFR-induced the negative inotropism(139.1±32. 1% vs 94. 9±20. 0%,P<0. 01),resisted the change ot FRP(266. 4±44. 7 vs 206. 6±44. 9 ms,P<0. 01),reduced the automaticity(5. 9±3. 4μmol·L^(-1) vs 1. 4 + 0. 9μmol·L^(-1),P<0. 01) by X-XOD. At the same time,GPS antagonized OFR-induced rise of MDA(86.1±14. 9 vs 137. 2±29. 3 nmol·g^(-1) wet wt ,P<0. 01)and decrease of SOD(0. 92±0. 30 vs 0. 61±0. 27U·mg^(-1) wet wt,P<0. 01). In the isolated rabbit thoracic aortacthe release of endothelium-derived relaxing factor (EDRF)induced by ACh decreased(RR:0. 34±0.16 vs 1. 00±0. 08,P<0. ODby X-XOD. GPS 50 mg·L^(-1) significantly protected the EDRF releasing capacity(RR:0. 80±0.16 vs 0. 34±0. 16,P<0. 01). It was concluded that GPS could protect the myocardium and arterial endothelium from OFR damage.
关键词
绞股蓝
自由基
皂甙
心血管功能
gypenosides
oxygen free radicals
endothelium—derived relaxing factors
guinea pig
rabbit
