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首页> 外文期刊>Life sciences >In vitro pharmacological actions of sinomenine on the smooth muscle and the endothelial cell activity in rat aorta.
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In vitro pharmacological actions of sinomenine on the smooth muscle and the endothelial cell activity in rat aorta.

机译：青藤碱对大鼠主动脉平滑肌和内皮细胞活性的体外药理作用。

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摘要

Vasodilating actions of sinomenine were examined using rat aorta ring strips. Sinomenine (0.1 to 100 microM) dilated norepinephrine (NE, 5 microM)-induced vasoconstriction in a concentration-dependent manner reaching 68.8+/-5.1% (n=6, P<0.01) at a concentration of 100 microM. Sinomenine (100 microM) also attenuated KCl (60 mM) and phorbol 12, 13-dibutyrate (PDB, a protein kinase C, PK-C, activator, 300 nM)-induced vasoconstriction by 86.9+/-8.5% (n=6, P<0.01) and 49.9+/-9.8% (n=6, P<0.01), respectively. Pretreatment with nicardipine (a Ca2+ channel antagonist), staurosporine (a PK-C inhibitor), NG-monomethyl-L-arginine acetate (L-NMMA, a nitric oxide, NO, synthesis inhibitor), and indomethacin (a cyclooxygenase inhibitor) were carried out. Nicardipine (0.1 microM) led to a significant decrease in the vasodilating potential of sinomenine (at 100 microM, 68.8+/-5.1% vs. 35.5+/-6.9%; n=5, P<0.001). Pretreatment with staurosporine (30 nM) reduced sinomenine-associated vasodilation from 68.8+/-5.1% to 49.5+/-7.7% (n=5, P<0.001), and L-NMMA (100 microM) and indomethacin (10 microM), to 25.3+/-2.3% (n=5, P<0.001) and to 37.1+/-9.3% (n=5, P<0.001), respectively. The responses were almost similar to the results without endothelium. Therefore, these results indicate that sinomenine causes the vasorelaxation by the mechanisms involved with the inhibitions of Ca2+ channel and PK-C activity, and also with the activations of NO and prostaglandin (PG) I2 syntheses in endothelium.
机译：用大鼠主动脉环带检查青藤碱的血管舒张作用。青藤碱（0.1至100 microM）以浓度依赖的方式使去甲肾上腺素（NE，5 microM）诱导的血管收缩扩张，浓度为100 microM时达到68.8 +/- 5.1％（n = 6，P <0.01）。青藤碱（100 microM）还减弱了KCl（60 mM）和佛波醇12、13-二丁酸酯（PDB，蛋白激酶C，PK-C，激活剂，300 nM）诱导的血管收缩86.9 +/- 8.5％（n = 6） ，P <0.01）和49.9 +/- 9.8％（n = 6，P <0.01）。分别用尼卡地平（一种Ca2 +通道拮抗剂），星形孢菌素（一种PK-C抑制剂），NG-单甲基-L-精氨酸乙酸酯（L-NMMA，一氧化氮，NO，合成抑制剂）和消炎痛（一种环加氧酶抑制剂）进行预处理。执行。尼卡地平（0.1 microM）导致青藤碱的血管舒张潜力显着降低（100 microM时为68.8 +/- 5.1％，而35.5 +/- 6.9％; n = 5，P <0.001）。星形孢菌素（30 nM）预处理将青藤碱相关的血管舒张从68.8 +/- 5.1％降至49.5 +/- 7.7％（n = 5，P <0.001）和L-NMMA（100 microM）和消炎痛（10 microM）分别为25.3 +/- 2.3％（n = 5，P <0.001）和37.1 +/- 9.3％（n = 5，P <0.001）。反应几乎与没有内皮的结果相似。因此，这些结果表明青藤碱可通过抑制Ca2 +通道和PK-C活性以及内皮中NO和前列腺素（PG）I2合成的激活机制引起血管舒张。

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