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Biochanin-A elicits relaxation in coronary artery of goat through different mechanisms.
Research in Veterinary Science ( IF 2.4 ) Pub Date : 2020-05-04 , DOI: 10.1016/j.rvsc.2020.05.003
Tarun Kumar 1 , Meemansha Sharma 1 , Abhinav Rana 1 , Madhu Cholenahalli Lingaraju 1 , Subhashree Parida 1 , Dinesh Kumar 1 , Thakur Uttam Singh 1
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Flavonoids have shown beneficial effects in various disease conditions as reported by various previous studies. Biochanin-A is a flavonoid present in various plants in nature. Present investigation was done to assess the vasorelaxant potential of biochanin-A on isolated coronary artery of goat and its possible mechanism of action. Vascular reactivity experiments were done on circumflex coronary artery of goats using the tension experiments. Goat coronary arterial rings were relaxed with biochanin-A in concentration (0.1-100 μM)-dependent manner. Endothelium had no effect on biochanin-A-induced relaxation. Maximum relaxation induced by biochanin-A was 116.54 ± 12.21% in endothelium-intact artery and it was not significantly different with maximal relaxation (108.22 ± 1.88%) of endothelium-denuded vessel. L-NAME (100 μM) did not show any effect on biochanin-A-induced relaxation. TEA (BKCa channel blocker), and BaCl2 (KIR blocker) had no effect on biochanin-A-induced relaxation. However, biochanin-A-induced maximal relaxation (71.72 ± 4.50%) was reduced significantly (P < .001) in the presence of 4-aminopyridine (KV channel blocker, 3 mM) in comparison with control (114.07 ± 4.33%). Glibenclaminde (KATP channel blocker), H89 (PKA inhibitor), ICI182780 (estrogen receptor antagonist) showed partial attenuation in the biochanin-A-induced relaxation. ODQ (sGC blocker) and HC067047 (TRPV4 channel blocker) had no effect on biochanin-A-induced relaxation. In K+-depolarized endothelium-denuded arterial rings, biochanin-A (30 μM) significantly (P < .05; P < .001) decreased CaCl2-induced contractions (0.02 ± 0.01 g vs. control 0.73 ± 0.30 g). Biochanin-A did not influence the fasudil (rho kinase inhibitor) and SNP (NO-donor)-induced relaxation in this vessel. Biochanin-A showed relaxation in goat coronary artery in endothelium-independent pathways and showed the partial involvement of KATP, protein kinase A and estrogen receptors and full involvement of Cav1.2 channels.

中文翻译:

Biochanin-A通过不同的机制引起山羊冠状动脉松弛。

如先前的各种研究所报道,类黄酮在各种疾病中均显示出有益的作用。Biochanin-A是存在于自然界的各种植物中的类黄酮。目前的研究是为了评估Biochanin-A对山羊离体冠状动脉血管舒张作用的潜力及其可能的作用机制。使用张力实验在山羊的回旋冠状动脉上进行了血管反应性实验。山羊冠状动脉环以浓度(0.1-100μM)依赖性的生物chanin-A松弛。内皮对生物素A诱导的松弛没有影响。由生物chanin-A引起的最大松弛在内皮完整动脉中为116.54±12.21%,与内皮剥除血管的最大松弛(108.22±1.88%)并无显着差异。L-NAME(100μM)对生物素A诱导的松弛没有任何影响。TEA(BKCa通道阻滞剂)和BaCl2(KIR阻滞剂)对生物素A诱导的松弛没有影响。但是,与对照(114.07±4.33%)相比,在存在4-氨基吡啶(KV通道阻滞剂,3 mM)的情况下,生物素A诱导的最大松弛(71.72±4.50%)显着降低(P <.001)。格列本脲(KATP通道阻滞剂),H89(PKA抑制剂),ICI182780(雌激素受体拮抗剂)在生物素A诱导的松弛中显示出部分减弱。ODQ(sGC阻滞剂)和HC067047(TRPV4通道阻滞剂)对生物素A诱导的松弛没有影响。在K +去极化的内皮剥脱的动脉环中,biochanin-A(30μM)显着(P <.05; P <.001)减少了CaCl2诱导的收缩(0.02±0.01 g,而对照组为0.73±0.30 g)。Biochanin-A不会影响fasudil(rho激酶抑制剂)和SNP(NO供体)诱导的血管舒张。Biochanin-A在山羊非依赖性内皮通路中显示出山羊冠状动脉的舒张,并显示出KATP,蛋白激酶A和雌激素受体的部分参与以及Cav1.2通道的完全参与。
更新日期:2020-05-04
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