Division of Pharmacology and Toxicology, ICAR-Indian Veterinary Research Institute, Izatnagar-243 122, Bareilly, Uttar Pradesh, India.
Division of Pharmacology and Toxicology, ICAR-Indian Veterinary Research Institute, Izatnagar-243 122, Bareilly, Uttar Pradesh, India.
Res Vet Sci. 2020 Aug;131:206-214. doi: 10.1016/j.rvsc.2020.05.003. Epub 2020 May 4.
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 (BK channel blocker), and BaCl (K 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 (K channel blocker, 3 mM) in comparison with control (114.07 ± 4.33%). Glibenclaminde (K 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 CaCl-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 K, protein kinase A and estrogen receptors and full involvement of Ca1.2 channels.
黄酮类化合物在各种疾病中的有益作用已被各种先前的研究报道。大豆苷元 A 是一种存在于自然界各种植物中的黄酮类化合物。本研究旨在评估大豆苷元 A 对山羊离体冠状动脉的血管舒张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血管反应性实验。山羊冠状动脉环以浓度（0.1-100 μM）依赖性方式用大豆苷元 A 松弛。内皮对大豆苷元 A 诱导的松弛没有影响。在完整内皮的动脉中，大豆苷元 A 诱导的最大松弛为 116.54±12.21%，与去内皮血管的最大松弛（108.22±1.88%）没有显著差异。L-NAME（100 μM）对大豆苷元 A 诱导的松弛没有影响。TEA（BK 通道阻滞剂）和 BaCl（K 通道阻滞剂）对大豆苷元 A 诱导的松弛没有影响。然而，在 4-氨基吡啶（K 通道阻滞剂，3 mM）存在的情况下，大豆苷元 A 诱导的最大松弛（71.72±4.50%）显著降低（P<.001），与对照相比（114.07±4.33%）。Glibenclamide（K 通道阻滞剂）、H89（PKA 抑制剂）和 ICI182780（雌激素受体拮抗剂）对大豆苷元 A 诱导的松弛表现出部分衰减。ODQ（sGC 阻滞剂）和 HC067047（TRPV4 通道阻滞剂）对大豆苷元 A 诱导的松弛没有影响。在 K 去极化去内皮的动脉环中，大豆苷元 A（30 μM）显著（P<.05；P<.001）降低了 CaCl 诱导的收缩（0.02±0.01 g 与对照 0.73±0.30 g）。在该血管中，大豆苷元 A 不影响 fasudil（rho 激酶抑制剂）和 SNP（NO 供体）诱导的松弛。大豆苷元 A 对山羊冠状动脉显示出非内皮依赖性的舒张作用，并显示 K、蛋白激酶 A 和雌激素受体的部分参与以及 Ca1.2 通道的完全参与。
