Vasodilatory Effect of <i>n</i>-Butanol Extract from <i>Sanguisorba officinalis</i> L. and Its Mechanism
The dried root of <i>Sanguisorba officinalis</i> L. (commonly known as Diyu) has been studied for its various pharmacological effects, including its antibacterial, antitumor, antioxidant, and anti-inflammatory activities. In the present study, primary cultured vascular endothelial cells...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2025-04-01
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| Series: | Plants |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2223-7747/14/7/1095 |
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| Summary: | The dried root of <i>Sanguisorba officinalis</i> L. (commonly known as Diyu) has been studied for its various pharmacological effects, including its antibacterial, antitumor, antioxidant, and anti-inflammatory activities. In the present study, primary cultured vascular endothelial cells (HUVECs) and isolated phenylephrine-precontracted rat thoracic aortic rings were examined to investigate the possible mechanism of a butanol extract of Diyu (BSO) in its vascular relaxant effect. HUVECs treated with BSO produced a significantly higher amount of nitric oxide (NO) compared to the control. However, its production was inhibited by pretreatment with N<sup>G</sup>-nitro-L-arginine methylester (L-NAME) or wortmannin. BSO also increased the phosphorylation levels of endothelial nitric oxide synthase (eNOS) and Akt. In the aortic ring, BSO relaxed PE-precontracted rat thoracic aortic rings in a concentration-dependent manner. The absence of the vascular endothelium significantly attenuated BSO-induced vasorelaxation. The non-selective NOS inhibitor, L-NAME, and the selective inhibitor of soluble guanylyl cyclase (sGC), 1H-[1,2,4]-oxadiazolo-[4,3-α]-quinoxalin-1-one (ODQ), dramatically inhibited the BSO-induced relaxation effect of the endothelium-intact aortic ring. Ca<sup>2+</sup>-free buffer and intracellular Ca<sup>2+</sup> homeostasis regulators (TG, Gd<sup>3+</sup>, and 2–APB) inhibited BSO-induced vasorelaxation. In Ca<sup>2+</sup>-free Krebs solution, BSO markedly reduced PE-induced contraction. Vasodilation induced by BSO was significantly inhibited by wortmannin, an inhibitor of Akt. Pretreatment with the non-selective inhibitor of Ca<sup>2+</sup>-activated K<sup>+</sup> channels (K<sub>Ca</sub>), tetraethylammonium (TEA), significantly attenuated the BSO-induced vasorelaxant effect. Furthermore, BSO decreased the systolic blood pressure and heart rate in a concentration-dependent manner in rats. In conclusion, BSO induces vasorelaxation via endothelium-dependent signaling, primarily through the activation of the PI3K-Akt-eNOS-NO signaling pathway in endothelial cells, and the activation of the NO-sGC-cGMP-K⁺ channels pathway in vascular smooth muscle cells. Additionally, store-operated Ca<sup>2+</sup> entry (SOCE)-eNOS pathways and the inhibition of Ca<sup>2</sup>⁺ mobilization from intracellular stores contribute to BSO-induced vasorelaxation. |
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| ISSN: | 2223-7747 |