Khamseekaew Juthamas, Duangjinda Monchai, Maneesai Putcharawipa, Labjit Chanon, Rattanakanokchai Siwayu, Rongpan Sudarat, Pakdeechote Poungrat, Potue Prapassorn
Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
Department of Animal Science, Faculty of Agriculture, Khon Kaen University, Khon Kaen 40002, Thailand.
Int J Mol Sci. 2025 Feb 22;26(5):1897. doi: 10.3390/ijms26051897.
Hemp ( L.) leaf oil (HLO) contains several bioactive compounds such as phenolics, flavonoids, and quercetin. However, the effects of HLO on hypertensive conditions have not yet been investigated. This study investigated the cardiovascular protective effects of HLO in a nitric oxide (NO) synthase inhibitor-induced hypertensive rat model. Five weeks of HLO administration significantly prevented blood pressure elevation, improved cardiac function, and mitigated cardiac hypertrophy. Furthermore, HLO ameliorated vascular dysfunction by reducing sympathetic nerve stimulation-induced vasoconstriction, increasing endothelium-dependent vasorelaxation, as well as decreasing vascular wall thickness and vascular smooth muscle cell proliferation. HLO inhibited renin-angiotensin system (RAS) activation and downregulated angiotensin II type 1 (AT1) receptor and NADPH oxidase expression. Additionally, HLO normalized the circulating NO metabolites, decreased oxidative stress, and enhanced antioxidant status. These findings suggest that HLO protects against cardiovascular dysfunction and preserves its morphology. The mechanism of action might involve the suppression of RAS overactivity and oxidative stress through the Ang II/AT1 receptor/NOX2 pathway in NO-deficient hypertension.
大麻(L.)叶油(HLO)含有多种生物活性化合物,如酚类、黄酮类和槲皮素。然而,HLO对高血压状况的影响尚未得到研究。本研究在一氧化氮(NO)合酶抑制剂诱导的高血压大鼠模型中研究了HLO的心血管保护作用。给予HLO五周可显著预防血压升高,改善心脏功能,并减轻心脏肥大。此外,HLO通过减少交感神经刺激引起的血管收缩、增加内皮依赖性血管舒张以及减少血管壁厚度和血管平滑肌细胞增殖来改善血管功能障碍。HLO抑制肾素-血管紧张素系统(RAS)激活,并下调血管紧张素II 1型(AT1)受体和NADPH氧化酶表达。此外,HLO使循环中的NO代谢产物正常化,降低氧化应激,并增强抗氧化状态。这些发现表明,HLO可预防心血管功能障碍并保持其形态。作用机制可能涉及在NO缺乏型高血压中通过Ang II/AT1受体/NOX2途径抑制RAS过度活性和氧化应激。