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The volatile oil of Nardostachyos Radix et Rhizoma induces endothelial nitric oxide synthase activity in HUVEC cells.

Maiwulanjiang M, Bi CW, Lee PS, Xin G, Miernisha A, Lau KM, Xiong A, Li N, Dong TT, Aisa HA, Tsim KW - PLoS ONE (2015)

Bottom Line: In parallel, the phosphorylation level of Akt kinase was markedly increased by the oil treatment, which was partially attenuated by PI3K/Akt inhibitor LY294002.This inhibitor also blocked the NRR-induced NO production and eNOS phosphorylation.In HUVECs, application of NRR volatile oil elevated the intracellular Ca(2+) level, and BAPTA-AM, a Ca(2+) chelator, reduced the Ca(2+) surge: the blockage were also applied to NRR-induced eNOS phosphorylation and NO production.

View Article: PubMed Central - PubMed

Affiliation: Division of Life Science and Centre for Chinese Medicine, The Hong Kong University of Science and Technology, Hong Kong, China.

ABSTRACT
Nardostahyos Radix et Rhizoma (NRR; the root and rhizome of Nardostachys jatamansi DC.) is a widely used medicinal herb. Historically, NRR is being used for the treatment of cardiovascular and neurological diseases. To search for active ingredients of NRR, we investigated the vascular benefit of NRR volatile oil in (i) the vasodilation in rat aorta ring, and (ii) the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in cultured human umbilical vein endothelial cells (HUVECs). By measuring the fluorescence signal in cultures, application of NRR volatile oil resulted in a rapid activation of NO release as well as the phosphorylation of eNOS: both inductions were markedly reduced by L-NAME. In parallel, the phosphorylation level of Akt kinase was markedly increased by the oil treatment, which was partially attenuated by PI3K/Akt inhibitor LY294002. This inhibitor also blocked the NRR-induced NO production and eNOS phosphorylation. In HUVECs, application of NRR volatile oil elevated the intracellular Ca(2+) level, and BAPTA-AM, a Ca(2+) chelator, reduced the Ca(2+) surge: the blockage were also applied to NRR-induced eNOS phosphorylation and NO production. These findings suggested the volatile oil of NRR was the major ingredient in triggering the vascular dilatation, and which was mediated via the NO production.

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NRR volatile oil induces vasodilation of rat aortic ring.(A): Rat aortic ring was isolated with or without intact endothelium, the vasoconstriction was induced by the applied phenylephrine (Phe, 0.5 µM); acetylcholine (ACh, 1 µM) was then added (left panel). (B): The contraction of aortic ring was tested similar to (A). Different concentrations of NRR volatile oil (1, 3, 10, 30 and 100 µg/mL) were added to induce the relaxation. Also, L-NAME (100 µM) was applied for 30 min, and then different concentrations of NRR volatile oil were added. Values are expressed as percentage of Phe tone as comparing to the control resting tension (right panel). Mean ± SEM, n = 3.
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pone.0116761.g001: NRR volatile oil induces vasodilation of rat aortic ring.(A): Rat aortic ring was isolated with or without intact endothelium, the vasoconstriction was induced by the applied phenylephrine (Phe, 0.5 µM); acetylcholine (ACh, 1 µM) was then added (left panel). (B): The contraction of aortic ring was tested similar to (A). Different concentrations of NRR volatile oil (1, 3, 10, 30 and 100 µg/mL) were added to induce the relaxation. Also, L-NAME (100 µM) was applied for 30 min, and then different concentrations of NRR volatile oil were added. Values are expressed as percentage of Phe tone as comparing to the control resting tension (right panel). Mean ± SEM, n = 3.

Mentions: The endothelial cells line the entire circulatory system, including the heart to the smallest capillary, which play a key role as sensor of chemical and physical stimuli. The endothelial cells possess the ability to release NO, a critical mediator for vasodilation in blood vessels. In an isolated rat aortic ring, acetylcholine (ACh) was shown to induce the endothelium-dependent relaxations, and the relaxations were abolished by removing the endothelium (Fig. 1A). The representative traces in Fig. 1B showed that phenylephrine (Phe), a vasoconstrictor, produced contraction effect in rat aorta. The Phe-induced contraction effects could be relaxed by application of NRR volatile oil (Fig. 1B). The NRR volatile oil-induced vasodilation could be reduced by pre-treatment of eNOS blocker L-NAME: this effect could be attenuated by removing the endothelium (Fig. 1B). These results indicated that the NRR volatile oil-induced rat aorta ring relaxation was mediated by NO, produced by endothelial cells.


The volatile oil of Nardostachyos Radix et Rhizoma induces endothelial nitric oxide synthase activity in HUVEC cells.

Maiwulanjiang M, Bi CW, Lee PS, Xin G, Miernisha A, Lau KM, Xiong A, Li N, Dong TT, Aisa HA, Tsim KW - PLoS ONE (2015)

NRR volatile oil induces vasodilation of rat aortic ring.(A): Rat aortic ring was isolated with or without intact endothelium, the vasoconstriction was induced by the applied phenylephrine (Phe, 0.5 µM); acetylcholine (ACh, 1 µM) was then added (left panel). (B): The contraction of aortic ring was tested similar to (A). Different concentrations of NRR volatile oil (1, 3, 10, 30 and 100 µg/mL) were added to induce the relaxation. Also, L-NAME (100 µM) was applied for 30 min, and then different concentrations of NRR volatile oil were added. Values are expressed as percentage of Phe tone as comparing to the control resting tension (right panel). Mean ± SEM, n = 3.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4359165&req=5

pone.0116761.g001: NRR volatile oil induces vasodilation of rat aortic ring.(A): Rat aortic ring was isolated with or without intact endothelium, the vasoconstriction was induced by the applied phenylephrine (Phe, 0.5 µM); acetylcholine (ACh, 1 µM) was then added (left panel). (B): The contraction of aortic ring was tested similar to (A). Different concentrations of NRR volatile oil (1, 3, 10, 30 and 100 µg/mL) were added to induce the relaxation. Also, L-NAME (100 µM) was applied for 30 min, and then different concentrations of NRR volatile oil were added. Values are expressed as percentage of Phe tone as comparing to the control resting tension (right panel). Mean ± SEM, n = 3.
Mentions: The endothelial cells line the entire circulatory system, including the heart to the smallest capillary, which play a key role as sensor of chemical and physical stimuli. The endothelial cells possess the ability to release NO, a critical mediator for vasodilation in blood vessels. In an isolated rat aortic ring, acetylcholine (ACh) was shown to induce the endothelium-dependent relaxations, and the relaxations were abolished by removing the endothelium (Fig. 1A). The representative traces in Fig. 1B showed that phenylephrine (Phe), a vasoconstrictor, produced contraction effect in rat aorta. The Phe-induced contraction effects could be relaxed by application of NRR volatile oil (Fig. 1B). The NRR volatile oil-induced vasodilation could be reduced by pre-treatment of eNOS blocker L-NAME: this effect could be attenuated by removing the endothelium (Fig. 1B). These results indicated that the NRR volatile oil-induced rat aorta ring relaxation was mediated by NO, produced by endothelial cells.

Bottom Line: In parallel, the phosphorylation level of Akt kinase was markedly increased by the oil treatment, which was partially attenuated by PI3K/Akt inhibitor LY294002.This inhibitor also blocked the NRR-induced NO production and eNOS phosphorylation.In HUVECs, application of NRR volatile oil elevated the intracellular Ca(2+) level, and BAPTA-AM, a Ca(2+) chelator, reduced the Ca(2+) surge: the blockage were also applied to NRR-induced eNOS phosphorylation and NO production.

View Article: PubMed Central - PubMed

Affiliation: Division of Life Science and Centre for Chinese Medicine, The Hong Kong University of Science and Technology, Hong Kong, China.

ABSTRACT
Nardostahyos Radix et Rhizoma (NRR; the root and rhizome of Nardostachys jatamansi DC.) is a widely used medicinal herb. Historically, NRR is being used for the treatment of cardiovascular and neurological diseases. To search for active ingredients of NRR, we investigated the vascular benefit of NRR volatile oil in (i) the vasodilation in rat aorta ring, and (ii) the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in cultured human umbilical vein endothelial cells (HUVECs). By measuring the fluorescence signal in cultures, application of NRR volatile oil resulted in a rapid activation of NO release as well as the phosphorylation of eNOS: both inductions were markedly reduced by L-NAME. In parallel, the phosphorylation level of Akt kinase was markedly increased by the oil treatment, which was partially attenuated by PI3K/Akt inhibitor LY294002. This inhibitor also blocked the NRR-induced NO production and eNOS phosphorylation. In HUVECs, application of NRR volatile oil elevated the intracellular Ca(2+) level, and BAPTA-AM, a Ca(2+) chelator, reduced the Ca(2+) surge: the blockage were also applied to NRR-induced eNOS phosphorylation and NO production. These findings suggested the volatile oil of NRR was the major ingredient in triggering the vascular dilatation, and which was mediated via the NO production.

Show MeSH
Related in: MedlinePlus