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Effects of Astragalus membranaceus and its main components on the acute phase endothelial dysfunction induced by homocysteine.
Vascul Pharmacol. 2007 Apr; 46(4):278-85.VP

Abstract

OBJECTIVE

This study was designed to investigate the effects of Astragalus membranaceus (AM) and its main components, astragalus saponin (ASP), astragalus polysaccharide (APS) and aminobutyric acid (GABA), on homocysteine (Hcy) induced acute impairment of vascular tone and to explore whether the antioxidant mechanism was involved in AM protective effect.

METHODS

Inhibitory effects of Hcy and protective effects of AM and its main components on endothelium-dependent relaxation of aortic rings were determined by isometric tension recordings and nitric oxide signaling was assayed with 125I-cGMP RIA Kit. Furthermore, generation of reactive oxygen species (ROS) in endothelial cells was detected using 5-(6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (CM-H2DCF-DA).

RESULTS

Hcy significantly inhibited endothelium-dependent relaxation to acetylcholine (ACh) in a dose-dependent manner, and decreased cGMP levels increased by ACh in aorta. Furthermore, superoxide dismutase (SOD), AM, and ASP markedly attenuated inhibition of vasorelaxation and downregulation of cGMP level by Hcy, and APS exerted a tendency to reverse both of the depressive responses, while GABA had no similar effects. Additionally, partially impaired relaxation by Hcy was completely blocked due to the presence of N(omega)-nitro-L-arginine-methyl ester (L-NAME), which could not be further altered by treatment with AM, ASP, APS or GABA. Finally, Hcy significantly increased intracellular ROS levels in endothelial cells as measured by CM-H2DCF-DA fluorescence. SOD, AM, ASP, and APS, but not GABA, inhibited Hcy-stimulated ROS generation.

CONCLUSION

This study demonstrated that AM and ASP, potently protected endothelium-dependent relaxation against the acute injury from Hcy through nitric oxide regulatory pathways, in which antioxidation played a key role.

Authors+Show Affiliations

Department of Cardiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, No. 79, Qingchun St, Hangzhou 310003, Zhejiang, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17196887

Citation

Zhang, Bi-Qi, et al. "Effects of Astragalus Membranaceus and Its Main Components On the Acute Phase Endothelial Dysfunction Induced By Homocysteine." Vascular Pharmacology, vol. 46, no. 4, 2007, pp. 278-85.
Zhang BQ, Hu SJ, Qiu LH, et al. Effects of Astragalus membranaceus and its main components on the acute phase endothelial dysfunction induced by homocysteine. Vascul Pharmacol. 2007;46(4):278-85.
Zhang, B. Q., Hu, S. J., Qiu, L. H., Zhu, J. H., Xie, X. J., Sun, J., Zhu, Z. H., Xia, Q., & Bian, K. (2007). Effects of Astragalus membranaceus and its main components on the acute phase endothelial dysfunction induced by homocysteine. Vascular Pharmacology, 46(4), 278-85.
Zhang BQ, et al. Effects of Astragalus Membranaceus and Its Main Components On the Acute Phase Endothelial Dysfunction Induced By Homocysteine. Vascul Pharmacol. 2007;46(4):278-85. PubMed PMID: 17196887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of Astragalus membranaceus and its main components on the acute phase endothelial dysfunction induced by homocysteine. AU - Zhang,Bi-Qi, AU - Hu,Shen-Jiang, AU - Qiu,Li-Hong, AU - Zhu,Jian-hua, AU - Xie,Xian-Ji, AU - Sun,Jian, AU - Zhu,Zhao-Hui, AU - Xia,Qiang, AU - Bian,Ka, Y1 - 2006/11/10/ PY - 2006/01/23/received PY - 2006/10/14/revised PY - 2006/11/02/accepted PY - 2007/1/2/pubmed PY - 2007/3/31/medline PY - 2007/1/2/entrez SP - 278 EP - 85 JF - Vascular pharmacology JO - Vascul. Pharmacol. VL - 46 IS - 4 N2 - OBJECTIVE: This study was designed to investigate the effects of Astragalus membranaceus (AM) and its main components, astragalus saponin (ASP), astragalus polysaccharide (APS) and aminobutyric acid (GABA), on homocysteine (Hcy) induced acute impairment of vascular tone and to explore whether the antioxidant mechanism was involved in AM protective effect. METHODS: Inhibitory effects of Hcy and protective effects of AM and its main components on endothelium-dependent relaxation of aortic rings were determined by isometric tension recordings and nitric oxide signaling was assayed with 125I-cGMP RIA Kit. Furthermore, generation of reactive oxygen species (ROS) in endothelial cells was detected using 5-(6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (CM-H2DCF-DA). RESULTS: Hcy significantly inhibited endothelium-dependent relaxation to acetylcholine (ACh) in a dose-dependent manner, and decreased cGMP levels increased by ACh in aorta. Furthermore, superoxide dismutase (SOD), AM, and ASP markedly attenuated inhibition of vasorelaxation and downregulation of cGMP level by Hcy, and APS exerted a tendency to reverse both of the depressive responses, while GABA had no similar effects. Additionally, partially impaired relaxation by Hcy was completely blocked due to the presence of N(omega)-nitro-L-arginine-methyl ester (L-NAME), which could not be further altered by treatment with AM, ASP, APS or GABA. Finally, Hcy significantly increased intracellular ROS levels in endothelial cells as measured by CM-H2DCF-DA fluorescence. SOD, AM, ASP, and APS, but not GABA, inhibited Hcy-stimulated ROS generation. CONCLUSION: This study demonstrated that AM and ASP, potently protected endothelium-dependent relaxation against the acute injury from Hcy through nitric oxide regulatory pathways, in which antioxidation played a key role. SN - 1537-1891 UR - https://www.unboundmedicine.com/medline/citation/17196887/Effects_of_Astragalus_membranaceus_and_its_main_components_on_the_acute_phase_endothelial_dysfunction_induced_by_homocysteine_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1537-1891(06)00630-6 DB - PRIME DP - Unbound Medicine ER -