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[Hypotensive effects of hydrogen sulfide via attenuating vascular inflammation in spontaneously hypertensive rats].
Zhonghua Xin Xue Guan Bing Za Zhi. 2008 Jun; 36(6):541-5.ZX

Abstract

OBJECTIVE

To investigate the effects of hydrogen sulfide (H2S) on vascular inflammation and blood pressure in spontaneously hypertensive rats (SHR).

METHODS

Four weeks old male SHR rats were treated with saline (control, n = 7), sodium hydrosulfide (NaHS, a H2S donor, n = 7) and propargylglycine (PPG, endogenous H2S production inhibitor, n = 6) for 5 weeks. Age-natched male Wistar Kyoto (WKY) rats served as normotensive controls (n = 8). Five weeks later, systolic blood pressure (SBP) was measured in conscious and quiet rats by means of the standard tail-cuff method. The protein expressions of intercellular adhesive molecule-1 (ICAM-1), nuclear transcriptional factor-kappaB p65 (NF-kappaB p65) and inhibitor of nuclear transcriptional factor-kappaB (IkappaB-alpha) in thoracic aorta of rats were detected by immunohistochemical assay, while the expression of ICAM-1 mRNA in thoracic aorta of rats were investigated by in situ hybridization.

RESULTS

SBP of control SHR rats was significantly higher than that of WKY rats (P < 0.05) accompanied by significantly upregulated expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells (all P < 0.01), while the expression of IkappaB-alpha protein in aortic endothelial cells in SHR control group was significantly lower than that of WKY control group (P < 0.01). NaHS treated SHR rats showed significantly reduced SBP and downregulated expressions of ICAM-1 mRNA, ICAM-1, NF-kappaB p65 in aortic endothelial cells and upregulated expression of IkappaB-alpha protein in aortic endothelial cells compared to untreated control SHR rats (all P < 0.05). In SHR rats treated with PPG, the expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells were further increased while the expression of IkappaB-alpha protein further decreased compared with control SHR rats (all P < 0.05).

CONCLUSION

H2S might attenuate the development of hypertension through by attenuating vascular inflammation reactions.

Authors+Show Affiliations

Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

chi

PubMed ID

19100070

Citation

Jin, Hong-fang, et al. "[Hypotensive Effects of Hydrogen Sulfide Via Attenuating Vascular Inflammation in Spontaneously Hypertensive Rats]." Zhonghua Xin Xue Guan Bing Za Zhi, vol. 36, no. 6, 2008, pp. 541-5.
Jin HF, Sun Y, Liang JM, et al. [Hypotensive effects of hydrogen sulfide via attenuating vascular inflammation in spontaneously hypertensive rats]. Zhonghua Xin Xue Guan Bing Za Zhi. 2008;36(6):541-5.
Jin, H. F., Sun, Y., Liang, J. M., Tang, C. S., & DU, J. B. (2008). [Hypotensive effects of hydrogen sulfide via attenuating vascular inflammation in spontaneously hypertensive rats]. Zhonghua Xin Xue Guan Bing Za Zhi, 36(6), 541-5.
Jin HF, et al. [Hypotensive Effects of Hydrogen Sulfide Via Attenuating Vascular Inflammation in Spontaneously Hypertensive Rats]. Zhonghua Xin Xue Guan Bing Za Zhi. 2008;36(6):541-5. PubMed PMID: 19100070.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Hypotensive effects of hydrogen sulfide via attenuating vascular inflammation in spontaneously hypertensive rats]. AU - Jin,Hong-fang, AU - Sun,Yan, AU - Liang,Jia-min, AU - Tang,Chao-shu, AU - DU,Jun-bao, PY - 2008/12/23/entrez PY - 2008/12/23/pubmed PY - 2009/9/11/medline SP - 541 EP - 5 JF - Zhonghua xin xue guan bing za zhi JO - Zhonghua Xin Xue Guan Bing Za Zhi VL - 36 IS - 6 N2 - OBJECTIVE: To investigate the effects of hydrogen sulfide (H2S) on vascular inflammation and blood pressure in spontaneously hypertensive rats (SHR). METHODS: Four weeks old male SHR rats were treated with saline (control, n = 7), sodium hydrosulfide (NaHS, a H2S donor, n = 7) and propargylglycine (PPG, endogenous H2S production inhibitor, n = 6) for 5 weeks. Age-natched male Wistar Kyoto (WKY) rats served as normotensive controls (n = 8). Five weeks later, systolic blood pressure (SBP) was measured in conscious and quiet rats by means of the standard tail-cuff method. The protein expressions of intercellular adhesive molecule-1 (ICAM-1), nuclear transcriptional factor-kappaB p65 (NF-kappaB p65) and inhibitor of nuclear transcriptional factor-kappaB (IkappaB-alpha) in thoracic aorta of rats were detected by immunohistochemical assay, while the expression of ICAM-1 mRNA in thoracic aorta of rats were investigated by in situ hybridization. RESULTS: SBP of control SHR rats was significantly higher than that of WKY rats (P < 0.05) accompanied by significantly upregulated expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells (all P < 0.01), while the expression of IkappaB-alpha protein in aortic endothelial cells in SHR control group was significantly lower than that of WKY control group (P < 0.01). NaHS treated SHR rats showed significantly reduced SBP and downregulated expressions of ICAM-1 mRNA, ICAM-1, NF-kappaB p65 in aortic endothelial cells and upregulated expression of IkappaB-alpha protein in aortic endothelial cells compared to untreated control SHR rats (all P < 0.05). In SHR rats treated with PPG, the expressions of ICAM-1 mRNA, ICAM-1 protein, NF-kappaB p65 protein in aortic endothelial cells were further increased while the expression of IkappaB-alpha protein further decreased compared with control SHR rats (all P < 0.05). CONCLUSION: H2S might attenuate the development of hypertension through by attenuating vascular inflammation reactions. SN - 0253-3758 UR - https://www.unboundmedicine.com/medline/citation/19100070/[Hypotensive_effects_of_hydrogen_sulfide_via_attenuating_vascular_inflammation_in_spontaneously_hypertensive_rats]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=0253-3758&amp;year=2008&amp;vol=36&amp;issue=6&amp;fpage=541 DB - PRIME DP - Unbound Medicine ER -