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Hydrogen sulfide improves endothelial dysfunction through inhibition of the vicious circle of NLRP3 and oxidative stress in spontaneously hypertensive rats
Author(s) -
Wu Yuming,
Li Jiabao
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.902.18
Subject(s) - inflammasome , oxidative stress , endothelial dysfunction , medicine , endocrinology , inflammation , pharmacology , chemistry
Aims The aim of this study is to elucidate whether the inhibition of inflammasome and oxidative stress mediated the ameliorative effect of hydrogen sulfide (H 2 S) on endothelial dysfunction in hypertension. Methods Spontaneously hypertensive rats (SHR) and normotensive Wistar kyoto rats (WKY) were injected with 100 μM NaSH intraperitoneally daily for 16 weeks. Systolic blood pressure (SBP) and plasma MDA and IL‐1β were measured. Renal vascular was used to determine endothelial dependent contraction (EDC) and endothelial dependent relaxation (EDR). Protein levels were detected by Western blot. Human umbilical vein endothelial cells (HUVECs) were used to confirm the protective role of H 2 S against AngII‐induced cell injury. Results Exogenous NaSH administration significantly lowered SBP and ameliorated damaged EDR and EDC. H 2 S reduced the activation of NLRP3 inflammasome and oxidative stress in SHR. The endothelial protective and anti‐oxidant effect of H2S was abolished by LPS, an inducer of NLRP3 inflammasome. In HUVECs, H 2 S significantly ameliorated AngII‐induced cellular impairment, NLRP3 inflammasome and ROS generation. After knocking down of Nrf2, the above protective effect of H2S was abolished. Conclusion Hydrogen sulfide could inhibit vicious circle of oxidative stress and inflammation, resulted in improved endothelial function and ameliorated hypertension. Our results throw light on the crucial role of H 2 S in regulation of endothelial function, which might provide the new target for treatment of hypertension. Support or Funding Information This work was supported by the National Natural Science Foundation of China (31171098, 31671185), the Specialized Research Fund for the Doctoral Program of Higher Education of China (20121323110008), the Hebei Province for Innovation Talents Support Plan (LJRC017) and the Natural Science Foundation of Hebei (C2012206063, H2016206264). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .