Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways
Abstract Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated g...
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Nature Portfolio
2017
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oai:doaj.org-article:50f6e801ffa04da7bc776657b798e3622021-12-02T11:41:20ZHydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways10.1038/s41598-017-00557-22045-2322https://doaj.org/article/50f6e801ffa04da7bc776657b798e3622017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00557-2https://doaj.org/toc/2045-2322Abstract Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.Dongdong WuNing LuoLianqu WangZhijun ZhaoHongmin BuGuoliang XuYongjun YanXinping CheZhiling JiaoTengfu ZhaoJingtao ChenAiling JiYanzhang LiGarrick D. LeeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-16 (2017) |
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Medicine R Science Q Dongdong Wu Ning Luo Lianqu Wang Zhijun Zhao Hongmin Bu Guoliang Xu Yongjun Yan Xinping Che Zhiling Jiao Tengfu Zhao Jingtao Chen Ailing Ji Yanzhang Li Garrick D. Lee Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| description |
Abstract Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways. |
| format |
article |
| author |
Dongdong Wu Ning Luo Lianqu Wang Zhijun Zhao Hongmin Bu Guoliang Xu Yongjun Yan Xinping Che Zhiling Jiao Tengfu Zhao Jingtao Chen Ailing Ji Yanzhang Li Garrick D. Lee |
| author_facet |
Dongdong Wu Ning Luo Lianqu Wang Zhijun Zhao Hongmin Bu Guoliang Xu Yongjun Yan Xinping Che Zhiling Jiao Tengfu Zhao Jingtao Chen Ailing Ji Yanzhang Li Garrick D. Lee |
| author_sort |
Dongdong Wu |
| title |
Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| title_short |
Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| title_full |
Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| title_fullStr |
Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| title_full_unstemmed |
Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways |
| title_sort |
hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ros/mapk and nf-κb signaling pathways |
| publisher |
Nature Portfolio |
| publishDate |
2017 |
| url |
https://doaj.org/article/50f6e801ffa04da7bc776657b798e362 |
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