About: Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

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About: Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways
Creator	Wu, Dongdong Bu, Hongmin Che, Xinping Chen, Jingtao Ji, Ailing Jiao, Zhiling Lee, Garrick Li, Yanzhang Luo, Ning Wang, Lianqu Xu, Guoliang Yan, Yongjun Zhao, Tengfu Zhao, Zhijun
Source	PMC
abstract	Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H(2)S) plays important roles in renal physiological and pathophysiological processes. However, whether H(2)S could protect against CRF in rats remains unclear. In this study, we found that H(2)S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H(2)S significantly improved the kidney structure and function of CRF rats. We found that H(2)S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H(2)S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H(2)S 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, H(2)S 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, H(2)S 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.
has issue date	2017-03-28(xsd:dateTime)
bibo:doi	10.1038/s41598-017-00557-2
bibo:pmid	28352125
has license	cc-by
sha1sum (hex)	f9700deed61ea92d41891cf29eccddac0ee0ca15
schema:url	https://doi.org/10.1038/s41598-017-00557-2
resource representing a document's title	Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways
has PubMed Central identifier	PMC5428696
has PubMed identifier	28352125
schema:publication	Sci Rep
resource representing a document's body	covid:f9700deed61ea92d41891cf29eccddac0ee0ca15#body_text
is schema:about of	named entity 'apoptosis' named entity 'problem' named entity 'signaling pathways' named entity 'levels' named entity 'Chronic renal failure' named entity 'remains' named entity 'CHRONIC RENAL FAILURE' named entity 'GLUTATHIONE PEROXIDASE' named entity 'PROCESSES' named entity 'INDUCED' named entity 'SIGNAL' named entity 'SIGNALING PATHWAYS' named entity 'PHYSIOLOGICAL' named entity 'REGULATED' named entity 'HYDROGEN SULFIDE' named entity 'PLAYS' named entity 'CELLS' named entity 'IMPROVED' named entity 'PROTEIN LEVELS' named entity 'NEPHROTOXICITY' named entity 'FOUND' named entity 'P65' named entity 'BCL-2' named entity 'SUPEROXIDE DISMUTASE' named entity 'CRF' named entity 'PHOSPHORYLATION' named entity 'ADENINE' named entity 'STUDY' named entity 'ROS' named entity 'INCREASED' named entity 'IL-10' named entity '10%' named entity 'EXTRACELLULAR' named entity 'A MAJOR' named entity 'EXPRESSION' named entity 'CLEAVED' named entity 'MALONDIALDEHYDE' named entity 'MEDIATED' named entity 'FUNCTION' named entity 'C-JUN N-TERMINAL KINASE' named entity 'CHRONIC RENAL FAILURE' named entity 'TUMOR NECROSIS FACTOR' named entity 'CASPASE-3' named entity 'HYDROGEN SULFIDE' named entity 'IMPORTANT' named entity 'IS A' named entity 'H 2' named entity 'KIDNEY' named entity 'PROTEIN KINASE' named entity 'DEMONSTRATED' covid:arg/f9700deed61ea92d41891cf29eccddac0ee0ca15 named entity 'RAT KIDNEY' named entity 'ROLES' named entity 'NORMAL' named entity 'INHIBITING' named entity 'INFLAMMATION' named entity 'BAB' named entity 'AMELIORATES' named entity 'ACTIVITIES' named entity 'INTERLEUKIN ' named entity 'RATS' named entity 'OPEN' named entity 'SIGNALING PATHWAYS' named entity 'ROS' named entity 'INHIBITING' named entity 'KIDNEY STRUCTURE' named entity 'RATS' named entity 'CONCLUSION'

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