Abstract | BACKGROUND: METHODS AND RESULTS: Mice subjected to LPS (10 mg/kg) treatment exhibited AKI demonstrated by markedly increased blood urea nitrogen and creatinine levels compared with controls (P<0.01). However, PDS and Dexamethasone induce similar reverse effects on renal function, such as reduced serum creatinine and blood urea nitrogen levels compared with the LPS group (P<0.05). PDS decreased the production and release of tumor necrosis factor (TNF)-α and interleukin (IL)-6 by inhibiting the NF-κB signaling pathway, down-regulating inducible nitric oxide synthase protein expression levels and inhibiting oxidative stress. In most anti-AKI mechanisms, PDS and dexamethasone were similar, but PDS are better at inhibition of TNF production, promote SOD activity and inhibition of IKB phosphorylation. In addition, nuclear glucocorticoid receptor expression was markedly enhanced in PDS and Dexamethasone treatment groups. Further research is required to determine whether PDS can combine with the glucocorticoid receptor to enter the nucleus. CONCLUSION: This study demonstrated that PDS and dexamethasone have similar reverse amelioration for renal functions, and have potential application prospects in the treatment of sepsis-induced AKI.
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Authors | Yan Chen, Yanwei Du, Yang Li, Xiaoqin Wang, Pin Gao, Guang Yang, Yuan Fang, Yan Meng, Xuejian Zhao |
Journal | PloS one
(PLoS One)
Vol. 10
Issue 7
Pg. e0134653
( 2015)
ISSN: 1932-6203 [Electronic] United States |
PMID | 26230340
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Ginsenosides
- Lipopolysaccharides
- Receptors, Glucocorticoid
- panaxadiol
- Nitric Oxide
- Malondialdehyde
- Dexamethasone
- Nitric Oxide Synthase Type II
- Superoxide Dismutase
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Topics |
- Acute Kidney Injury
(chemically induced, metabolism, physiopathology)
- Animals
- Dexamethasone
(pharmacology)
- Disease Models, Animal
- Ginsenosides
(pharmacology)
- Kidney
(drug effects, physiopathology)
- Lipopolysaccharides
(toxicity)
- Malondialdehyde
(metabolism)
- Mice
- Mice, Inbred C57BL
- Nitric Oxide
(metabolism)
- Nitric Oxide Synthase Type II
(metabolism)
- Receptors, Glucocorticoid
(metabolism)
- Superoxide Dismutase
(metabolism)
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