The NLRP3 inflammasome is a potential target of ozone therapy aiming to ease chronic renal inflammation in chronic kidney disease
Ozone therapy is an effective medical treatment for various diseases. A previous study has demonstrated its reno-protective effect in chronic kidney disease (CKD), but the mechanism involved is not completely known. This study produced the 5/6 nephrectomized CKD rat model and investigated whether th...
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Veröffentlicht in: | International immunopharmacology 2017-02, Vol.43, p.203-209 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Ozone therapy is an effective medical treatment for various diseases. A previous study has demonstrated its reno-protective effect in chronic kidney disease (CKD), but the mechanism involved is not completely known. This study produced the 5/6 nephrectomized CKD rat model and investigated whether the reno-protective effect of ozone therapy was achieved by its anti-inflammatory property through the modulation of the NLRP3 inflammasome. The results showed that ozone therapy at a low concentration improved renal function and ameliorated renal morphological injury in 5/6 nephrectomized rats. The expression of NLRP3, ASC, and caspase-1-p10 in the kidney of these rats was simultaneously lowered by ozone therapy. Moreover, renal inflammation caused by IL-1β was significantly alleviated by ozone therapy. The Pearson correlation analysis indicated that the protein level of IL-1β was positively correlated with renal injury scores. Taken together, these results indicated that ozone therapy might reduce sterile renal inflammation and slow down CKD progression through the modulation of the NLRP3 inflammasome in 5/6 nephrectomized rats.
•Ozone therapy slows down the CKD progression of 5/6 nephrectomized rats.•Chronic renal injury is ameliorated by ozone therapy in 5/6 nephrectomized rats.•Ozone therapy reduces chronic renal inflammation by modulating NLRP3 inflammasome.•Ozone therapy might be a promising reno-protecting treatment for CKD patients. |
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ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2016.12.022 |