Ozone Oxidative Preconditioning Protects the Rat Kidney from Reperfusion Injury: The Role of Nitric Oxide

Chen, Hui; Xing, Bianzhi; Liu, Xiuheng; Zhan, Bin; Zhou, Jiangqiao; Zhu, Hengcheng; Chen, Zhiyuan

doi:10.1016/j.jss.2007.12.756

Cited by 65 publications

(61 citation statements)

References 42 publications

(32 reference statements)

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“…25 The protective effect of ozone is shown at the rat kidney from reperfusion injury by upregulation of antioxidant defense system and beneficial effects on blood circulation and in oxygen metabolism. 26 In conclusion, our study results are consistent with encouraging data for ozone therapy on APAPinduced nephrotoxicity in rats by improving antioxidant …”

Section: Discussionsupporting

confidence: 90%

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats

et al. 2010

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Acetaminophen (APAP), also known as paracetamol, is the commonest cause of toxic ingestion in the world. Because overdose of APAP has life-threatening effects on kidney, treatment of APAP-induced nephrotoxicity has life-saving importance. Aim of the study was to evaluate the efficacy of medical ozone therapy in experimental model of APAP toxication. Twenty-one male Wistar rats (200-250 g) were randomly assigned into three groups containing seven rats each: Sham, control (only APAP treated), and APAP + ozone therapy groups. Rats were killed 48 hours after administration of APAP. Urea, creatinine levels in the blood, and malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activity in renal tissue were measured. Kidney tissues were stained with hematoxylin and eosin for histological assessment. APAP administration deteriorated the renal functions and significantly elevated renal MDA levels and depleted SOD and GSH-Px activities. Ozone therapy significantly reduced the MDA level, increased the SOD and GSHPx activities, and normalized the renal histology. In conclusion, our study results are consistent with encouraging data for ozone therapy on APAP-induced nephrotoxicity in rats by improving antioxidant mechanism and oxidative stress.

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Section: Discussionsupporting

confidence: 90%

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats

et al. 2010

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“…Several studies have indicated that NO induces cellular cytotoxicity and tissue injury via lipid peroxidation, as well as DNA damage and pro-apoptotic effects in I/R injury (12,16,24). Conversely, there are studies which demonstrate that the increased activity of NOS is associated with reduced I/R-induced injury (25). Alterations in the expression of various NOS isoforms have been described in renal I/R injury (17).…”

Section: Discussionmentioning

confidence: 99%

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

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Küçük

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxy nucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by realtime polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and antiapoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

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“…It has been demonstrated that ozone oxidative preconditioning (OzoneOP) induced protective effects in renal I/R injury [4][5][6][7] . It is a simple and harmless method which provides a new tool to protect organ from I/R injury.…”

Section: Ischemia-reperfusionmentioning

confidence: 99%

“…Before the I/R procedure (as in group 2), rats were treated with ozone as previously described [5][6][7] . Briefly, rats received 15 ozone treatments by rectal insufflations 1 mg kg−1, once a day, at an ozone concentration of 50 μg ml−1.…”

Section: Animal Preparation and Experimental Designmentioning

confidence: 99%

Ozone oxidative preconditioning protects the rat kidney from reperfusion injury via modulation of the TLR4-NF-κB pathway

et al. 2015

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PURPOSE:To investigate the protective effects of ozone oxidative preconditioning (OzoneOP) were associated with the modulation of TLR4-NF-κB pathway. METHODS:Thirty six rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated and immunohistochemistry was also performed for localization of TLR4 and NF-κB. The expression of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 were studied by Real-time PCR. Western blot was performed to detect the expression of TLR4 and NF-κB. RESULTS:The results indicated that blood urea nitrogen and creatinine levels increased significantly in I/R group. Rats treated with OzoneOP showed obviously less renal damage. Immunohistochemistry showed that TLR4 were ameliorated by OzoneOP. Realtime PCR showed that OzoneOP could significantly inhibit the increased mRNA levels of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 induced by I/R. Western blot indicated that the expression of TLR4 and NF-κB were upregulated in I/R group, but OzoneOP could inhibit this increase. CONCLUSION:These findings indicated that OzoneOP had potent anti-inflammatory properties by the modulation of the TLR4-NF-κB pathway in renal ischemia/reperfusion injury.Key words: Ozone. Ischemia. Reperfusion. Toll-Like Receptor 4. NF-kappa B. Kidney. Rats. Ozone oxidative preconditioning protects the rat kidney from reperfusion injury via modulation of the TLR4-NF-κB pathway

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Ozone Oxidative Preconditioning Protects the Rat Kidney from Reperfusion Injury: The Role of Nitric Oxide

Cited by 65 publications

References 42 publications

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Ozone oxidative preconditioning protects the rat kidney from reperfusion injury via modulation of the TLR4-NF-κB pathway

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