Pioglitazone protects against renal ischemia-reperfusion injury by enhancing antioxidant capacity

Zou, Cong; Hu, Honglin; Xi, Xiaoqing; Shi, Zimin; Wang, Gongxian; Huang, Xueming

doi:10.1016/j.jss.2013.03.027

Cited by 42 publications

(41 citation statements)

References 19 publications

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“…Moreover, the current results verified the pioglitazone ability to reduce oxidative stress and its deleterious leverage on renal tissue, where it reduced the tissue level of MDA and enhanced that of GSH. Our data mimicked that reported previously by Shah et al [59] and Zou et al [50] in an experimental model of renal I/R, which attested the antioxidant activity of pioglitazone in diminishing renal injury. Nevertheless, combining both drugs, at the low dose level, boosted the GSH content significantly even above the effect mediated by the high doses, indicating a possible synergistic effect between the two drugs.…”

Section: Discussionsupporting

confidence: 92%

“…To our knowledge, the current study is the first to address the possible renoprotective mechanisms interceded by cilostazol in renal I/R rat model. Cilostazol pretreatment improved renal glomerular filtration function as confirmed by the inhibition of the serum levels of creatinine, BUN, and cystatin C. The same results have been seen in the pioglitazone pretreated groups, effects that coincide with the recent findings of Zou et al [50]. The ability of pioglitazone to prevent podocytes apoptosis may be partially behind its positive effect [49].…”

Section: Discussionsupporting

confidence: 80%

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Cilostazol Renoprotective Effect: Modulation of PPAR-γ, NGAL, KIM-1 and IL-18 Underlies Its Novel Effect in a Model of Ischemia-Reperfusion

2014

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Cilostazol, a phosphodiesterase-III inhibitor, reportedly exhibits positive effects against ischemia/reperfusion (I/R)-induced injury in several models. However, its potential role against the renal I/R insult has not been elucidated. To test whether the PPAR-γ (of peroxisome proliferator activated receptor gamma) pathway is involved in the cilostazol effect, rats were randomized into sham, I/R, cilostazol (50 and 100 mg/kg per day, orally), pioglitazone (3 and 10 mg/kg per day, orally) and their combination at the low dose levels. Drugs regimens were administered for 14 days prior to the I/R induction. Pretreatment with cilostazol or pioglitazone provided significant protection against the I/R-induced renal injury as manifested by the attenuated serum levels of creatinine, blood urea nitrogen and cystatin C. Both drugs have also opposed the I/R-induced elevation in tissue contents/activity of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Κim-1), nuclear factor-κB, interleuκin-18, caspase-1, as well as malondialdehyde, iNOS, myeloperoxidase, ICAM-1 and VCAM-1. Nevertheless, the drugs increased both the PPAR-γ transcriptional activity and the content of glutathione. Furthermore, combining the two low doses of both drugs produced effects comparable to that of the high dose level of either drug, advocating the fortification of pioglitazone renoprotective effect when given concomitantly with cilostazol. In conclusion, cilostazol purveyed conceivable novel renoprotective mechanisms and alleviated incidents associated with acute renal injury either alone or in combination with pioglitazone partially via the elevation of PPAR-γ besides the amendment of the aforementioned biomarkers.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 80%

Cilostazol Renoprotective Effect: Modulation of PPAR-γ, NGAL, KIM-1 and IL-18 Underlies Its Novel Effect in a Model of Ischemia-Reperfusion

2014

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“…Previous studies showed that reduction of oxidative stress can protect kidney from renal IRI [42]. Zou et al found that pioglitazone protected against renal ischemia-reperfusion injury by increasing the level of enzymatic activities of superoxide dismutase and enhancing antioxidant capacity [43]. Similar mechanisms were seen in the protective effects of curcumin and intermedin [44] It was reported that propofol had anti-oxidative activity [45].…”

Section: Discussionmentioning

confidence: 90%

Propofol Prevents Renal Ischemia-Reperfusion Injury via Inhibiting the Oxidative Stress Pathways

Zhong

Lei

et al. 2015

Cell Physiol Biochem

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Background/Aims: Renal ischemia/reperfusion injury (IRI) is a risk for acute renal failure and delayed graft function in renal transplantation and cardiac surgery. The purpose of this study is to determine whether propofol could attenuate renal IRI and explore related mechanism. Methods: Male rat right kidney was removed, left kidney was subjected to IRI. Propofol was intravenously injected into rats before ischemia. The kidney morphology and renal function were analyzed. The expression of Bax, Bcl-2, caspase-3, cl-caspase-3, GRP78, CHOP and caspase-12 were detected by Western blot analysis. Results: IR rats with propofol pretreatment had better renal function and less tubular apoptosis than untreated IR rats. Propofol pretreated IR rats had lower Bax/Bcl-2 ratio and less cleaved caspase-3. The protein expression levels of GRP78, CHOP and caspase-12 decreased significantly in propofol pretreated IR rats. In vitro cell model showed that propofol significantly increased the viability of NRK-52E cells that were subjected to hypoxia/reoxygenation (H/R) in a dose-dependent manner. The effect of propofol on the expression regulation of Bax, Bcl-2, caspase-3, GRP78, CHOP was consistent in both in vitro and in vivo models. Conclusion: Experimental results suggest that propofol prevents renal IRI via inhibiting oxidative stress.

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“…In the previous studies on the role of PPAR in diabetic kidney disease, it was found that the PPAR agonist could modulate systemic metabolism in a number of ways, including improvement of glycaemic control, insulin sensitivity and dyslipidaemia, and these modulatory effects might influence the outcome of the disease [31][32][33][34]. Later on, Zou et al [21] and Reel et al [35] concluded that pioglitazone was capable of protecting the kidney from renal injury by enhancing the antioxidative and anti-inflammatory capacity of the kidney. Furthermore, it was reported that pioglitazone significantly increased the expression of VEGF and accelerated the angiogenesis process following kidney injuries [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Pioglitazone, a Peroxisome Proliferator-Activated Receptor γ Agonist, Ameliorates Chronic Kidney Disease by Enhancing Antioxidative Capacity and Attenuating Angiogenesis in the Kidney of a 5/6 Nephrectomized Rat Model

Sun

Yuan

et al. 2016

Cell Physiol Biochem

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Background/Aims: Pioglitazone is a type of peroxisome proliferator-activated receptor γ agonist and is capable of alleviating renal ischemia-reperfusion injury. Methods: A5/6 nephrectomized rat model was established to induce renal impairments mimicking chronic kidney diseases (CKDs). The effect of pioglitazone on renal structure, function, antioxidative capacity, and angiogenesis in the nephrectomized rats was assessed. Moreover, the expression of HIF-1α, eNOS, VEGF, Flt-1 and Flk-1 was determined to reveal the possible pathways through which pioglitazone exerted its beneficial effect on CKDs. Results: Subtotal nephrectomy caused severe damages to rat renal tissues, and administration of pioglitazone dramatically restored the structure and function of the kidney, which was evidenced by Periodic acid- Schiff staining and the reduced levels of urinary proteins, blood urea nitrogen, and creatinine. Furthermore, pioglitazone decreased the level of malondialdehyde and increased the level of superoxide dismutase in the injured renal tissues, suggesting that the antioxidative capacity in the injured kidney was augmented by pioglitazone. Additionally, pioglitazone inhibited HIF-1α-dependent angiogenesis by down-regulating the expression of a panel of angiogenic factors. Conclusion: The current study demonstrates that pioglitazone benefits renal failure through activation of the antioxidative system and inhibition of angiogenesis in the injured kidney. Our study provides preliminary evidences for the potential application of this agent in the treatment of CKDs.

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Pioglitazone protects against renal ischemia-reperfusion injury by enhancing antioxidant capacity

Cited by 42 publications

References 19 publications

Cilostazol Renoprotective Effect: Modulation of PPAR-γ, NGAL, KIM-1 and IL-18 Underlies Its Novel Effect in a Model of Ischemia-Reperfusion

Cilostazol Renoprotective Effect: Modulation of PPAR-γ, NGAL, KIM-1 and IL-18 Underlies Its Novel Effect in a Model of Ischemia-Reperfusion

Propofol Prevents Renal Ischemia-Reperfusion Injury via Inhibiting the Oxidative Stress Pathways

Pioglitazone, a Peroxisome Proliferator-Activated Receptor γ Agonist, Ameliorates Chronic Kidney Disease by Enhancing Antioxidative Capacity and Attenuating Angiogenesis in the Kidney of a 5/6 Nephrectomized Rat Model

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