Protective effects of curcumin on acute gentamicin-induced nephrotoxicity in rats

He, Liyu; Peng, Xiaofei; Zhu, Jiefu; Liu, Guoyong; Chen, Xian; Tang, Chengyuan; Liu, Hong; Liu, Fuyou; Peng, Youming

doi:10.1139/cjpp-2014-0459

Cited by 68 publications

(53 citation statements)

References 38 publications

(29 reference statements)

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“…It has also revealed that high glucose obviously decreased SIRT1 mRNA and protein expression in rat mesangial cells [18]. Other studies have reported that SIRT1 expression was decreased in rats with gentamicin or cisplatin-induced nephrotoxicity [19,20]. Moreover, reduced SIRT1 expression has been found in mouse cortical collecting duct cells [14], in human kidney proximal tubule epithelial cells [21], and in rats with AKI induced by severe burns [22] and renal ischaemia-reperfusion injury [23].…”

Section: Discussionmentioning

confidence: 99%

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Lin¹,

Geng²,

Lin³

et al. 2016

Med Sci Monit Basic Res

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BackgroundAquaporin-2 (AQP2) plays a major role in water reabsorption in the renal collecting duct, and is involved in a variety of renal disease. Recent studies have indicate that sirtuin1 (SIRT1) exerts renoprotective properties against kidney diseases. This study aimed to determine the potential role of SIRT1 in AQP2 expression induced by tumor necrosis factor-alpha (TNF-α) and to disclose the underlying mechanism in renal inner medullary collecting duct (IMCD) cells.Material/MethodsQuantitative real-time PCR and Western blotting were respectively identified mRNA and protein expression. Immunofluorescence staining was used to detect the localization of AQP2. Small-interfering RNA (siRNA) was carried out for mechanism study.ResultsResults showed that AQP2 was clearly increased in the plasma membrane and decreased in the cytoplasm of IMCD cells treated with AVP. TNF-α treatment in IMCD cells significantly reduced SIRT1 and AQP2 expression, and increased acetylated NF-κBp65 protein level in time- and concentration-dependent manners. Moreover, SIRT1 overexpression or the activator SRT1720 augmented AQP2 expression and reduced the acetylation of NF-κBp65, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol in TNF-α-induced IMCD cells. Knockdown of NF-κBp65 or NF-κBp65 inhibition by pyrrolidine dithiocarbamate (PDTC) enhanced AQP2 expression in IMCD cells exposed to TNF-α. Importantly, knockdown of NF-κBp65 augmented the up-regulation of SIRT1 on AQP2 expression in IMCD cells induced by TNF-α.ConclusionsThese findings indicate that SIRT1 increases AQP2 expression in TNF-α-induced IMCD cells via the NF-κB-dependent signalling pathway, which might provide novel insight to understanding the renoprotective effects of SIRT1 in kidney diseases.

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Section: Discussionmentioning

confidence: 99%

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Lin¹,

Geng²,

Lin³

et al. 2016

Med Sci Monit Basic Res

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“…12 In this study, significant increases in serum urea and creatinine levels after exposure to cisplatin were accepted as an indicator of nephrotoxicity. A marked improvement was detected in renal histopathology and function parameters supporting the protective effect of curcumin against oxidative stress, inflammation, and tubular cell death caused by cisplatin-induced nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10] Curcumin, a major component of turmeric, is known to have anti-inflammatory and antioxidant effects in various pathologies. [11][12][13][14][15][16][17] In addition, recent studies have revealed that the antiapoptotic properties of curcumin against different agent-mediated acute renal injury. 11,12,15 It has been reported that curcumin prevents and ameliorates the severity of cisplatin nephrotoxicity, by inhibiting various cytokines and chemokines such as TNF-a and IL-1b and scavenging free radicals.…”

Section: Introductionmentioning

confidence: 99%

“…[11][12][13][14][15][16][17] In addition, recent studies have revealed that the antiapoptotic properties of curcumin against different agent-mediated acute renal injury. 11,12,15 It has been reported that curcumin prevents and ameliorates the severity of cisplatin nephrotoxicity, by inhibiting various cytokines and chemokines such as TNF-a and IL-1b and scavenging free radicals. 4,14,[17][18][19] However, there is no any study to support the antiapoptotic effect of curcumin in cisplatininduced nephrotoxicity, yet.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin counteracts cisplatin-induced nephrotoxicity by preventing renal tubular cell apoptosis

2016

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Curcumin has several biological functions particularly antioxidant and anti-inflammatory. The aims of this study are determination of the protective effects of curcumin on cisplatin-induced renal tubular cell apoptosis and related pathways in kidney. Eighteen male Wistar albino rats were randomly divided into three groups (n ¼ 6): the control, cisplatin (CP), and cisplatin þ curcumin (CP þ CUR). Acute renal damage was induced by single dose of cisplatin (7.5 mg/ kg) injected by intraperitoneally (i.p). The animals of curcumin-treated group were received daily 200 mg/kg curcumin per os (po), starting from 2 days before the injection of cisplatin to the day of sacrifice. Forty-eight hours after cisplatin injection, samples of cardiac blood and kidneys were harvested from the animals. In this study, the major finding is that curcumin treatment ameliorates the following conditions associated with cisplatin-induced nephrotoxicity: (1) the development of kidney injury (histopathology), (2) inflammatory responses [myeloperoxidase (MPO) and tumor necrosis factor-alpha (TNF-a), interleukin-1 beta (IL-1b), IL-6, IL-10 levels], (3) the degree of lipid peroxidation [malondialdehyde (MDA) level], (4) renal tubular cell apoptosis (active caspase-3) and expression of related proteins [p53, Fas, and Fas ligand (Fas-L)] by immunohistochemistry, (5) renal dysfunction (serum urea and creatinine). In a conclusion, this study suggests that curcumin has antiapoptotic effect against cisplatin nephrotoxicity, in addition to anti-inflammatory and antioxidant properties. ARTICLE HISTORY

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“…Lysates of cultured cells were prepared as previously described [37] . After centrifugation, the protein level was determined in supernatants using a Micro BCA protein assay kit with BSA as a standard (Pierce, Thermo).…”

Section: Western Blottingmentioning

confidence: 99%

Regulation of IgA Class Switch Recombination in Immunoglobulin A Nephropathy: Retinoic Acid Signaling and BATF

Peng²,

Chen³

et al. 2016

Am J Nephrol

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Background: Immunoglobulin (Ig) A nephropathy (IgAN) is the ﬁnding of immune deposits predominantly containing polymeric IgA in the glomerular mesangium on renal biopsy. Increasing evidence suggested that retinoic acid (RA) signaling selectively induces IgA isotype switching and basic leucine zipper transcription factor, ATF-like (BATF) controls the global regulators of class switch recombination (CSR) in lymphocytes. Great effort has been paid to identify whether impaired immune regulation along the ‘mucosa-bone marrow (BM) axis' play an important role in the pathogenesis of IgAN. Methods: The aim of the study was to investigate the expression of all-trans-RA (ATRA) and BATF, and to identify their impact on IgA CSR in IgAN patients and rat animal models. Blood samples and tonsillar tissue specimens were obtained from 22 patients with IgAN and 24 patients with chronic tonsillitis as control. Results: Immunohistochemical, RT-PCR and western blotting examination revealed that RA signaling and BATF productions are activated in IgAN patients compared with controls. Lipopolysaccharide and α-hemolytic streptococcus stimulation upregulated RA receptor (RAR) and BATF expression, promote IgA CSR and ATRA productions in tonsil mononuclear cells. RAR alpha (RARα) or BATF siRNA decreases IgA expression. We also built IgAN rat models and found that RARα, BATF and activation-induced cytidine deaminase were upregulated in the peripheral blood, spleen and BM. With ATRA (500 μg/kg body weight) treatment for 8 weeks, IgA deposition on glomeruli and mesangial cells proliferation increased. It also revealed that ATRA activated BATF and IgA CSR in vivo. Conclusion: These data point toward the role of RA signaling together with BATF in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with neoantigen results in impaired mucosal and systemic IgA responses.

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Protective effects of curcumin on acute gentamicin-induced nephrotoxicity in rats

Abstract: Our data clearly demonstrate that curcumin protects kidney from gentamicin-induced AKI via the amelioration of oxidative stress and apoptosis of renal tubular cells, thus providing hope for the amelioration of gentamicin-induced nephrotoxicity.

Cited by 68 publications

References 38 publications

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Curcumin counteracts cisplatin-induced nephrotoxicity by preventing renal tubular cell apoptosis

Regulation of IgA Class Switch Recombination in Immunoglobulin A Nephropathy: Retinoic Acid Signaling and BATF

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