Diallyl sulfide enhances antioxidants and inhibits inflammation through the activation of Nrf2 against gentamicin-induced nephrotoxicity in Wistar rats

Srinivasan, Kannan; Prabhu, Ponnuraj Nagendra; Narayanan, Sriram; Manikandan, R.; Arumugam, Muthu; Sudhandiran, Ganapasam

doi:10.1016/j.ejphar.2008.12.055

Cited by 159 publications

(96 citation statements)

References 71 publications

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“…For histological study, mice treated with gentamicin with high doses for long term showed progressive tubular, glomerular and interstitial alterations. The tubular damage and degenerative changes seen in the present work confirm with the findings of previous work (Ali et al, 2011;Dehghani et al, 2011;Kalayarasan et al, 2009).…”

Section: Discussionsupporting

confidence: 83%

Administration of gentamicin induced hematobiochemical and renal morphological alterations in Swiss albino mice

Jannat¹,

Sultana²,

Islam³

2017

Afr. J. Pharm. Pharmacol.

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Gentamicin is widely used as an effective antibiotic. A study was conducted to investigate the effects of intramuscular administration of gentamicin on 20, 5 to 6 weeks male Swiss albino mice weighing 25 to 30 g. The mice were divided into 4 groups: Group A (kept as control); groups B, C and D (treated with gentamicin intramuscularly daily at the dose rate of 5 mg/kg for 7 days, 5 mg/kg for 30 days, and 10 mg/kg for 30 days, respectively). The mice of treated groups showed specific clinical signs such as dullness, roughness of the body coat, anorexia and weakness. Blood was collected by cardiac puncture for estimation of various blood chemical parameters, such as total erythrocyte count (TEC), total leucocyte count (TLC), hemoglobin percentage (Hb%), alanine amino transferase (ALT), and serum creatinine. Kidneys were collected for gross and histological study. Body weight (P<0.01) and kidney weight (P<0.05) decreased significantly in gentamicin treated group. In hematological study, TEC, TLC, and Hb% values decreased significantly (P<0.01), whereas in biochemical study, serum creatinine and ALT values increased significantly (P<0.01) in treated group when compared with control group. Gross study of kidneys showed abnormal characteristics, such as, soft, flabby, brownish color with decreased size of left kidney in treated group. Histological study revealed desquamation of glomerulus, loss of glomerular architecture, distortion of renal tubules and hemorrhage in tubules of treated group. These data supports the view that gentamicin has a toxic effect on the morphology of kidney after long term treatment with higher dose.

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Section: Discussionsupporting

confidence: 83%

Administration of gentamicin induced hematobiochemical and renal morphological alterations in Swiss albino mice

Jannat¹,

Sultana²,

Islam³

2017

Afr. J. Pharm. Pharmacol.

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“…We showed that TNF induces the expression and activation of the transcription factor Nrf2, which leads to the upregulation of cytoprotective and detoxification genes, including NQO1, GCLM, and GSTA1. The regulation of such genes by Nrf2 has been shown to regulate innate immune responses in various experimental disease models (25,26). This is the first time, to our knowledge, that TNF alone has been shown to regulate the expression and activation of Nrf2.…”

Section: Discussionmentioning

confidence: 87%

TNF Mediates the Sustained Activation of Nrf2 in Human Monocytes

Rushworth

Shah

MacEwan

2011

The Journal of Immunology

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Modulation of monocyte function is a critical factor in the resolution of inflammatory responses. This role is mediated mainly by the production of TNF-a. Investigations of the actions of TNF have mostly focused on acute activation of other cell types such as fibroblasts and endothelial cells. Less is known about the effects of TNF on monocytes themselves, and little is known about the regulation of cell responses to TNF beyond the activation of NF-?B. In this study, we investigated the regulation of NF-E2–related factor 2 (Nrf2) cyctoprotective responses to TNF in human monocytes. We found that in monocytes TNF induces sustained Nrf2 activation and Nrf2 cytoprotective gene induction in a TNFR1-dependent manner. Under TNF activation, monocytes increased their expression of Nrf2-dependent genes, including NAD(P)H:quinone oxidoreductase 1 and glutamyl cysteine ligase modulatory, but not heme oxygenase-1. We also showed that autocrine TNF secretion was responsible for this sustained Nrf2 response and that Nrf2 activation by TNF was mediated by the generation of reactive oxygen species. Moreover, we showed that Nrf2-mediated gene induction can modulate TNF-induced NF-?B activation. These results show for the first time, to our knowledge, that TNF modulates prolonged Nrf2-induced gene expression, which in turn regulates TNF-induced inflammatory responses

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“…However, when the cell experiences oxidative stress, Nrf2 becomes dissociated from Keap1 and translocates to the nucleus, where it induces expression of ARE-dependent target genes. The Nrf2/HO-1 pathway plays an important role in the nephrotoxicity of antibiotics and toxins, including gentamicin, cisplatin, adriamycin, and manganese (22,(26)(27)(28)(29)(30).…”

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confidence: 99%

Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

Dai

Tang

Deng

et al. 2015

Antimicrob Agents Chemother

107

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bNephrotoxicity is the major dose-limiting factor for the clinical use of colistin against multidrug-resistant (MDR) Gram-negative bacteria. This study aimed to investigate the protective effect of lycopene on colistin-induced nephrotoxicity in a mouse model. Fifty mice were randomly divided into 5 groups: the control group (saline solution), the lycopene group (20 mg/kg of body weight/day administered orally), the colistin group (15 mg/kg/day administered intravenously), the colistin (15 mg/kg/day) plus lycopene (5 mg/kg/day) group, and the colistin (15 mg/kg/day) plus lycopene (20 mg/kg/day) group; all mice were treated for 7 days. At 12 h after the last dose, blood was collected for measurements of blood urea nitrogen (BUN) and serum creatinine levels. The kidney tissue samples were obtained for examination of biomarkers of oxidative stress and apoptosis, histopathological assessment, and quantitative reverse transcription-PCR (qRT-PCR) analysis. Colistin treatment significantly increased concentrations of BUN and serum creatinine, tubular apoptosis/necrosis, lipid peroxidation, and heme oxygenase 1 (HO-1) activity, while the treatment decreased the levels of endogenous antioxidant biomarkers glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Notably, the changes in the levels of all biomarkers were attenuated in the kidneys of mice treated with colistin by lycopene (5 or 20 mg/kg). Lycopene treatment, especially in the colistin plus lycopene (20 mg/kg) group, significantly downregulated the expression of NF-B mRNA (P < 0.01) but upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 mRNA (both P < 0.01) in the kidney compared with the results seen with the colistin group. Our data demonstrated that coadministration of 20 mg/kg/day lycopene can protect against colistin-induced nephrotoxicity in mice. This effect may be attributed to the antioxidative property of lycopene and its ability to activate the Nrf2/HO-1 pathway.

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Diallyl sulfide enhances antioxidants and inhibits inflammation through the activation of Nrf2 against gentamicin-induced nephrotoxicity in Wistar rats

Cited by 159 publications

References 71 publications

Administration of gentamicin induced hematobiochemical and renal morphological alterations in Swiss albino mice

Administration of gentamicin induced hematobiochemical and renal morphological alterations in Swiss albino mice

TNF Mediates the Sustained Activation of Nrf2 in Human Monocytes

Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

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