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. 2014;58(4):1872-8.
doi: 10.1128/AAC.02431-13. Epub 2014 Jan 6.

Gingerol fraction from Zingiber officinale protects against gentamicin-induced nephrotoxicity

Francisco A P Rodrigues  1 , Mara M G Prata, Iris C M Oliveira, Natacha T Q Alves, Rosa E M Freitas, Helena S A Monteiro, Jame's A Silva, Paulo C Vieira, Daniel A Viana, Alexandre B Libório, Alexandre Havt
Affiliations

Gingerol fraction from Zingiber officinale protects against gentamicin-induced nephrotoxicity

Francisco A P Rodrigues et al. Antimicrob Agents Chemother. 2014.

Abstract

Nephrotoxicity is the main complication of gentamicin (GM) treatment. GM induces renal damage by overproduction of reactive oxygen species and inflammation in proximal tubular cells. Phenolic compounds from ginger, called gingerols, have been demonstrated to have antioxidant and anti-inflammatory effects. We investigated if oral treatment with an enriched solution of gingerols (GF) would promote a nephroprotective effect in an animal nephropathy model. The following six groups of male Wistar rats were studied: (i) control group (CT group); (ii) gingerol solution control group (GF group); (iii) gentamicin treatment group (GM group), receiving 100 mg/kg of body weight intraperitoneally (i.p.); and (iv to vi) gentamicin groups also receiving GF, at doses of 6.25, 12.5, and 25 mg/kg, respectively (GM+GF groups). Animals from the GM group had a significant decrease in creatinine clearance and higher levels of urinary protein excretion. This was associated with markers of oxidative stress and nitric oxide production. Also, there were increases of the mRNA levels for proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], IL-2, and gamma interferon [IFN-γ]). Histopathological findings of tubular degeneration and inflammatory cell infiltration reinforced GM-induced nephrotoxicity. All these alterations were attenuated by previous oral treatment with GF. Animals from the GM+GF groups showed amelioration in renal function parameters and reduced lipid peroxidation and nitrosative stress, in addition to an increment in the levels of glutathione (GSH) and superoxide dismutase (SOD) activity. Gingerols also promoted significant reductions in mRNA transcription for TNF-α, IL-2, and IFN-γ. These effects were dose dependent. These results demonstrate that GF promotes a nephroprotective effect on GM-mediated nephropathy by oxidative stress, inflammatory processes, and renal dysfunction.

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Figures

FIG 1
FIG 1
Effects of GF on lipid peroxidation (MDA) in gentamicin-induced nephrotoxicity. The results are expressed as means ± SEM (n = 7). Statistical analysis was performed by ANOVA followed by the Newman-Keuls post hoc test. *, significant difference compared to saline (CT); #, significant difference compared to gentamicin (GM) (P < 0.05); **, significant difference compared to saline (P < 0.01).
FIG 2
FIG 2
Effect of GF on serum nitrite levels in gentamicin-induced nephrotoxicity. The results are expressed as means ± SEM (n = 6). Statistical analysis was performed by ANOVA followed by the Newman-Keuls post hoc test. **, significant difference compared to saline (CT); #, significant difference compared to gentamicin (GM) (P < 0.05); ##, significant difference compared to gentamicin (P < 0.01).
FIG 3
FIG 3
Effect of GF on the amount of glutathione (GSH) in gentamicin-induced nephrotoxicity. The results are expressed as means ± SEM (n = 7). Statistical analysis was performed by ANOVA followed by the Newman-Keuls post hoc test. **, significant difference compared to saline (CT); #, significant difference compared to gentamicin (GM) (P < 0.05).
FIG 4
FIG 4
Effect of GF on superoxide dismutase (SOD) activity in gentamicin-induced nephrotoxicity. The results are expressed as means ± SEM (n = 7). Statistical analysis was performed by ANOVA followed by the Newman-Keuls post hoc test. *, significant difference compared to saline (CT); #, significant difference compared to gentamicin (GM) (P < 0.05); **, significant difference compared to saline (P < 0.01).
FIG 5
FIG 5
Effects of GF on relative expression of the TNF-α, IL-1β, IL-2, and IFN-γ genes in gentamicin-induced nephrotoxicity. Statistical analysis was performed by the Mann-Whitney test (n = 6). *, significant difference compared to saline (CT); #, significant difference compared to gentamicin (GM) (P < 0.05); **, significant difference compared to saline (P < 0.01); ##, significant difference compared to gentamicin (P < 0.01).
FIG 6
FIG 6
Photomicrographs depicting H&E-stained sections of kidneys from rats receiving saline (control) (A), GM (100 mg/kg) (B and C), saline plus oral treatment with GF at a dose of 25 mg/kg (D), or gentamicin plus GF at 25 mg/kg (E and F). There was vacuolar degeneration in proximal tubule cells (B) and an inflammatory infiltrate (C) associated with GM administration. These features were attenuated by concomitant GF treatment (E and F). Magnification, ×400.
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