Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Abstract

BackgroundThe metabolic syndrome is associated with an increased risk of development and progression of chronic kidney disease. Renal inflammation is well known to play an important role in the initiation and progression of tubulointerstitial injury of the kidneys. Ginger, one of the most commonly used spices and medicinal plants, has been demonstrated to improve diet-induced metabolic abnormalities. However, the efficacy of ginger on the metabolic syndrome-associated kidney injury remains unknown. This study aimed to investigate the impact of ginger on fructose consumption-induced adverse effects in the kidneys.MethodsThe fructose control rats were treated with 10% fructose in drinking water over 5 weeks. The fructose consumption in ginger-treated rats was adjusted to match that of fructose control group. The ethanolic extract of ginger was co-administered (once daily by oral gavage). The indexes of lipid and glucose homeostasis were determined enzymatically, by ELISA and/or histologically. Gene expression was analyzed by Real-Time PCR.ResultsIn addition to improve hyperinsulinemia and hypertriglyceridemia, supplement with ginger extract (50 mg/kg) attenuated liquid fructose-induced kidney injury as characterized by focal cast formation, slough and dilation of tubular epithelial cells in the cortex of the kidneys in rats. Furthermore, ginger also diminished excessive renal interstitial collagen deposit. By Real-Time PCR, renal gene expression profiles revealed that ginger suppressed fructose-stimulated monocyte chemoattractant protein-1 and its receptor chemokine (C-C motif) receptor-2. In accord, overexpression of two important macrophage accumulation markers CD68 and F4/80 was downregulated. Moreover, overexpressed tumor necrosis factor-alpha, interleukin-6, transforming growth factor-beta1 and plasminogen activator inhibitor (PAI)-1 were downregulated. Ginger treatment also restored the downregulated ratio of urokinase-type plasminogen activator to PAI-1.ConclusionsThe present results suggest that ginger supplement diminishes fructose-induced kidney injury through suppression of renal overexpression of macrophage-associated proinflammatory cytokines in rats. Our findings provide evidence supporting the protective effect of ginger on the metabolic syndrome-associated kidney injury.

Ginger Water Reduces Body Weight Gain and Improves Energy Expenditure in Rats

“…Ginger extract weakened the kidney injury induced by chronic fructose consumption. This was mediated by suppressing renal over-expression of proinflammatory cytokines [20]. The important active component of ginger root is the unpredictable oil and impactful phenol compounds, for example, gingerol, which is a very powerful anti-inflammatory compound [21].…”

Fructose downregulates miR‐330 to induce renal inflammatory response and insulin signaling impairment: Attenuation by morin

“…In our previous studies, rats receiving 10% w/v fructose in the drinking water induced hyperuricemia and renal injury , as well as podocyte injury and proteinuria . Fibrosis in renal cortex and podocyte dysfunction , as well as tubulointerstitial injury with inflammation are also observed in rats with 10% w/v fructose consumption in other reports. Therefore, 10% w/v fructose was chosen in vitro experiments.…”

“…All animals were received regular standard chow for 8 wk. They were given normal drinking water (normal control group, n = 7/group) or 10% w/v fructose in drinking water and standard chow for 8 wk ad libitum. Fresh drinking water was replaced every 2 days.…”

Ginger (Zingiber officinaleRosc.) and its bioactive components are potential resources for health beneficial agents

“…Supplementation with ginger ethanol extract at 50 mg/kg, (p.o.) reversed the fructose consumption‐induced chronic kidney injury in rats, with decreased damage of tubules in the cortex and ratio of the Masson's trichrome‐stained area to the total tissue area in the renal interstitium (Yang et al, 2014). In another study, this extract at doses of 100 and 200 mg/kg (p.o., 4 weeks) displayed an improvement in cadmium (5 mg/kg)‐induced renal cell dysfunction, severity of tubular cells, and DNA damage (Gabr et al, 2019).…”