Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Fan, Shao‐Hua; Zhang, Zi-Feng; Zheng, Yuxin; Lü, Jun; Wu, Dongmei; Shan, Qun; Hu, Bin; Wang, Yanyan

doi:10.1016/j.intimp.2008.10.008

Cited by 121 publications

(74 citation statements)

References 44 publications

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“…Our previous studies have demonstrated that troxerutin has many different biological activities, including antioxidant and anti-inflammatory activities (27)(28)(29)(30)(31). Recently, our preliminary data showed that troxerutin blocked the phosphorylation of MAPK/ ERK1/2 (MEK1/2) in the hippocampus of DA-treated mice and reversed DA-induced memory deficits.…”

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confidence: 95%

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Lü

Zheng

et al. 2013

The Journal of Immunology

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The C/EBP β is a basic leucine zipper transcription factor that regulates a variety of biological processes, including metabolism, cell proliferation and differentiation, and immune response. Recent findings show that C/EBP β–induced inflammatory responses mediate kainic acid–triggered excitotoxic brain injury. In this article, we show that protein kinase C ζ enhances K-ras expression and subsequently activates the Raf/MEK/ERK1/2 pathway in the hippocampus of domoic acid (DA)–treated mice, which promotes C/EBP β expression and induces inflammatory responses. Elevated production of TNF-α impairs mitochondrial function and increases the levels of reactive oxygen species by IκB kinase β/NF-κB signaling. The aforementioned inflammation and oxidative stress lead to memory deficits in DA-treated mice. However, troxerutin inhibits cyclin-dependent kinase 1 expression, enhances type 1 protein phosphatase α dephosphorylation, and abolishes MEK/ERK1/2/C/EBP β activation, which subsequently reverses the memory impairment observed in the DA-treated mice. Thus, troxerutin is recommended as a potential candidate for the prevention and therapeutic treatment of cognitive deficits resulting from excitotoxic brain damage and other brain disorders.

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confidence: 95%

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Lü

Zheng

et al. 2013

The Journal of Immunology

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“…Free radicals attack essential cell constituents and also induce lipid peroxidation, damage the membranes of cells and organelles in liver and kidney, cause the swelling and necrosis of hepatocytes and nephrocytes, and ultimately result in liver and kidney injury (Fan et al 2009;Zhang et al 2009b). D-Gal overload increases the production of free radicals, diminishes antioxidant enzyme activity, and attenuates immune responses.…”

Section: Introductionmentioning

confidence: 99%

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

Feng

Wang

et al. 2016

Pharmaceutical Biology

112

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Context Oxidative stress and inflammation are implicated in the aging process and its related hepatic and renal function decline. Chlorogenic acid (CGA) is one of the most abundant polyphenol compounds in the human diet. Recently, CGA has shown in vivo and in vitro antioxidant properties. Objective The current study investigates the effects of protective effects of chlorogenic acid (CGA) on D-galactose-induced liver and kidney injury. Materials and methods Hepatic and renal injuries were induced in a mouse model by subcutaneously injection of D-galactose (D-gal; 100 mg/kg) once a day for 8 consecutive weeks and orally administered simultaneously with CGA included in the food (200 mg/kg of diet). The liver and renal functions were examined. Histological analyses of liver and kidney were done by haematoxylin and eosin staining. The oxidative stress markers and pro-inflammatory cytokines in the liver and the kidney were measured. Results CGA significantly reduced the serum aminotransferase, serum creatinine (SCr) and blood urea nitrogen (BUN) levels in D-gal mice (p50.05). CGA also restored superoxide dismutase, catalase, and malondialdehyde levels and decreased glutathione content in the liver and kidney in D-gal mice (p50.05). Improvements in liver and kidney were also noted in histopathological studies. CGA reduced tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6) protein levels in the liver and kidney in D-gal mice (p50.05). Discussion and conclusion These findings suggest that CGA attenuates D-gal-induced chronic liver and kidney injury and that this protection may be due to its antioxidative and antiinflammatory activities.ARTICLE HISTORY

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“…ROS are associated with the inflammatory response and frequently contribute to the tissue-damaging effects of inflammatory reactions (15,47). d-Galactose can induce renal injury, including oxidative stress and inflammation, in mice, which can lead to renal dysfunction (18,48). Moreover, obesity is reported to expedite the aging process (24).…”

Section: Discussionmentioning

confidence: 99%

“…When rats are injected with d-galactose for 6 wk, free radical production is increased in renal and other tissues (16). d-Galactose has been used to induce oxidative stress in vivo to mimic the natural aging process in rats and mice (17)(18)(19)(20). In addition, a high-fat diet (HFD) was found to be a significant risk factor for kidney disease (21)(22)(23).…”

Section: J Nutr Scimentioning

confidence: 99%

A High-Fat Diet Increases Oxidative Renal Injury and Protein Glycation in D-Galactose-Induced Aging Rats and Its Prevention by Korea Red Ginseng

Park

Kim

Min

et al. 2014

J Nutr Sci Vitaminol

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Summary Declining renal function is commonly observed with age. Obesity induced by a high-fat diet (HFD) may reduce renal function. Korean red ginseng (KRG) has been reported to ameliorate oxidative tissue injury and have an anti-aging effect. This study was designed to investigate whether HFD would accelerate the d-galactose-induced aging process in the rat kidney and to examine the preventive effect of KRG on HFD and d-galactose-induced aging-related renal injury. When rats with d-galactose-induced aging were fed an HFD for 9 wk, enhanced oxidative DNA damage, renal cell apoptosis, protein glycation, and extracellular high mobility group box 1 protein (HMGB1), a signal of tissue damage, were observed in renal glomerular cells and tubular epithelial cells. However, treatment of rats with HFDplus d-galactose-induced aging with KRG restored all of these renal changes. Our data suggested that a long-term HFD may enhance d-galactose-induced oxidative renal injury in rats and that this age-related renal injury could be suppressed by KRG through the repression of oxidative injury.

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Troxerutin protects the mouse kidney from d-galactose-caused injury through anti-inflammation and anti-oxidation

Cited by 121 publications

References 44 publications

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Chlorogenic acid protects d-galactose-induced liver and kidney injury via antioxidation and anti-inflammation effects in mice

A High-Fat Diet Increases Oxidative Renal Injury and Protein Glycation in D-Galactose-Induced Aging Rats and Its Prevention by Korea Red Ginseng

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