Protective role of chrysin against oxidative stress in <scp>d</scp>‐galactose‐induced aging in an experimental rat model

Anand, Kalaiselvi Velayutham; Jaabir, Mohamed; Thomas, Philip A.; Geraldine, Pitchairaj

doi:10.1111/j.1447-0594.2012.00843.x

Cited by 106 publications

(61 citation statements)

References 49 publications

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“…SOD, the main endogenous antioxidant enzyme, could protect tissues against the harmfulness of free radicals [31,32]. GSH-Px activity is a major mechanism for intracellular decomposition of lipid peroxidase [33]. MDA could reflect the status of oxidative stress [34].…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

Zhang

Gao

Guo

et al. 2016

Biol Trace Elem Res

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Lead (Pb) exposure is a global environmental problem that can deplete body antioxidant enzymes, causing damage to various macromolecules and ultimately cell death. Pb exposure could lead to serious renal damage. Baicalin, a traditional Chinese medicine, could protect against renal injury through inhibition of oxidative stress and apoptosis. This study was designed to investigate the protective efficacy of baicalin against Pb-induced nephrotoxicity in mice and to elucidate the potential mechanisms using animal experiment. The results revealed that baicalin decreased Pb-induced bodyweight loss, declined kidney coefficients, and ameliorated renal function and structure in a dose-dependent manner. Meanwhile, baicalin dose dependently increased Pb-induced activity of SOD and GSH-Px, while the content of MDA in the kidney was decreased. In addition, baicalin enhanced the Bcl-2/Bax ratio associated with apoptosis in the kidney. These data indicated that further investigation of the use of baicalin as a new natural chemopreventive agent against Pd poisoning is warranted.

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Section: Discussionmentioning

confidence: 99%

The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

Zhang

Gao

Guo

et al. 2016

Biol Trace Elem Res

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“…Some of these investigations yielded promising results. For example, Uhl et al [13] demonstrated antimutagenic properties against benzo(a)pyrene B(a)P induced DNA-damage in HepG2 cells and Salmonella typhimurium ; Anand et al [14] showed that CR reduces the disturbances of redox status, named superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) in liver, kidney, and brain tissues of rats treated with D-galactose.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of the Flavonoid Chrysin against Methylmercury-Induced Genotoxicity and Alterations of Antioxidant Status,In Vivo

Manzolli

Serpeloni

Grotto

et al. 2015

Oxidative Medicine and Cellular Longevity

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The use of phytochemicals has been widely used as inexpensive approach for prevention of diseases related to oxidative damage due to its antioxidant properties. One of dietary flavonoids is chrysin (CR), found mainly in passion fruit, honey, and propolis. Methylmercury (MeHg) is a toxic metal whose main toxic mechanism is oxidative damage. Thus, the study aimed to evaluate the antioxidant effects of CR against oxidative damage induced by MeHg in Wistar rats. Animals were treated with MeHg (30 µg/kg/bw) in presence and absence of CR (0.10, 1.0, and 10 mg/kg/bw) by gavage for 45 days. Glutathione (GSH) in blood was quantified spectrophotometrically and for monitoring of DNA damage, comet assay was used in leukocytes and hepatocytes. MeHg led to a significant increase in the formation of comets; when the animals were exposed to the metal in the presence of CR, higher concentrations of CR showed protective effects. Moreover, exposure to MeHg decreased the levels of GSH and GSH levels were restored in the animals that received CR plus MeHg. Taken together the findings of the present work indicate that consumption of flavonoids such as CR may protect humans against the adverse health effects caused by MeHg.

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“…Chronic administration of D -galactose ( D -gal) which induces neurotoxicity is a common model used to study aging and memory impairment [1,2,3,4,5]. There are 3 main aspects of the mechanism of D -gal-induced aging.…”

Section: Introductionmentioning

confidence: 99%

The Neurovascular Protective Effects of Huperzine A on D-Galactose-Induced Inflammatory Damage in the Rat Hippocampus

Ruan

et al. 2014

Gerontology

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Background: Chronic administration of D-galactose (D-gal) results in oxidative stress and chronic inflammatory aging. Age-related changes in the brain result in neurovascular damage and blood-brain barrier (BBB) dysfunction. However, little is known regarding D-gal-induced neurovascular damage, as well as the protective effects of huperzine A. Objective: The purpose of this study was to utilize a D-gal-induced rat model to investigate the activation of neurovascular inflammatory damage and apoptosis in the rat hippocampus and to understand whether huperzine A alleviates D-gal-induced neuronal and vascular inflammatory injury. Methods: Aging rats were treated with D-gal (300 mg/kg s.c. for 8 weeks), were coadministered D-gal and huperzine A (D-gal 300 mg/kg and huperzine A 0.1 mg/kg s.c. for 8 weeks) or served as the saline-treated control group rats (same volume of saline given subcutaneously for 8 weeks). Changes in hippocampal morphology and biomarkers of inflammatory damage were analyzed. Results: Our study revealed that chronic administration of D-gal resulted in the activation of glia and vascular endothelial cells and upregulation of mRNA and protein levels of cell-associated adhesion molecules and inflammatory cytokines via nuclear factor (NF)-κB inhibitor degradation and NF-κB nuclear translocation. The inflammatory injury caused significant BBB dysfunction, decreased density of tight junctions (TJs) and apoptosis in the rat hippocampus. Coadministration of huperzine A not only markedly inhibited the D-gal-induced increase in acetylcholinesterase (AChE) activity, but also alleviated D-gal-induced neurovascular damage by inhibiting D-gal-induced NF-κB activation, improving cerebrovascular function and suppressing the D-gal-induced decrease in the density and protein levels of TJs and cell apoptosis. Conclusions: Our findings provided evidence that D-gal induced a proinflammatory phenotype mediated by NF-κB in the rat hippocampus. Moreover, huperzine A suppressed D-gal-induced neurovascular damage and BBB dysfunction, partly by preventing NF-κB nuclear translocation. The inhibiting effect of huperzine A on AChE activity might play an important role in attenuating D-gal-induced inflammatory damage.

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Protective role of chrysin against oxidative stress in d‐galactose‐induced aging in an experimental rat model

Abstract: These results suggest that chrysin protects against oxidative stress-induced tissue damage in D-galactose-induced aging in an experimental rat model.

Cited by 106 publications

References 49 publications

The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

Protective Effects of the Flavonoid Chrysin against Methylmercury-Induced Genotoxicity and Alterations of Antioxidant Status,In Vivo

The Neurovascular Protective Effects of Huperzine A on D-Galactose-Induced Inflammatory Damage in the Rat Hippocampus

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