Neuroprotection of Grape Seed Extract and Pyridoxine against Triton‐Induced Neurotoxicity

Abdou, Heba M.; Wahby, Mayssaa M.

doi:10.1155/2016/8679506

Cited by 20 publications

(14 citation statements)

References 55 publications

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“…Administration of the DEX-induced rats with either dose of GSE significantly improved the hematological parameters compared with rats treated with dexamethasone alone. Our results in the line of those of Abdou and Wahby [29] who demonstrated that GSE administration improves the hematological alteration induced by Triton.…”

Section: Discussionsupporting

confidence: 93%

Grape Seed Extract Alleviates Dexamethasone-Induced Hyperlipidemia, Lipid Peroxidation, and Hematological Alteration in Rats

Hasona

Morsi

2018

Ind J Clin Biochem

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The ameliorative effects of dietary natural compounds have drawn increasing attention. Dietary antioxidant is considered a common practice adopted in traditional and alternative medicine. The current study was considered to assess the ameliorative effect of grape seed extract on dexamethasone-induced hepatotoxicity in rats. Rats were injected with dexamethasone, (0.1 mg/kg; i.m.), three times per week, for 30 days. The other groups; dexamethasone (0.1 mg/kg) and grape seed extract at a dose of 200 and 400 mg/kg were given orally to rats, respectively. Dexamethasone treatment resulted in a significant elevation in liver function markers activities, lipid profile, and hematological alterations; also, a remarkable increase in hepatic lipid peroxidation marker whereas decreased antioxidant activities in rats. However, administration of grape seed extract resulted in a reversal of dexamethasoneinduced lipid peroxidation, antioxidant enzyme activities, liver function markers and lipid profile, and hematological alterations. Moreover, grape seed extract demonstrated preventive action against dexamethasone-induced histopathological changes in rat liver tissues. In conclusion, grape seed extract exhibited a protective effect in rats against oxidative stress, hyperlipidemia and hematological alterations induced by dexamethasone.

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Section: Discussionsupporting

confidence: 93%

Grape Seed Extract Alleviates Dexamethasone-Induced Hyperlipidemia, Lipid Peroxidation, and Hematological Alteration in Rats

Hasona

Morsi

2018

Ind J Clin Biochem

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“…Figure 4 showed mild DNA fragmentation that indicates Triton-induced neurotoxicity in brain tissues (lane 2) as compared to the control (lane 1).While, Triton WR-1339 plus soybean oil treatment (lane 3) caused partial inhibition in the DNA fragmentation compared to the Triton WR-1339-treated group (lane 2). In further support of our results, a previous study indicated that Triton WR-1339 efficiently induced DNA degradation indicating its necrotic effect (Abdou & Wahby, 2016). Thus, the increase in lipid peroxidation and depletion of antioxidant enzymes play major role in Triton WR-1339-induced genotoxicity.…”

Section: Discussionsupporting

confidence: 90%

“…Hyperlipidemia is characterized by elevated serum total cholesterol, low-density cholesterol, and very low density lipoprotein cholesterol and decreased high-density lipoprotein cholesterol levels (Ibrahim, Mohamed, Banjar, & Kamal, 2013). The increase of oxidative metabolic activity in addition to the low concentrations of the endogenous antioxidants causes liver and brain oxidative damage (Abdou & Wahby, 2016;Küçükgergin et al, 2010). Currently, available hypolipidemic drugs have been associated with a number of side effects (Al-Awadi, Rashid, & Hassen, 2013b).…”

Section: Introductionmentioning

confidence: 99%

Triton WR-1339-induced hyperlipidemia, DNA fragmentation, neurotransmitters inhibition, oxidative damage, histopathological and morphometric changes: the protective role of soybean oil

Abdou

Yousef

Newairy

2018

JoBAZ

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Background: Triton WR1339 (Tyloxapol) is the nonionic detergent, which is able to increase the oxidative markers. This oxidation have a crucial effect on the pathological processes. Vegetable oils, such as soy, are recommended for human consumption due to the presence of high content of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA). Therefore, the effect of Triton WR1339 and soybean oil on biochemical parameters was tested in our study. Aim: The objective of this study is to investigate the possible protective effects of soybean oil against Triton WR-1339-induced hyperlipidemia, DNA fragmentation, oxidative damage, neurotransmitters inhibition, and changes in histological and morphometric analysis of the liver and dorsal aorta of male rats. Methods: Animals were treated with Triton WR-1339 (50 mg/kg BW) and soybean oil (50 mg/kg BW) for 28 days. Oxidative stress markers; antioxidant enzymes activity; biochemical parameters, such as acetylcholinesterase and mono aminoxidase, transaminases, phosphatases, lactate dehydrogenase, urea, creatinine, bilirubin, and lipid profile; DNA fragmentation; as well as histopathological and morphmetric analysis of the liver and dorsal aorta were investigated. Results: Triton WR-1339 increased oxidative stress through an elevation in TBARS associated with depletion in glutathione and the activities of GST, SOD, GSH-Px, and CAT in plasma, liver, and brain. Triton WR-1339 induced DNA fragmentation and inhibited the activities of acetylcholinesterase and mono aminoxidase in the brain. Plasma biochemical parameters including transaminases, phosphatases, lactate dehydrogenase, urea, creatinine, bilirubin, total lipid, cholesterol, triglyceride, and LDL were increased, while total protein, albumin, and high HDL were decreased due to Triton WR-1339-treatment. The histopathological and morphmetric analysis of the liver and dorsal aorta revealed alterations after Triton WR-1339-treatment. The presence of soybean oil with Triton WR-1339 minimized its hepatotoxicity and neurotoxicity via hypolipidemic effects and attenuated the oxidative damage. Conclusion: Soybean oil showed hypolipidemic effects and antioxidant activity, so it could be used as a hypolipidemic agent.

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“…The EtOH (current study) caused an increased expression of both apoptotic (caspase-3) and antiapoptotic (survivin) markers, and those changes were alleviated by GLE, which correlated well with its hepatoprotective effects demonstrated in the current study. Importantly, grape-seed extract was previously found to exert neuro-, cardio-, and renoprotective effects via apoptosis suppression [55,56], with no previous reports on the antiapoptotic effects of GLE in the liver.…”

Section: (A)mentioning

confidence: 99%

Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway

et al. 2020

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Grape (Vitis vinifera) leaf extracts (GLEs) are known to be rich in phenolic compounds that exert potent antioxidant effects. Given the vulnerability of the liver to oxidative damage, antioxidants have been proposed as therapeutic agents and coadjuvant drugs to ameliorate liver pathologies. The current study was designed to characterize secondary metabolites and investigate the hepatoprotective effects of GLE and its underlying mechanisms. The secondary metabolites were profiled using HPLC–PDA–ESI-MS, and forty-five compounds were tentatively identified. In experimental in vivo design, liver injury was induced by oral administration of high doses of ethanol (EtOH) for 12 days to male Sprague Dawley rats that were split into five different groups. Blood samples and livers were then collected, and used for various biochemical, immunohistochemical, and histopathological analyses. Results showed that GLE-attenuated liver injury and promoted marked hepatic antioxidant effects, in addition to suppressing the increased heat-shock protein-70 expression. Moreover, GLE suppressed EtOH-induced expression of nuclear factor-κB (NF-κB) p65 subunit and proinflammatory cytokine tumor necrosis factor-α. Caspase-3 and survivin were enhanced by EtOH intake and suppressed by GLE intake. Finally, EtOH-induced histopathological changes in liver sections were markedly normalized by GLE. In conclusion, our results suggested that GLE interferes with NF-κB signaling and induces antioxidant effects, which both play a role in attenuating apoptosis and associated liver injury in a model of EtOH-induced liver damage in rats.

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Neuroprotection of Grape Seed Extract and Pyridoxine against Triton‐Induced Neurotoxicity

Cited by 20 publications

References 55 publications

Grape Seed Extract Alleviates Dexamethasone-Induced Hyperlipidemia, Lipid Peroxidation, and Hematological Alteration in Rats

Grape Seed Extract Alleviates Dexamethasone-Induced Hyperlipidemia, Lipid Peroxidation, and Hematological Alteration in Rats

Triton WR-1339-induced hyperlipidemia, DNA fragmentation, neurotransmitters inhibition, oxidative damage, histopathological and morphometric changes: the protective role of soybean oil

Grape-Leaf Extract Attenuates Alcohol-Induced Liver Injury via Interference with NF-κB Signaling Pathway

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