Protective effect of grape seed proanthocyanidin extract against oxidative stress induced by cisplatin in rats

Yousef, Mokhtar I.; Saad, Abeer A.; El-Shennawy, Lamiaa

doi:10.1016/j.fct.2009.02.007

Cited by 214 publications

(167 citation statements)

References 49 publications

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“…Furthermore, the obtained enzymatic improvement by administration of GSPE may be due to protecting the cell membranes by the scavenging property of the free radical by the antioxidative phytochemicals present in GSPE such as flavonoids (Yousef et al 2009) and/or due to the fact that GSPE improves hepatic ischemic injury (Sehirli et al 2008). The recorded improvement of TP, urea and creatinine levels by administration of GSPE may be due to the antioxidant effects of GSPE which improved the liver cells function and consequently increased protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

Grape seeds proanthocyanidin extract as a hepatic-reno-protective agent against gibberellic acid induced oxidative stress and cellular alterations

Hassan

Al-Rawi

2012

Cytotechnology

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The present study aims to investigate the heptonephro-protective effect of grape seeds proanthocyanidin extract (GSPE) against the risks induced by gibberellic acid (GA3) in male rats. The results recorded that GA3 caused a significant increase in total lipids, total cholesterol, triglycerides and LDL-C levels in serum, concomitant with a significant decrease in serum HDL-C. A significant increase in serum AST, ALT, urea and creatinine, while, a significant decrease in total protein content in serum was observed in rats given GA3. Hepatic and renal lipid peroxidation product (MDA) was significantly increased, meanwhile, total antioxidant capacity (TAC), glutathione, and catalase levels were significantly decreased. In addition, there was a negative change in liver structure including dilatation in the central veins with degeneration of endothelium cells and cellular injury around the veins as well as in the kidney structure such as lesion in both glomeruli and tubules, detachment of the Malpighian corpuscles from the Bowman's capsule's epithelium, shrinkage in the glomerular capillary network. However, almost all of these adverse effects seemed to be ameliorated by oral administration of GSPE with GA3 to rats for 2 month indicating the protective effect of grape seeds GSPE on GA3 induced oxidative stress in rats.

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Section: Discussionmentioning

confidence: 99%

Grape seeds proanthocyanidin extract as a hepatic-reno-protective agent against gibberellic acid induced oxidative stress and cellular alterations

Hassan

Al-Rawi

2012

Cytotechnology

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“…Proanthocyanidins exhibit antioxidant (Yousef et al 2009), anti-inflammatory (Terra et al 2009) and anticancer (Kaur et al 2006) activities. It has been shown that grape seed proanthocyanidins (GSP) reduces oxidative stress, hyperglycemia and hyperinsulinemia in high fructose dietinduced insulin resistant rats (Suwannaphet et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Grape seed proanthocyanidins and metformin act by different mechanisms to promote insulin signaling in rats fed high calorie diet

Yogalakshmi

Bhuvaneswari

Sreeja

et al. 2013

Journal of Cell Communication and Signaling

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Key pathways like insulin signaling, AMP activated kinase (AMPK) activation and inflammatory signaling are involved in the complex pathological network of hepatic insulin resistance. Our aim is to investigate whether grape seed proanthocyanidins (GSP) and metformin (MET) target any of these pathways in insulin resistant rat liver. Albino Wistar rats were rendered insulin resistant by feeding a high fat-fructose diet (HFFD). Either GSP (100 mg/kg b.w), MET(50 mg/kg b.w) or both were administered to insulin resistant rats as therapeutic options. HFFD-feeding caused hyperglycemia, hyperinsulinemia, increased gluconeogenesis, decreased tyrosine phosphorylation of insulin receptor-β (IR-β) and insulin receptor substrate-1 (IRS-1) and increased serine phosphorylation of IRS-1. The association of p85α subunit of phosphotidyl inositol 3 kinase(PI3K) with IRS-1 and subsequent Akt phosphorylation were reduced while the expression of mitogen activated protein kinases (MAPK) were increased in HFFD rats. Both MET and GSP reduced hyperglycemia and hyperinsulinemia and improved glycolysis, tyrosine phosphorylation of IR-β and IRS-1, IRS-1-PI3K association and Akt activation. However, activation of tumor necrosis factor-α, interleukin-6, leptin and suppressor of cytokine signaling-3 and reduction in adiponectin caused by chronic HFFD feeding were reversed by GSP better than by MET. Activation of AMPK by GSP was much less compared to that by MET. These findings suggest that GSP might activate PI3K pathway and promote insulin action by reducing serine kinase activation and cytokine signaling and MET by targeting AMPK. The beneficial effects were enhanced during combination therapy. Thus, combination therapy with MET and GSP may be considered for the management of metabolic syndrome.

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“…Oxidative stress is reportedly associated with cisplatin-induced toxicity. The decrease of antioxidant enzymes (GST, SOD, CAT, GSH-Px and GSH) is involved in the cisplatin-induced toxicity process (9). The increased type III collagen in the heart, as shown by our results, suggests that the tissues were greatly damaged when subjected to cisplatin-induced toxicity.…”

Section: Discussionmentioning

confidence: 50%

“…Cisplatin-induced toxicity is known to be involved in the changes of antioxidant enzymes (GST, SOD, CAT, GSH-Px and GSH), serum superoxide dismutase (SOD), glutathione (GSH), malondiethylaldehyde (MDA), nitric oxide (NO) (9) and DNA (2,10). However, little is known about the changes in endothelin (ET)-1 and type III collagen expression in the heart following cisplatin-induced toxicity.…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 and type III collagen alterations in the heart of rats following cisplatin-induced toxicity

Huang

Liu

2011

Mol Med Report

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Abstract. Cisplatin-induced heart damage is associated with enzymes and protein alterations. The purpose of this study was to investigate cisplatin-induced alterations in cardiac endothelin (ET)-1 and type III collagen following administration of cisplatin. Male Wistar rats were randomly divided into two groups: a control and a cisplatin group. The cisplatin group received cisplatin intraperitoneally (i.p.) at a single dose of 7 mg/kg on day 6, while the controls were given the same amount of saline via the same route. On day 11, the rats were anesthetized and a thoracotomy was performed on all animals. Immunohistochemical analysis was performed to evaluate the protein expression of ET-1 and type III collagen. Sections were analyzed by digital image analysis. Results showed that the cardiac protein expression of ET-1 and type III collagen was altered following cisplatin-induced toxicity in rats. The expression of ET-1 and type III collagen was significantly increased after cisplatin treatment, supported by integrated optical density, when compared to the control group (P<0.05). The present findings indicate that such alterations may be reflected in abnormal cardiac function. Additionally, the proteins identified in this study may benefit investigations into the mechanisms underlying cisplatin-induced toxicity, thereby providing the necessary evidence for further research. IntroductionCisplatin is a chemotherapeutic agent widely used to treat a variety of solid tumors (1,2). It is also an antineoplastic drug that causes an array of adverse effects on various organs and tissues (3). Nephrotoxicity is one of the major side-effects of cisplatin chemotherapy (4) limiting the promising efficacy of cisplatin (5). Cisplatin-based chemotherapy also has a variety of vascular side-effects (6). Acute administration of cisplatin induces nausea/emesis and diarrhea (7). Chronic cisplatin may induce an enteric neuropathy characterized by changes in myenteric neurons associated with marked gastrointestinal motor dysfunction (7). Dysfunction in immune surveillance during anticancer chemotherapy of patients often causes weakness of the host defense system and a subsequent increase in microbial infections (8).Cisplatin-induced toxicity is known to be involved in the changes of antioxidant enzymes (GST, SOD, CAT, GSH-Px and GSH), serum superoxide dismutase (SOD), glutathione (GSH), malondiethylaldehyde (MDA), nitric oxide (NO) (9) and DNA (2,10). However, little is known about the changes in endothelin (ET)-1 and type III collagen expression in the heart following cisplatin-induced toxicity.The present study used immunohistochemical analysis to evaluate the expression of ET-1 and type III collagen in the heart, and to determine whether or not the protein expression is altered with cisplatin-induced toxicity. Materials and methodsAnimals and study design. Sixteen healthy adult male Wistar rats, weighing 210-250 g, were used in this study. The animals were housed individually in stainless-steel wire-bottomed cages in an air-conditione...

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Protective effect of grape seed proanthocyanidin extract against oxidative stress induced by cisplatin in rats

Cited by 214 publications

References 49 publications

Grape seeds proanthocyanidin extract as a hepatic-reno-protective agent against gibberellic acid induced oxidative stress and cellular alterations

Grape seeds proanthocyanidin extract as a hepatic-reno-protective agent against gibberellic acid induced oxidative stress and cellular alterations

Grape seed proanthocyanidins and metformin act by different mechanisms to promote insulin signaling in rats fed high calorie diet

Endothelin-1 and type III collagen alterations in the heart of rats following cisplatin-induced toxicity

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