Protective role of grape seed proanthocyanidins against cadmium induced hepatic dysfunction in rats

Nazimabashir,; Manoharan, Vaihundam; Prabu, S. Milton

doi:10.1039/c3tx50085c

Cited by 19 publications

(15 citation statements)

References 47 publications

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“…Therefore, the Furthermore, DIC has been reported to decline the activity of antioxidant enzymes such as SOD and CAT (Giridharan & Sabina, 2017;Nouri, Heidarian, & Nikoukar, 2017). SOD and CAT have essential role in the body against oxidative stress (Manoharan & Prabu, 2014;Sikander et al, 2013). Superoxide dismutase has a key role to eliminate the toxic effects of superoxide anion (Han et al, 2014;Wei, Tian, Liu, & Xie, 2014).…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Nouri

Heidarian

2019

J Food Biochem

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Diclofenac (DIC) can cause nephrotoxicity in humans. In this study, we evaluated the protective effects of N‐acetyl cysteine (NAC) on DIC‐induced nephrotoxicity. Rats were assigned to four groups. Group 1 was control group; group 2 administrated with DIC only; group 3 administrated with DIC plus NAC and group 4 was treated with DIC and silymarin. Then, the oxidative biomarkers in serum and kidney were evaluated. In group 2, DIC caused a remarkable elevation (p < 0.05) in the levels of serum uric acid, TNF‐α, creatinine, urea, GOT, and GPT, protein carbonyl, malondialdehyde (MDA), and renal TNF‐α gene expression, relative to control group. In treated groups with NAC and silymarin, a noticeable reduction (p < 0.05) was seen in mentioned levels of biochemical parameters. NAC showed that it could reduce the abnormality of biochemical parameters and histopathological changes which is induced by DIC. Practical applications N‐acetyl cysteine (NAC) has a potential to ameliorate renal histopathological changes and improving renal activity of antioxidant enzymes in nephrotoxicity by diclofenac. Also, NAC has a potential to reduce inflammatory gene expression in the diclofenac‐induced nephrotoxicity. Additionally, NAC can be considered as an antioxidant which reduces renal MDA and serum protein carbonyl due to nephrotoxicity by diclofenac.

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Section: Discussionmentioning

confidence: 99%

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Nouri

Heidarian

2019

J Food Biochem

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“…One of the most advantageous features of proanthocyanidin free radical scavenging activity is that it is easily incorporated within the cell membranes [9] . The presence of both, hydrophobic and hydrophilic residues within the flavan-3-ol molecule, allows these compounds to interact with phospholipid head groups and be adsorbed onto the surface of membranes [10] . Several authors have studied the mitoprotective effect of some types of flavonoids, such as resveratrol [11] and quercetin [12] .…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

2016

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The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats.

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“…Oral administration of GSP significantly reduces the postprandial levels of TG-rich and apolipoprotein-B-containing lipoproteins and improves several atherosclerotic risk indexes in normolipidemic rats (Delbas et al, 2005). We have studied the protective role of GSP on cadmium induced hepatic dysfunction in rats (Nazimabashir et al, 2014) now the present study was devoted to investigate the influence of (GSP) on some metabolic and biochemical changes associated with hyperglycemia, antihyperlipidemic and antiperoxidative effect on cadmium intoxicated rats.…”

Section: +mentioning

confidence: 99%

Ameliorative effects of grape seed proanthocyanidins on cadmium induced metabolic alterations in rats

Bashir

Manoharan

Prabu

2014

International Journal of Biological Research

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Objective: To study the ameliorative effects of grape seed proanthocyanidins (GSP) against cadmium (Cd) induced hyperglycemia, hypercholesterolemia and hyperlipidemia in rats. Methods: Wistar rats, body weight 180-200g, were randomly divided into four groups, six rats in each group. First group (control) represented the control animal, the second group (Cd) was fed orally with Cd in the form of CdCl 2 (5mg/kg bw), the third group (GSP) was fed with GSP (200 mg/kg bw) and to the fourth group (Cd+GSP), CdCl 2 was administered orally at a dose of (5 mg/kg bw) and pretreated with GSP (200 mg/kg bw) 90 min before Cd intoxication for 4 weeks. At the end of experiment, rats were sacrificed; blood and liver samples were collected and used for analysis of various metabolic parameters. Results: The result of the present study revealed that Cd exposure caused significant reduction in food intake and body weight gain, but increased the liver weight. GSP administration significantly revert all these changes to normal level. Cd intoxication induced hyperglycemia, elevate plasma glucose and lipid profiles and decline in high density lipoprotein (HDL) -cholesterol respectively. The GSP pretreatment regimen was beneficial in the restoration of the increased serum levels of TC, TG and lipid profiles and of the suppressed insulin and total antioxidants on Cd exposure. Conclusion: From the present investigation, it may be concluded that Cd intoxication caused deleterious effects on the metabolism of rats which were successfully restored by GSP. Therefore, the present work suggests that GSP is a feasible therapeutic agent to improve and treat patients with hyperlipidemia, obesity, hyperglycemia in addition to its anti-oxidant properties and can be used as a component in food to promote the health of people.

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Protective role of grape seed proanthocyanidins against cadmium induced hepatic dysfunction in rats

Cited by 19 publications

References 47 publications

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Ameliorative effects ofN‐acetyl cysteine on diclofenac‐induced renal injury in male rats based on serum biochemical parameters, oxidative biomarkers, and histopathological study

Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

Ameliorative effects of grape seed proanthocyanidins on cadmium induced metabolic alterations in rats

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