Hepatoprotective and Antioxidant Effects of Saponarin, Isolated from<i>Gypsophila trichotoma</i>Wend. on Paracetamol-Induced Liver Damage in Rats

Simeonova, Rumyana; Vitcheva, Vessela; Kondeva-Burdina, Magdalena; Krasteva, Ilina; Manov, Vasil; Mitcheva, Mitka

doi:10.1155/2013/757126

Cited by 54 publications

(43 citation statements)

References 32 publications

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“…This shows that the plasma MDA level can be used as a biomarker for oxidative stress [ 13 ]. The MDA value of the liver tissue was detected to be increased in the group with induced paracetamol toxicity and the values obtained were in line with the results from the recent relevant trials [ 14 – 16 ]. In our trial, we detected that the increased oxidative stress could be prevented by leptin.…”

Section: Discussionsupporting

confidence: 88%

Assessing the Effect of Leptin on Liver Damage in Case of Hepatic Injury Associated with Paracetamol Poisoning

Polat

Cerrah

Albayrak

et al. 2015

Gastroenterology Research and Practice

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Background Aim. In case of high-dose acetaminophen intake, the active metabolite can not bind to the glutathione, thereby inducing cellular necrosis through binding to the cytosol proteins. This trial was performed to histologically and biochemically investigate whether leptin was protective against liver damage induced by paracetamol at toxic doses. Material and Method. In our trial, 30 female rats, divided into 5 groups, were used. IP leptin administration was performed after an hour in the group of rats, in which paracetamol poisoning was induced. The groups were as follows: Group 1: the control group, Group 2: 20 µg/kg leptin, Group 3: 2 g/kg paracetamol, Group 4: 2 g/kg paracetamol + 10 µg/kg leptin, and Group 5: 2 g/kg paracetamol + 20 µg/kg leptin. Results. The most significant increase was observed in the PARA 2 g/kg group, while the best improvement among the treatment groups occurred in the PARA 2 g/kg + LEP 10 µg/kg group (p < 0.05). While the most significant glutathione (GSH) reduction was observed in the PARA 2 g/kg group, the best improvement was in the PARA 2 g/kg + LEP 10 µg/kg group (p < 0.05). Conclusion. Liver damage occurring upon paracetamol poisoning manifests with hepatocyte breakdown occurring as a result of inflammation and oxidative stress. Leptin can prevent this damage thanks to its antioxidant and anti-inflammatory efficacy.

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Section: Discussionsupporting

confidence: 88%

Assessing the Effect of Leptin on Liver Damage in Case of Hepatic Injury Associated with Paracetamol Poisoning

Polat

Cerrah

Albayrak

et al. 2015

Gastroenterology Research and Practice

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“… reported that APAP intoxication raises MDA and decreases GSH levels in rats. Similarly, a statistically significant increase in MDA quantity and depletion in GSH levels have been shown both in vitro and in vivo . Because of the inhibition of lipid peroxidation by the defence mechanisms of the body itself, the reduced lipid peroxidation cannot cause this severe hepatic injury alone.…”

Section: Discussionmentioning

confidence: 98%

Biochemical and Histological Effects of Thiamine Pyrophosphate against Acetaminophen‐Induced Hepatotoxicity

Uysal

Dağlı

Yılmaz

et al. 2015

Basic Clin Pharma Tox

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The aim of this study was to investigate whether thiamine pyrophosphate (TPP) has biochemical and histological preventive effects on oxidative liver damage induced by paracetamol (APAP). Rats were divided into the following groups: healthy control (HG), APAP (AG, 1500 mg/kg, orally), thiamine pyrophosphate (TPPG, 100 mg/kg, intraperitoneally), APAP+NAC (ANAC, 100 mg/kg, intraperitoneally), APAP+TPP (ATPG) and APAP+NAC+TPP (ANTG). Oxidant, antioxidant parameters, liver function tests and histological assessment were performed between groups. Malondialdehyde levels in the AG, HG, TPPG, ANAC, ATPG and ANTG groups were 0.470 AE 0.210, 0.213 AE 0.004, 0.194 AE 0.001, 0.197 AE 0.06, 0.199 AE 0.008 and 0.173 AE 0.010 lmol/g protein, respectively. Total glutathione levels were 7.787 AE 0.395, 14.925 AE 0.932, 13.200 AE 0.984, 13.162 AE 0.486, 13.287 AE 0.787 and 13.500 AE 0.891 lM/g protein, respectively. In the AG group, marked liver damage occurred with the elevation of liver function tests and oxidative stress markers, such as malondialdehyde, myeloperoxidase and nitric oxide (p < 0.05). Biochemical results were congruent with the histological changes of oxidative damage. Compared to the AG group (p < 0.05), TPP significantly reduced oxidant parameter levels in the ATPG group and simultaneously increased the antioxidant parameter levels of catalase and glutathione. The histological changes were improved to almost normal hepatic structure. Moreover, TPP had nearly the same hepatoprotective effect as NAC, and there was statistically no additional benefit with NAC co-treatment. There was no statistically significant difference (p > 0.05) among the ANAC, ANTG and ATPG groups in terms of oxidant/ antioxidant levels. TPP proved to be as efficacious as standard therapy and may be beneficial in APAP-induced hepatotoxicity.Acetaminophen (Paracetamol, APAP) is widely used for its antipyretic and analgesic efficacy. APAP is safe and has few side effects when used at therapeutic levels. However, an overdose either in therapeutic contexts or in suicide can induce severe hepatotoxicity and acute liver failure [1,2]. Nearly 50% of all acute liver failure cases are due to APAP toxicity and carry 30% mortality [3]. In the United States, more than 100,000 cases of APAP intoxication occur annually [4]. Hepatotoxicity is the outcome of the reactive, toxic metabolite of APAP. If taken at recommended daily doses, nearly 85-90% of APAP is metabolized by glucuronidation and sulphation in the liver and subsequently excreted in the urine. In normal conditions, reactive metabolite N-acetyl-p-benzo-quinoneimine (NAPQI) is detoxified by endogenous glutathione (GSH). However, after APAP overdose, the GSH stores are depleted and sufficient NAPQI detoxification cannot be processed. This leads NAPQI to covalently bind to intracellular proteins [5]. Covalent binding is thought to be the progenitor mechanism of centrilobular hepatic necrosis, causing oxidative stress, lipid peroxidation and the depletion of protein thiols [6].In APAP hepatot...

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“…Silymarin has hepatoprotective properties and is used in treatment of various liver diseases [ 11 ]. Various studies indicate that Silymarin exhibits strong antioxidant activity [ 36 ] and shows protective effects against hepatic toxicity induced by a wide variety of agents by inhibiting lipid peroxidation [ 30 , 37 ]. Higher total phenolic content has been known to contribute to the antioxidant activity of extracts [ 38 ], while antioxidant activity has also been linked to the hepatoprotective effect of some extracts [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective Effect of Silymarin (Silybum marianum) on Hepatotoxicity Induced by Acetaminophen inSpontaneously Hypertensive Rats

Freitag

Cardia

Rocha

et al. 2015

Evidence-Based Complementary and Alternative Medicine

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This study was aimed to investigate the effect of Silymarin (SLM) on the hypertension state and the liver function changes induced by acetaminophen (APAP) in spontaneously hypertensive rat (SHR). Animals normotensive (N) or hypertensive (SHR) were treated or not with APAP (3 g/kg, oral) or previously treated with SLM. Twelve hours after APAP administration, plasmatic levels of liver function markers: alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose (GLU), gamma glutamyl transferase (γ-GT), and alkaline phosphatase (ALP) of all groups, were determined. Liver injury was assessed using histological studies. Samples of their livers were then used to determine the myeloperoxidase (MPO) activity and nitric oxide (NO) production and were also sectioned for histological analysis. No differences were observed for ALT, γ-GT, and GLU levels between SHR and normotensive rats groups. However, AST and ALP levels were increased in hypertensive animals. APAP treatment promoted an increase in ALT and AST in both SHR and N. However, only for SHR, γ-GT levels were increased. The inflammatory response evaluated by MPO activity and NO production showed that SHR was more susceptible to APAP effect, by increasing leucocyte infiltration. Silymarin treatment (Legalon) restored the hepatocyte functional and histopathological alterations induced by APAP in normotensive and hypertensive animals.

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Hepatoprotective and Antioxidant Effects of Saponarin, Isolated fromGypsophila trichotomaWend. on Paracetamol-Induced Liver Damage in Rats

Cited by 54 publications

References 32 publications

Assessing the Effect of Leptin on Liver Damage in Case of Hepatic Injury Associated with Paracetamol Poisoning

Assessing the Effect of Leptin on Liver Damage in Case of Hepatic Injury Associated with Paracetamol Poisoning

Biochemical and Histological Effects of Thiamine Pyrophosphate against Acetaminophen‐Induced Hepatotoxicity

Hepatoprotective Effect of Silymarin (Silybum marianum) on Hepatotoxicity Induced by Acetaminophen inSpontaneously Hypertensive Rats

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