Silymarin modulates the oxidant–antioxidant imbalance during diethylnitrosamine induced oxidative stress in rats

Pradeep, Kannampalli; Chandrasekaran, Victor Raj Mohan; Gobianand, Kuppannan; Karthikeyan, S.

doi:10.1016/j.ejphar.2006.12.023

Cited by 171 publications

(146 citation statements)

References 40 publications

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“…Recent studies shown that orally or subcutaneous IAA has no toxic action on rats leukocytes measured by analyzing the DNA integrity, membrane integrity, and enzyme activities. [12][13][14] However, the genotoxic carcinogen DEN induced extensive DNA damage 42 in accordance with the present study. Moreover, IAA was partially efficient in providing protection to DENinduction of DNA fragmentation; similarly, guarana has a protective effect against DEN-induced DNA damage in mouse liver.…”

Section: Discussionsupporting

confidence: 92%

Protective action of indole‐3‐acetic acid on induced hepatocarcinoma in mice

Mourão

Cruz

Paulo

et al. 2008

Cell Biochemistry & Function

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In this study, we report the protective effects of IAA on diethylnitrosamine (DEN)-induced hepatocarcinogenesis. BALB/c mice received daily IAA at 50 (T 50 ), 250 (T 250 ), and 500 (T 500 ) mg Kg À1 per body mass by gavage for 15 days. At day 15, animals were administered DEN and sacrificed 4 h later. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed in sera. In addition, hepatomorphologic alterations, activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), gene expression of antioxidant enzymes and DNA integrity were evaluated in the liver. IAA administration did not show any alterations in any of the parameters available, except for a reduction of the gene expression for antioxidant enzymes by 55, 56, 27, and 28% for SOD, CAT, GPx, and GR upon T 500 , respectively compared with the control. Several hepatic alterations were observed by DEN exposure. Moreover, IAA administration at 3 doses was shown to provide a total prevention of the active reduction of CAT and GR induced by DEN exposure compared with the control. IAA at T 500 was shown to give partial protection (87, 71, 57, and 90% for respectively SOD, CAT, GPx, and GR) on the down-regulation of the enzymes induced by DEN and this auxin showed a partial protection (50%) on DEN-induced DNA fragmentation for both parameters when compared to DEN alone. This work showed IAA hepatocarcinogenesis protection for the first time by means of a DEN-protective effect on CAT and GR activity, and by affecting antioxidant gene expression and DNA fragmentation.

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Section: Discussionsupporting

confidence: 92%

Protective action of indole‐3‐acetic acid on induced hepatocarcinoma in mice

Mourão

Cruz

Paulo

et al. 2008

Cell Biochemistry & Function

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“…On the contrary, it improved the antioxidant capacity and decreased the oxidative stress markers. These results are in accordance with the previous reports suggested that SIL possess antioxidant, antiapoptotic, anti-inflammatory and immunomodulatory properties (Al-Rasheed et al, 2015Fraschini et al, 2002;Karimi et al, 2011;Pradeep et al, 2007). The hepatoprotective role of SIL was suggested to be due to its enhancement of CYP2E1 activity which has a major role in drug metabolism (Dejanovic et al, 2014;Jorgačević et al, 2014;Mahli et al, 2015;Wong et al, 1998).…”

Section: Discussionsupporting

confidence: 91%

Inulin nanoparticles and silymarin counteract chlorpromazine-induced injury in the liver and kidney of rats

Abdel-Wahhab¹,

Eid²,

Ahmed³

et al. 2017

J App Pharm Sci

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The aim of the current study was to evaluate the protective role of inulin nanoparticles (INPs) prepared by the emulsion method alone or plus silymarin (SIL) against chlorpromazine (CPZ)-induced hepatonephrotoxicity in rats. Eleven groups of female Sprague-Dawley rats were treated orally for 3 weeks as follow: control group, the group treated with CPZ (38.7 mg/kg. b.w in 1 ml saline each 72 h), the groups treated with INPs at low (100 mg/kg b.w) or high (200 mg/ kg b.w) dose, the group treated with SIL (50 mg/kg b.w), the groups treated with SIL plus INPs at the two doses and the groups treated with CPZ plus SIL and INPs at the two tested doses. At the end of the treatment period, blood and tissue samples were collected for different biochemical and histological analyses. The results indicated that CPZ induced significant disturbances in liver and kidney function indices, oxidative stress markers, lipid profile, antioxidant enzyme activity and DNA fragmentation as well as the histological changes in the liver and kidney. SIL alone or plus INPs alone at the low or high dose induce insignificant changes in all the tested parameters or pathological changes in the liver and kidney. SIL and INPs at the two doses could induce a pronounced protection in liver and kidney of CPZ-treated animals due to their antioxidant activity and the role of INPs in the enhancement of SIL solubility. It could be concluded that INPs is a promise drug delivery for SIL and could prevent the liver and kidney injury induced by CPZ.

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“…Several reports have demonstrated a strong relationship between oxidative stress and cancer in the case of NDEA-induced hepatocellular carcinoma (HCC) (Pradeep et al 2007;Santos et al 2012;Paula Santos et al 2014). Since a growing body of evidence has suggested that epicatechins, which are found in large amounts in green tea, display anticancer and chemopreventive properties, we investigated whether catechin-rich yellow tea can provide some protection against NDEA-induced hepatocarcinogenesis in rats.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

Kujawska

Ewertowska

Adamska

et al. 2016

Pharmaceutical Biology

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Context Yellow tea containing the same catechins as other types of tea but in different proportions has been suggested to possess potent anticancer activities. Objective This study investigates the chemopreventive effect of yellow tea aqueous extract against N-nitrosodiethylamine (NDEA)-induced liver carcinogenesis in rats by employing histological and biochemical methods. Materials and methods Wistar rats were divided randomly into four groups: control (I), yellow tea (II), NDEA (III), and yellow tea + NDEA (IV). Groups II and IV were exposed via a diet to yellow tea extract in a concentration of 10 g/kg feed; groups III and IV received 0.01% NDEA in drinking water. The experiment lasted for 13 weeks. Results Daily intake of yellow tea in an average dose of 800 mg/kg b.w. alleviated the carcinogenic effect of NDEA as evidenced by reversed histopathological changes towards normal hepatocellular architecture and decreased lipid peroxidation, protein carbonyl formation, and DNA degradation by 64%, 37% and 15%, respectively, as compared with values obtained in NDEA alone-treated rats. Treatment with yellow tea extract caused protection of superoxide dismutase (SOD) and catalase (CAT); their activity was recovered by 47% and 12%, respectively, as compared with the NDEAtreated rats. Moreover, the extract normalized the NDEA-induced activity of paraoxonase 1 (PON1) and glutathione peroxidase (GPx), while a further increase in the level of reduced glutathione (GSH) was noticed. Conclusions On the basis of these findings, it can be concluded that treatment with yellow tea partially protected the livers of rats from NDEA-induced hepatocarcinogenesis and that its antioxidant activity contributed to this effect. ARTICLE HISTORY

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Silymarin modulates the oxidant–antioxidant imbalance during diethylnitrosamine induced oxidative stress in rats

Cited by 171 publications

References 40 publications

Protective action of indole‐3‐acetic acid on induced hepatocarcinoma in mice

Protective action of indole‐3‐acetic acid on induced hepatocarcinoma in mice

Inulin nanoparticles and silymarin counteract chlorpromazine-induced injury in the liver and kidney of rats

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

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