Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Chen, An-Shu; Taguchi, Tadao; Sakai, Kazuo; Matahira, Yoshiharu; Wang, Min Wei; Miwa, Ichitomo

doi:10.1248/bpb.28.1971

Cited by 39 publications

(17 citation statements)

References 15 publications

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“…Increased lipid peroxidation and impaired antioxidant enzyme function in the liver tissue are characteristic observations in PCM-treated rats (Weber et al, 2003). In the present study, MDA concentration significantly increased (p ˂ 0.05) 24hr after PCM treatment alone as demonstrated in other studies (Ohta et al, 1997;Chen et al, 2005).This elevated level of MDA in plasma or liver tissue caused by PCM treatment was significantly depressed by the pretreatment with ghrelin. This was attributed to the decreased bioactivation of PCM caused by the ghrelin pretreatment.…”

Section: Discussionsupporting

confidence: 83%

Protective effect of ghrelin on paracetamol induced acute hepatotoxicity in rats

Alantary¹,

Rezk²,

Soliman³

2014

J. Physiol. Pathophysiol.

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In this study we investigated if ghrelin plays a protective role against paracetamol-induced acute hepatotoxicity in rats and the possible mechanism of action. Forty adult male albino rats were divided into four equal groups; control, ghrelin, paracetamol and ghrelin plus paracetamol. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Liver histopathology was also performed. Paracetamol (PCM) treatment increased plasma and liver tissue malondialdehyde (MDA) content and plasma nitric oxide (NO) level, and decreased erythrocyte and liver tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities when compared to control group. At the same time, PCM treatment increased the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities. By contrast, ghrelin pretreatment reduced plasma and liver MDA content and plasma NO level, and increased erythrocyte, liver tissue SOD, CAT and GPx activities when compared with paracetamoltreated group. The PCM-induced histopathological changes were also reduced by the ghrelin pretreatment. In conclusion, our results proved that ghrelin was found to protect the liver against paracetamol-induced oxidative damage in rats and the hepatoprotective effect may be correlated with its antioxidant effect.

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Section: Discussionsupporting

confidence: 83%

Protective effect of ghrelin on paracetamol induced acute hepatotoxicity in rats

Alantary¹,

Rezk²,

Soliman³

2014

J. Physiol. Pathophysiol.

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“…agreement with the findings of Boll et al 36 and Chen et al 37 Boll et al 36 explained that the trichloromethyl radicals generated during the biotransformation of CCl 4 bind triacylglycerol and phospholipid, with phosphatidylcholine binding being the highest; the binding therefore promotes the peroxidation of these lipids. The ability of KV, FI, FII, and vitamin E to attenuate the toxic assault imposed on lipids by CCl 4 points to either their free radical-chain breaking or scavenging activities.…”

supporting

confidence: 88%

Hepatoprotective Activity of Purified Fractions fromGarcinia kolaSeeds in Mice Intoxicated with Carbon Tetrachloride

Adaramoye

Farombi

Nssien

et al. 2008

Journal of Medicinal Food

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The hepatoprotective activity of kolaviron (KV), a biflavonoid complex from Garcinia kola seeds, and its purified fractions was investigated in mice intoxicated with carbon tetrachloride (CCl(4)). The ability of vitamin E to attenuate the toxicity was also examined. KV was extracted from powdered seeds of G. kola and then separated by thin-layer chromatography into three fractions--Fraction I (FI), Fraction II (FII), and Fraction III (FIII), with ratio of fronts values of 0.48, 0.71, and 0.76, respectively. Pretreatment with KV, FI, and FII at a dose of 100 mg/kg of body weight for 2 weeks and then challenge with CCl(4) at a dose of 1.2 g/kg of body weight, three times a week for 2 consecutive weeks, decreased the CCl(4)-induced increase in activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) by 31%, 30%, and 31% and 41%, 55%, and 42%, respectively. CCl(4) intoxication also caused a significant (P < .05) accumulation of lipid peroxidation (LPO) products as revealed by the formation of the thiobarbituric acid-reactive substances: CCl(4) induced LPO levels in serum and microsomes by 112% and 89%, respectively. However, pretreatment with KV, FI, and FII decreased LPO levels in serum by 31%, 41%, and 40% and in microsomes by 48%, 39%, and 35%, respectively. Vitamin E was protective in reducing the CCl(4)-induced increase in levels of AST, ALT, and gamma-glutamyl transferase as well as LPO. Furthermore, CCl(4) intoxication significantly (P < .05) decreased the activities of microsomal glucose-6-phosphatase, aniline hydroxylase, and cytosolic glutathione-S-transferase (GST). While pretreatments with KV, FI, and FII were able to ameliorate the levels of glucose-6-phosphatase and GST, there were no significant (P > .05) effects on the levels of aniline hydroxylase and DT-diaphorase. This study confirms that FI and FII from KV enhanced recovery from CCl(4)-induced hepatotoxicity by decreasing the extent of LPO and also inducing the levels of phase II enzyme (GST). These fractions are responsible for the observed antihepatotoxic effect of KV.

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“…It is known that chitosan is not to be absorbable by orally administration on account of only chitobiose or chitotriose can be absorbed by the digestive tract among various chitooligosaccharides (Chen et al, 2005). In previous study, 85% of FITC-CM-chitosan was excreted in urine within 11 d. Our present work showed that through the intraperitoneal injection of FITC-HP-chitosan at a dose of 10 mg per rat, 98.62% of the content was rapidly absorbed in 24 h, 88.47% was excreted in urine within 11 d. The GPC analysis in vivo and in vitro also indicated that a significant degradation process occurred in abdominal cavity, plasma and liver.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and biodegradation performance of a hydroxypropyl chitosan derivative

Shao

Han

Dong

et al. 2015

J. Ocean Univ. China

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Hydroxypropyl chitosan (HP-chitosan) has been shown to have promising applications in a wide range of areas due to its biocompatibility, biodegradability and various biological activities, especially in the biomedical and pharmaceutical fields. However, it is not yet known about its pharmacokinetics and biodegradation performance, which are crucial for its clinical applications. In order to lay a foundation for its further applications and exploitations, here we carried out fluorescence intensity and GPC analyses to determine the pharmacokinetics mode of fluorescein isothiocyanate-labeled HP-chitosan (FITC-HP-chitosan) and its biodegradability. The results showed that after intraperitoneal administration at a dose of 10 mg per rat, FITC-HP-chitosan could be absorbed rapidly and distributed to liver, kidney and spleen through blood. It was indicated that FITC-HP-chitosan could be utilized effectively, and 88.47% of the FITC-HP-chitosan could be excreted by urine within 11 days with a molecular weight less than 10 kDa. Moreover, our data indicated that there was an obvious degradation process occurred in liver (< 10 kDa at 24 h). In summary, HP-chitosan has excellent bioavailability and biodegradability, suggesting the potential applications of hydroxypropyl-modified chitosan as materials in drug delivery, tissue engineering and biomedical area.

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Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Cited by 39 publications

References 15 publications

Protective effect of ghrelin on paracetamol induced acute hepatotoxicity in rats

Protective effect of ghrelin on paracetamol induced acute hepatotoxicity in rats

Hepatoprotective Activity of Purified Fractions fromGarcinia kolaSeeds in Mice Intoxicated with Carbon Tetrachloride

Pharmacokinetics and biodegradation performance of a hydroxypropyl chitosan derivative

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