Protective role of catechin on D-galactosamine induced hepatotoxicity through a p53 dependent pathway

P. Vasanth Raj, K. Nitesh, S. Sagar Gang, V. Hitesh Jagani, H. Raghu Chandrashekhar, J. Venkata Rao, C. Mallikarjuna Rao, N. Udupa

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Objective of this study was to obtain a better understanding of the mechanism responsible for the D-galactosamine (D-GalN) induced hepatotoxicity and to study the effect of catechin against D-GalN induced hepatotoxicity. Catechin 50 and 100 mg/kg b.wt was administered for 1 week by oral route. Liver damage was induced by intra-peritoneal administration of 400 mg/kg b.wt D-galactosamine on the last day of catechin treatment. At the end of treatment all animals were killed and liver enzyme levels were estimated. Dissected hepatic samples were used for histopathology, RNA isolation, expression studies of Bax, Bcl-2 and p53 mRNA levels and mitochondrial membrane potential studies. We found that increases in the liver enzyme activity and decrease in antioxidant enzyme activity by D-GalN were significantly restricted by oral pretreatment with catechin. Disruption of mitochondrial membrane potential, up regulation of p53, Bax and down regulation of Bcl-2 mRNA levels in the liver of D-GalN intoxicated rats were effectively prevented by pretreatment with catechin.

Original languageEnglish
Pages (from-to)349-356
Number of pages8
JournalIndian Journal of Clinical Biochemistry
Volume25
Issue number4
DOIs
Publication statusPublished - 2010

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Galactosamine
Catechin
Liver
Mitochondrial Membrane Potential
Enzyme activity
4 alpha-glucanotransferase
Membranes
Messenger RNA
Enzymes
Rats
Animals
Up-Regulation
Down-Regulation
Antioxidants
RNA

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry

Cite this

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abstract = "Objective of this study was to obtain a better understanding of the mechanism responsible for the D-galactosamine (D-GalN) induced hepatotoxicity and to study the effect of catechin against D-GalN induced hepatotoxicity. Catechin 50 and 100 mg/kg b.wt was administered for 1 week by oral route. Liver damage was induced by intra-peritoneal administration of 400 mg/kg b.wt D-galactosamine on the last day of catechin treatment. At the end of treatment all animals were killed and liver enzyme levels were estimated. Dissected hepatic samples were used for histopathology, RNA isolation, expression studies of Bax, Bcl-2 and p53 mRNA levels and mitochondrial membrane potential studies. We found that increases in the liver enzyme activity and decrease in antioxidant enzyme activity by D-GalN were significantly restricted by oral pretreatment with catechin. Disruption of mitochondrial membrane potential, up regulation of p53, Bax and down regulation of Bcl-2 mRNA levels in the liver of D-GalN intoxicated rats were effectively prevented by pretreatment with catechin.",
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Protective role of catechin on D-galactosamine induced hepatotoxicity through a p53 dependent pathway. / Vasanth Raj, P.; Nitesh, K.; Sagar Gang, S.; Hitesh Jagani, V.; Raghu Chandrashekhar, H.; Venkata Rao, J.; Mallikarjuna Rao, C.; Udupa, N.

In: Indian Journal of Clinical Biochemistry, Vol. 25, No. 4, 2010, p. 349-356.

Research output: Contribution to journalArticle

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AU - Nitesh, K.

AU - Sagar Gang, S.

AU - Hitesh Jagani, V.

AU - Raghu Chandrashekhar, H.

AU - Venkata Rao, J.

AU - Mallikarjuna Rao, C.

AU - Udupa, N.

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AB - Objective of this study was to obtain a better understanding of the mechanism responsible for the D-galactosamine (D-GalN) induced hepatotoxicity and to study the effect of catechin against D-GalN induced hepatotoxicity. Catechin 50 and 100 mg/kg b.wt was administered for 1 week by oral route. Liver damage was induced by intra-peritoneal administration of 400 mg/kg b.wt D-galactosamine on the last day of catechin treatment. At the end of treatment all animals were killed and liver enzyme levels were estimated. Dissected hepatic samples were used for histopathology, RNA isolation, expression studies of Bax, Bcl-2 and p53 mRNA levels and mitochondrial membrane potential studies. We found that increases in the liver enzyme activity and decrease in antioxidant enzyme activity by D-GalN were significantly restricted by oral pretreatment with catechin. Disruption of mitochondrial membrane potential, up regulation of p53, Bax and down regulation of Bcl-2 mRNA levels in the liver of D-GalN intoxicated rats were effectively prevented by pretreatment with catechin.

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