Chemoprotective Role of Triphala Against 1,2-Dimethylhydrazine Dihydrochloride Induced Carcinogenic Damage to Mouse Liver |
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| Authors: | Aditi Sharma Krishan Kumar Sharma |
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| Institution: | (1) Department of Biochemistry and Microbiology, Dr Rajendra Prasad Govt Medical College Kangra at Tanda, Himachal Pradesh, 176001, HP, India; |
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| Abstract: | The present study was carried out to investigate the protective role of Triphala (a combination in equal proportions by weight
of fruit powder of Terminalia belerica, Terminalia chebula and Emblica officinalis) against 1,2-dimethylhydrazinedihydrochloride (DMH) induced Endoplasmic reticulum stress (ER stress) in mouse liver. An oral
dose of 3 mg/kg body wt in drinking water for 5 weeks significantly (P < 0.001) increased the levels of serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase
(SGPT), serum Alkaline phosphatase (ALP) and total bilirubin thus suggesting damage to mouse liver and biliary dysfunction.
The DMH administration invariably led to increase in the liver microsomal proteins of molecular weight of about 29 (ERp29)
and 53 kDa (ERp53) and decrease in the protein of molecular weight of 36 kDa (ERp36) thereby suggesting the interference of
DMH and its metabolites with normal protein biosynthesis and folding, in the reticular membranes of the liver cells thus developing
ER stress. Histological studies show necrosis, large sized hepatocytes with increased N:C ratio, aberrant mitotic figures
and prominent nucleoli in the liver of DMH treated mice. In animals fed 5% Triphala in diet (w/w) during DMH administration,
there was significant decrease in the above changes in the liver suggesting the suppression of DMH induced ER stress in liver.
Triphala significantly (P < 0.05) decreased lipid peroxidation and also the activity of lactate dehydrogenase (LDH) in mouse liver. It simultaneously
increased the level of reduced glutathione (GSH) and the activity of glutathione-S-transferase (GST) thereby suggesting that
it prevents peroxidative damage and also diverts the active metabolites (electrophiles) of DMH from their interactions with
critical cellular bio-molecules which could be responsible for its protective action against DMH. |
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| Keywords: | 1 2-Dimethylhydrazinedihydrochloride Neoplastic lesions Triphala ER stress ERp29 ERp53 Antioxidant status Chemoprotective effect |
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