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The effects of administration of Embelin (EMB) and Curcumin (CUR) on lipid peroxidation, hepatic glutathione antioxidant defense and hematopoietic cells were examined during N-nitrosodiethylamine (DENA-200 mg kg(-1)body wt, single I.P injection) initiated and Phenobarbital (PB-0.05% in drinking water orally for 13 weeks) promoted hepatocarcinogenesis in Wistar strain male albino rats. DENA/PB-induced hepatic damage was manifested by a significant drop in the hepatic glutathione antioxidant defense, increased lipid peroxidation and histological alterations like dysplasia, and atypical cells with abnormal chromatin pattern. Treatment with Curcumin (100 mg kg(-1)body wt) and Embelin (50 mg kg(-1)body wt) prevented the drop in hepatic glutathione antioxidant defense, decreased lipid peroxidation, minimized the histological alterations induced by DENA/PB, but showed toxic effects on the hematopoietic cells. Results indicate the beneficial effects of Embelin and Curcumin against oxidative tissue damage during chemically-induced hepatocarinogenesis in rats.

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Background Embelin is a benzoquinone reported to possess anticancer activity in several in vivo and in vitro models of carcinogenesis, especially hematopoietic and prostate malignancy. A detailed investigation on the influence of embelin on epithelial malignancy model system, especially colon adenocarcinoma, is lacking. The objective of the current study is to investigate the antiproliferative, antiinvasive and proapoptotic potential of embelin on colon adenocarcinoma cell line HT-29. Methods The effect of embelin (35 µg/mL for 24 h) on cell proliferation was assessed by Sulforhodamine B assay and bromodeoxyuridine incorporation test, antiinvasive effect by Boyden chamber assay and scratch assay. Proapoptotic effects of embelin were determined by studies on DNA fragmentation, annexin V-FITC labeling, TUNEL assay, COMET assay and assay of caspase-3 activity. Influence of embelin on the expression of genes regulating apoptosis (caspase 3 and 9, Bcl-2, Bax, cytochrome C and X-linked inhibitor of apoptosis protein) and migration/invasion (matrix metalloproteinase [MMP]-2 and MMP-9) was investigated by reverse transcription polymerase chain reaction (PCR). Further, the effect of embelin on the levels of reactive oxygen species (ROS), lipid peroxides, nitric oxide, mitochondrial membrane potential and antioxidant status (total reduced glutathione [GSH] and GSH-S-transferase) was evaluated. Results Results implicated that embelin treatment inhibited proliferation (IC50 35 µg/mL), induced DNA fragmentation, phosphatidyl serine externalization, increased caspase expression, decreased cell migration and expression of MMPs in HT-29 cells. Interestingly, embelin exhibited prooxidant effect on HT-29 cells and induced excessive ROS generation resulting in apoptotic cell death. Conclusions To conclude, embelin treatment could be a promising strategy for the chemotherapy of colon cancer.

Allurement of herbs as health beneficial foods (physiologically functional foods) and as a source material for the development of new drugs, has led to greater furtherance in the study of herbal medicines during recent years. Plant extracts are being utilized to treat a wide variety of diseases like hepatotoxicity. Premna tomentosa is one such medicinal plant used widely in Indian ayurvedic medicine for the treatment of liver disorders. This study appraised the effectiveness of P. tomentosa leaf extract in protecting the liver against mitochondrial damage induced by acetaminophen, since mitochondrial injury has been investigated as a potential initiator of hepatotoxicity. Normal Wistar strain rats were pre-treated with P. tomentosa extract (750 mg/kg, orally) for 15 days and then intoxicated with acetaminophen (640 mg/kg, orally). Mitochondria were isolated from liver of experimental animals and assessed for the levels of lipid peroxide products, GSH and mitochondrial enzymes (isocitrate dehydrogenase, alpha-keto glutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and cytochrome-C-oxidase). The levels of Lipid peroxidation products were increased and the levels of the other assessed parameters were significantly decreased in hepatotoxicity induced animals. Whereas, the levels were brought back to normal in P. tomentosa pre-treated rats, which shows the protective effect of the extract against mitochondrial damage. Presence of anti-oxidant compound D-limonene (58%) in P. tomentosa leaves, which is known to enhance conjugation of toxic metabolites by maintaining liver GSH concentrations may explain the hepatoprotective property of the extract.