Protective effect of Amorphophallus campanulatus (Roxb.) Blume. tuber against thioacetamide induced oxidative stress in rats.

Biochemistry and Pharmacognosy Research Laboratory, School of Biosciences, M. G. University, P.D. Hills. P.O, Kottayam, Kerala-686560, India.
Asian Pacific Journal of Tropical Medicine (Impact Factor: 0.5). 11/2011; 4(11):870-7. DOI: 10.1016/S1995-7645(11)60211-3
Source: PubMed

ABSTRACT To identify the phytochemical constituents of Amorphophallus campanulatus (A. campanulatus) tuber and to evaluate its antioxidant potential through in vitro and in vivo models.
Phytochemical screening and in vitro antioxidant activities of A. campanulatus tuber n-hexane extract (ACHE) and methanolic extract (ACME) were evaluated using DPPH, hydroxyl radical, reducing power and total antioxidant capacity assays. The total phenolic and flavonoid contents were also investigated. The protective potential of two different doses of ACME (125 and 250 mg/kg) was also evaluated against thioacetamide (TAA) induced oxidative stress in rats. Silymarin used as a standard drug control. Hepatotoxicity was assessed by quantifying the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). The antioxidant potential of ACME were also evaluated by the estimation of catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (Thiobarbituric acid reactive substances) in hepatic and renal tissues. Histopathologic changes of liver were also evaluated.
In vitro studies revealed that ACME has higher antioxidant and radical scavenging activity than ACHE, which may be attributed to its higher phenolic and flavonoid content. ACME significantly prevented the elevation of serum AST, ALT, ALP, LDH, and tissue malondialdehyde levels(P < 0.05). Hepatic and renal GSH, GST, GR, GPx, and catalase levels were remarkably increased by the treatment with the extract. Quantification of histopathological changes also supported the dose dependent protective effects of ACME.
The results do suggest that A. campanulatus tuber could be considered as a potential source of natural antioxidant.

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    ABSTRACT: Colorectal cancer is one of the leading causes of cancer death worldwide and is the third most common form of malignancy in both men and women. Several possible colon cancer chemopreventive agents are found in edible plants. Amorphophallus campanulatus (Roxb.) Blume (family: Araceae) is a tuber crop, largely cultivated throughout the plains of India for using its corm as food. This tuber has also been traditionally used for the treatment of abdominal tumors, liver diseases, piles etc. The aim of this study was to evaluate the dose-dependent cytotoxic and apoptosis inducing effects of the sub fractions of Amorphophallus campanulatus tuber methanolic extract (ACME) viz. petroleum ether fraction (PEF), chloroform fraction (CHF), ethyl acetate fraction (EAF) and methanolic fraction (MEF) on colon cancer cell line, HCT-15. Antiproliferative effects of the sub fractions of ACME were studied by MTT assay. Apoptotic activity was assessed by DAPI, annexin V-FITC and JC-1 fluorescent staining. The chemotherapeutic drug, 5-flurouracil (5-FU) was used as positive drug control. The sub fractions of ACME significantly inhibited the proliferation of HCT-15 cells in a dose-dependent manner. In addition, the extracts were found to induce apoptosis and were confirmed by DAPI, annexin V-FITC and JC-1 fluorescent staining. A pronounced results of cytotoxic and apoptotic activities were observed in the cells treated with 5-FU and CHF, whereas, EAF and MEF treated cells exhibited a moderate result and the least effect were observed in PEF treated cells. Our results suggested that, among the sub fractions of ACME, CHF had potent cytotoxic and apoptotic activity and thus it could be explored as novel target for anticancer drug development. Furthermore, these findings confirm that the sub fractions of ACME dose-dependently suppress the proliferation of HCT-15 cells by inducing apoptosis.
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