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: 0.93).
11/2011; 4(11):870-7. DOI: 10.1016/S1995-7645(11)60211-3
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.
Available from: Sherein, Saied Abdelgayed
- "Thioacetamide is metabolized to acetamide and thioacetamideـــsــoxide. The latter binds to tissue macromolecules and is responsible for the change in cell permeability, increased intracellular concentration of Ca ++ , increase in nuclear volume and enlargement of nucleoli and inhibits mitochondria activity eventually leading to hepatic necrosis (Ansil et al., 2011). Histopathological studies of liver and brain tissue of TAA rats confirmed hepatic necrosis and mononuclear inflammatory cells infiltration. "
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ABSTRACT: Hepatic encephalopathy (HE) is a syndrome resulting from acute or chronic liver failure. The main hypothesis suggests a state of hyperammonemia which is responsible for both direct and indirect alterations in cerebral metabolism with increased production of reactive oxygen and nitrogen species. The effect of milk-derived alpha-lactalbumin (α-LAC) and vitamin C (vit. C) was evaluated in thioacetamide (TAA)-induced HEmodel in the current study. Animals were treated with TAA (100 mg/kg, i.p.) or saline thrice weekly for six weeks to induce HE then treatment groups received orally α-LAC (100 or150 mg/kg) and /or vit. C (500 mg/kg)daily for two weeks. Twenty-four hours after last treatment sera, liver and brain samples were collected to assess serum ammonia level, activities of alanine transaminase (ALT), and aspartate transaminase (AST), brain and liver oxidative stress parameters as well as histopathological investigations.TAA rats experienced increases in serum activities of ALT and AST as well as serum levels of ammonia. Furthermore, TAA induced hepatic and brain oxidative damage as indicated by increase in lipid peroxidation (LP), decrease in reduced glutathione (GSH) and decrease in superoxide dismutase (SOD) activity as well as increased nitric oxide (NO) levels. TAA caused distortion of hepatic and brain architecture as shown by histopathological examination. Treatment with α-LAC either alone or combined with vit. C resulted in improved liver functions by decline in serum AST and ALT activities and reduction in serum ammonia level. Alpha-LAC and vit. C reduced LP and NO levels while increased GSH concentration and SOD activity in hepatic and brain tissues. Finally, α-LAC-vit. C combination improved the hepatic and brain histological picture. Alpha-LAC-vit. C combination may be a promising pharmacological tool in providing a natural source of branched-chain amino acids and powerful antioxidants to combat hepatic encephalopathy-associated hyperammonemia and its consequential oxidative damage in liver and brain.
Journal of Applied Pharmaceutical Science 01/2015; 5(9):072-081. DOI:10.7324/JAPS.2015.50914 · 0.47 Impact Factor
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To evaluate the antioxidant and antihepatotoxic effect of methanolic extract of Gardenia gummifera Linn. f. root (MEGG) on thioacetamide (TAA) induced oxidative stress in male Wistar rats.Methods
In the preventive study, rats were administered with 125 and 250 mg/kg of MEGG for 9 days prior to TAA administration (100 mg/kg s.c.). In post-treatment groups, rats were treated with MEGG at doses of 125 and 250 mg/kg, 2, 24 and 48 h after TAA intoxication. Silymarin was used as a standard drug control (100 mg/kg). 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 MEGG was 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 (TBARS)] in hepatic and renal tissues. Histopathological changes were also evaluated.ResultsMEGG significantly (P≤0.05) prevented the elevation of serum AST, ALT, ALP, LDH and tissue malondialdehyde levels in both experimental groups, when compared to the TAA alone treated groups. The rats receiving TAA plus MEGG exhibited significant (P≤0.05) increases in hepatic and renal antioxidant activities including GSH, GST, GR, GPx and CAT levels. Quantification of histopathological changes also supported the dose dependent protective effects of MEGG.Conclusions
These observations suggest that MEGG has dose dependent hepatoprotective and antioxidant effect against TAA induced oxidative stress.
Asian Pacific Journal of Tropical Disease 04/2012; 2(2):90–98. DOI:10.1016/S2222-1808(12)60023-1
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ABSTRACT: A comparison of analysis in evaluating the hepatoprotective action of fractional ethanolic (F0), ethyl acetic (F1), n-butanol (F2) and aqueous (F3) extracts of E. ulmoides Oliv. (EUO) against thioacetamide (TAA) induced hepatic damage was studied in mice. The extract (453 mg/kg-F0, 104 mg/kg-F1, 95 mg/kg-F2 and 237 mg/kg-F3 body weight, po, once daily for 15 days) restored serum marker enzymes levels to normal in TAA treated mice. The biochemical biomarkers viz., total protein, albumin and total bilirubin were also restored forward normal level expression pattern of liver protein profile of mice by using sodium dodecyl sulfate polyacrylamide gel electrophoresis and two-dimensional gel electrophoresis showed 144 spots in TAA administered group which were significantly reduced in EUO extracts treated group. Among the four extracts ethyl acetate (F1) and n-butanol (F2) extracts showed more significant liver protection. TAA induced injury can be correlated with its high phenolic content in these extracts which may have hepatoprotective effects in regulating liver proteins by scavenging free radicals.
Indian journal of experimental biology 12/2012; 50(12):875-82. · 0.84 Impact Factor
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