Protective effect of Pisonia aculeata on thioacetamide induced hepatotoxicity in rats

Anbarasu, C.; Balasubramanian, Ravikumar; Bhat, Krishna L.; Giridharan, John; Amuthan, Arul; Kumar, Satish

doi:10.1016/s2221-1691(12)60087-2

Cited by 23 publications

(14 citation statements)

References 12 publications

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“…Significant decrease in the body weight in animals treated with TAA could be attributed to the toxic effect of TAA decreasing the levels of nutrient absorption, energy utilization, and metabolic efficiency [8][9][10]13]. While animals treated with MSCs showed significant increase in the body weight that could be contributed to the effect of MSCs.…”

Section: Discussionmentioning

confidence: 97%

Use of Bone Marrow-Derived Mesenchymal Stem Cells in Improving Thioacetamide Induced Liver Fibrosis in Rats

Mansour

Shaheed

Hassan

2015

Springer Proceedings in Physics

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Liver fibrosis, is one of big problems usually ends with cirrhosis which considered a life threatening disease as the only way of treatment is the liver transplantation, this study aimed to find a new way for fibrosis treatment by the use of bone marrow isolated Mesenchymal stem cells (MSCs). Thioacetamide (TAA) was used for fibrosis induction in male Sprague Dawely (SD) rats which divided into two random groups: group infused with TAA for fibrosis induction and group as control negative group. MSCs were isolated from bone marrow of twenty five (4-5) weeks male SD rats, and labeled with fluorescent material (PKH26) to confirm the homing of cells. After fibrosis induction, rats were divided into four subgroups to study the effect of MSCs injection in fibrosis treatment. After 4 weeks from MSCs administration, all rats were sacrificed. Liver tissue were collected for histopathological and immunohistopathological studies. In comparison with control groups, the treated groups with MSCs showed improvement in the amount of deposited collagen which decreased compared to control positive group. So MSCs can be used to replace liver transplantation in the treatment of fibrosis.

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Section: Discussionmentioning

confidence: 97%

Use of Bone Marrow-Derived Mesenchymal Stem Cells in Improving Thioacetamide Induced Liver Fibrosis in Rats

Mansour

Shaheed

Hassan

2015

Springer Proceedings in Physics

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“…This leads to oxidative stress (Lena and Subramanian, 2004;Norenberg et al, 2004b), which eventually results in increased levels of lipid peroxidation products (MDA) and decreased levels of antioxidants (GSH and SOD) in TAA-treated rats. Consequently, CLF following TAA administration is well established by the elevated activities of liver transaminases (ALT and AST) in the present study, indicating cellular leakage and loss of functional integrity of hepatic membrane (Chen et al, 2008;AlAttar, 2012;Anbarasu et al, 2012;Farjam et al, 2012). The extensive liver injury induced by TAA through its free radical generation mechanism, which in turn has the ability to cause hepatic damage resulting in increased leakage of cellular enzymes.…”

Section: Resultsmentioning

confidence: 51%

“…Moreover, results demonstrated significant elevation in LP during TAA-induced HE in liver and brain. Most of the hepatotoxic agents including TAA damaged liver mainly by inducing lipid peroxidation (LPO) directly or indirectly (Sanz et al, 2002;Hessien et al, 2010;Chi et al, 2011;Anbarasu et al, 2012). As brain is structurally rich in polyunsaturated fatty acids and has high oxygen demand, making it the most vulnerable organ to undergo oxidative damage during un-physiological challenges.…”

Section: Resultsmentioning

confidence: 99%

“…These changes include necrosed hepatocytes, infiltrated and replaced by mononuclear inflammatory cells and perineuronal edema in brain (Kucera et al, 2011;Farjam et al, 2012).The hepatic architecture of TAA-treated rats resulted in necrotic changes and inflammatory cell infiltration, which basically supported the alterations observed in biochemical analysis. It might be due to TAA-intermediates and the reactive oxygen species that can covalently bind to biologically important molecules and increase cellular oxidative stress (Pallottini et al, 2006;Chilakapati et al, 2007), and lipid peroxidation, and glutathione depletion (Sanz et al, 2002;Kucera et al, 2011).TAA interferes with the movement of RNA from the nucleus to the cytoplasm which may cause membrane injury (Anbarasu et al, 2012), also astrogliosis was evaluated at the area of cerebellum and hippocampus in TAA-treated animals (Avraham et al, 2009), which may explain changes observed in brain histology. Alpha-LAC markedly counteracted the histological alterations induced by TAA in liver and brain tissues.…”

Section: Resultsmentioning

confidence: 99%

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Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Mansour¹,

Nada²,

Elmahmoudy³

et al. 2015

J App Pharm Sci

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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 alphalactalbumin (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.

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“…It removes free radical species such as hydrogen peroxide, superoxide radicals and maintains membrane protein thiols. 18 Prophylactic treatment with Silymarin (100 mg / kg) and UNLE at both doses (200 and 400 mg / kg) causes a significant increase in hepatic GSH, SOD and CAT activity and thus reduces reactive free radical induced oxidative damage to liver by decreasing LPO levels depicted in Table 4. From comparative histopathological study, the histological observations of the control animals showed normal hepatocytes with well preserved cytoplasm, prominent nucleus, nucleolus and central vein.…”

Section: Ementioning

confidence: 99%

Attenuating Effect of Uvaria Narum (Dunal) Wall. Leaves on Thioacetamide Induced Hepatic Injury

Patel¹,

Moses²,

Shenoy³

et al. 2013

Int. Res. J. Pharm.

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The objective of the present study was to evaluate the hepatoprotective potential of Uvaria narum leaf extract at two different doses (200 and 400 mg / kg b.w.) against thioacetamide induced Hepatic injury. Thioacetamide at dose of 100 mg / kg induced liver toxicity, which was assessed by quantifying the serum hepatic biomarkers like SGPT, SGOT, ALP, total and direct bilirubin, serum biochemical parameters like albumin, total protein, cholesterol, triglycerides, glucose and urea and oxidative parameters like glutathione, catalase, superoxide dismutase and lipid peroxidation in hepatic tissue. Further study was supported by histopathology studies. The results revealed that Silymarin (100 mg / kg b.w.) and Uvaria narum leaf extract at both doses prevented the elevation of serum hepatic biomarkers and also altered serum biochemical parameters dose dependently. Whereas decrease in lipid peroxidation and elevation in catalase, glutathione and superoxide dismutase was observed in Silymarin and extract treated animals. Histopathological changes in hepatic tissue also supported the dose dependent protective effect of Uvaria narum leaf extract. The results were comparable to reference standard Silymarin.

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Protective effect of Pisonia aculeata on thioacetamide induced hepatotoxicity in rats

Cited by 23 publications

References 12 publications

Use of Bone Marrow-Derived Mesenchymal Stem Cells in Improving Thioacetamide Induced Liver Fibrosis in Rats

Use of Bone Marrow-Derived Mesenchymal Stem Cells in Improving Thioacetamide Induced Liver Fibrosis in Rats

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Attenuating Effect of Uvaria Narum (Dunal) Wall. Leaves on Thioacetamide Induced Hepatic Injury

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