The protective effect of an aqueous extract from Smilax excelsa l. against carbon tetrachloride-induced liver injury in rats

Background: Because reactive oxygen species (ros) contribute to the pathogenesis of various acute and chronic liver diseases, dietary antioxidants and drugs from herbal origins have been proved to be beneficial as therapeutic agents in reversing hepatotoxicity and oxidative stress. The objective of this study was to investigate the protective effect of an aqueous extract from smilax excelsa l. Shoots and leaves against acute ccl4-induced liver injury as well as the changes in antioxidative defense system in female wistar albino rats.Materials and Methods: S. Excelsa extract was administered orally in doses of 100, 200 and 400 mg/kg body weight, once daily for 9 days. Acute hepatic toxicity was induced by intraperitoneal injection of ccl4 (1 ml/kg) on the 10th day. 24 h after ccl4 intoxication, biochemical and histopathological analyses were undertaken on sera and liver tissues.Results: Ccl4 challenge caused significant increases in the activities of liver enzymes as well as the levels of bilirubin, malondialdehyde and nitric oxide, while total serum protein levels and antioxidant defense system parameters were reduced significantly compared to the normal group. Administration of s. Excelsa extract at a dose of 400 mg/kg resulted in a suppression of ccl4-induced lipid peroxidation and altered oxidative stress parameters to nearly normal values in comparison to ccl4-treated rats. Nevertheless the extract did not reduce the extent of ccl4-induced mild liver injury, as seen by the histopathology of liver damage.Conclusion: The results of this study suggest that s. Excelsa could protect the liver tissues against ccl4-induced oxidative stress probably by increasing antioxidative defense activities.Keywords: Antioxidant enzymes, carbon tetrachloride, liver injury, smilax excelsa, hepatoprotective activit

THE PROTECTIVE EFFECT OF AN AQUEOUS EXTRACT FROM SMILAX EXCELSA L. AGAINST CARBON TETRACHLORIDE-INDUCED LIVER INJURY IN RATS

Background: Because reactive oxygen species (ros) contribute to the pathogenesis of various acute and chronic liver diseases, dietary antioxidants and drugs from herbal origins have been proved to be beneficial as therapeutic agents in reversing hepatotoxicity and oxidative stress. The objective of this study was to investigate the protective effect of an aqueous extract from smilax excelsa l. Shoots and leaves against acute ccl4-induced liver injury as well as the changes in antioxidative defense system in female wistar albino rats. Materials and Methods: S. Excelsa extract was administered orally in doses of 100, 200 and 400 mg/kg body weight, once daily for 9 days. Acute hepatic toxicity was induced by intraperitoneal injection of ccl4 (1 ml/kg) on the 10th day. 24 h after ccl4 intoxication, biochemical and histopathological analyses were undertaken on sera and liver tissues. Results: Ccl4 challenge caused significant increases in the activities of liver enzymes as well as the levels of bilirubin, malondialdehyde and nitric oxide, while total serum protein levels and antioxidant defense system parameters were reduced significantly compared to the normal group. Administration of s. Excelsa extract at a dose of 400 mg/kg resulted in a suppression of ccl4-induced lipid peroxidation and altered oxidative stress parameters to nearly normal values in comparison to ccl4-treated rats. Nevertheless the extract did not reduce the extent of ccl4-induced mild liver injury, as seen by the histopathology of liver damage. Conclusion: The results of this study suggest that s. Excelsa could protect the liver tissues against ccl4-induced oxidative stress probably by increasing antioxidative defense activities

The role of glucagon-like peptide-2 on apoptosis, cell proliferation, and oxidant-antioxidant system at a mouse model of intestinal injury induced by tumor necrosis factor-alpha/actinomycin D

Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine, which has the ability to produce cytotoxicity via induction of cell death and cell cycle arrest. Blocking the synthesis of protective proteins through a transcriptional inhibitor such as actinomycin D (Act D) sensitizes many cell types to TNF-alpha toxicity. Teduglutide, h[Gly(2)]GLP-2, is a protease-resistant synthetic analog of glucagon-like peptide-2 (GLP-2) which is an intestinotrophic peptide. In this study, we evaluated this potential of GLP-2 on apoptosis, cell proliferation, and oxidant-antioxidant system on a mouse model of intestinal injury induced by TNF-alpha/Act D. The intestinal injury was induced by intraperitoneal administration of 15 mu g/kg TNF-alpha and 800 mu g/kg Act D per mouse. Animals were injected subcutaneously 200 mu g/kg h[Gly(2)]GLP-2 every 12 h for 10 consecutive days prior to the administration of TNF-alpha and Act D. The model of intestinal injury induced by TNF-alpha/Act D, which is the new animal model for the intestinal disorders, was characterized by the degeneration of intestinal mucosa, an increase in apoptotic index, expression of active caspase-3, lipid peroxidation and glutathione (GSH) levels, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities; a decrease in cell proliferation and catalase (CAT) activity. h[Gly(2)]GLP-2 pretreatment prevented the TNF-alpha/Act D-induced oxidative injury by a significant reduction in the intestinal injury, apoptotic index, expression of active caspase-3, lipid peroxidation and GSH levels, GPx and SOD activities; a markedly increase in cell proliferation, and CAT activity. These results demonstrate that GLP-2 has a protective, antiapoptotic, proliferative, and antioxidant effects against to TNF-alpha/Act D-induced intestinal injury. It is suggested that GLP-2 may potentially be useful as a therapeutic agent in TNF-alpha-mediated intestinal disorders

The role of epidermal growth factor in prevention of oxidative injury and apoptosis induced by intestinal ischemia/reperfusion in rats

Intestinal ischemia/reperfusion is a major problem which may lead to multiorgan failure and death. The aim of the Study was to evaluate the effects of epidermal growth factor (EGF) on apoptosis, cell proliferation, oxidative stress and the antioxidant system in intestinal injury induced by ischemia/reperfusion in rats and to determine if EGF can ameliorate these toxic effects. Intestinal ischemia/reperfusion injury was produced by causing complete occlusion of the superior mesenteric artery for 60 thin followed by a 60-min reperfusion period. Animals received intraperitoneal injections of 150 mu g/kg human recombinant EGF 30 min prior to the mesenteric ischemia/reperfusion. Mesenteric ischemia/reperfusion caused degeneration of the intestinal mucosa, inhibition of cell proliferation, stimulation of apoptosis and oxidative stress in the small intestine of rats. In the ischemia/reperfusion group, lipid peroxidation was stimulated accompanied by increased intestinal catalase and glutathione peroxidase activities, however, glutathione levels and superoxide dismutase activities were markedly decreased. EGF treatment to rats with ischemia/reperfusion prevented the ischemia/reperfusion-induced oxidative injury by reducing apoptosis and lipid peroxidation, and by increasing antioxidant enzyme activities. These results demonstrate that EGF has beneficial antiapoptotic and antioxidant effects on intestinal injury induced by ischemia/reperfusion in rats. (C) 2013 Elsevier GmbH. All rights reserved

Galectin-1 reduces the severity of dextran sulfate sodium (DSS)-induced ulcerative colitis by suppressing inflammatory and oxidative stress response

Ulcerative colitis is an inflammatory bowel disease that affects a large number of people around the world. Galectin-1 is a β-galactoside-binding lectin with a broad range of biological activities. The effects of galectin-1 on dextran sulfate sodium (DSS)-induced ulcerative colitis in vivo is not clear. We investigated the effect of galectin-1 on colon morphology, cell proliferation, oxidative stress, antioxidant system, and proinflammatory/antiinflammatory cytokines in a DSS-induced mouse model of ulcerative colitis. Thirty-two C57BL/6 mice were randomly assigned to one of the four groups: control, acute colitis, galectin-1, and DSS+galectin-1. Controls were treated with phosphate-buffered saline (PBS) for seven days. Acute colitis was induced by 3% DSS in drinking water administered orally for five days. Mice in galectin-1 groups were treated with 1 mg/kg recombinant human galectin-1 in PBS for seven consecutive days. Oral DSS administration resulted in acute colitis by causing histopathological changes; an increase in disease activity index (DAI), lipid peroxidation (malondialdehyde [MDA]), myeloperoxidase (MPO), and tumor necrosis factor (TNF)-α levels; a decrease in body weight, colon length, cell proliferation index, catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, and GSH and interleukin (IL)-10 levels. The treatment with galectin-1 attenuated DSS-induced acute colitis by reducing DAI, MDA, MPO, and TNF-α levels and by increasing body weight, colon length, cell proliferation, antioxidant enzyme activity, GSH, and IL-10 levels. These findings suggest that galectin-1 has proliferative, antioxidant, antiinflammatory, and cytoprotective effects against DSS-induced ulcerative colitis in mice. Due to its antiinflammatory and antioxidant activity galectin-1 may be effective in preventing and treating ulcerative colitis

Galectin-1 reduces the severity of dextran sulfate sodium (DSS)-induced ulcerative colitis by suppressing inflammatory and oxidative stress response

Ulcerative colitis is an inflammatory bowel disease that affects a large number of people around the world. Galectin-1 is a beta-galactoside-binding lectin with a broad range of biological activities. The effects of galectin-1 on dextran sulfate sodium (DSS)-induced ulcerative colitis in vivo is not clear. We investigated the effect of galectin-1 on colon morphology, cell proliferation, oxidative stress, antioxidant system, and proinflammatory/antiinflammatory cytokines in a DSS-induced mouse model of ulcerative colitis. Thirty-two C57BL/6 mice were randomly assigned to one of the four groups: control, acute colitis, galectin-1, and DSS+galectin-1. Controls were treated with phosphate-buttered saline (PBS) for seven days. Acute colitis was induced by 3% DSS in drinking water administered orally for five days. Mice in galectin-1 groups were treated with 1 mg/kg recombinant human galectin-1 in PBS for seven consecutive days. Oral DSS administration resulted in acute colitis by causing histopathological changes; an increase in disease activity index (DAI), lipid peroxidation (malondialdehyde MDA]), myeloperoxidase (MPO), and tumor necrosis factor (TNF)-alpha levels; a decrease in body weight, colon length, cell proliferation index, catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, and GSH and interleukin (IL)-10 levels. The treatment with galectin-1 attenuated DSSinduced acute colitis by reducing DAI, MDA, MPO, and TNF-alpha levels and by increasing body weight, colon length, cell proliferation, antioxidant enzyme activity, GSH, and IL-10 levels. These findings suggest that galectin-1 has proliferative, antioxidant, antiinflammatory, and cytoprotective effects against DSS-induced ulcerative colitis in mice. Due to its antiinflammatory and antioxidant activity galectin-1 may be effective in preventing and treating ulcerative colitis