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 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

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

The role of zinc sulfate and metallothionein in protection against ethanol-induced gastric damage in rats

In this study, the effects of zinc sulfate against ethanol-induced acute gastric damage in rats were investigated, morphologically and biochemically. In addition, the present investigation has demonstrated the distribution of metallothionein stimulated by zinc in gastric mucosal tissues, immunohistochemically. The gastric damage was induced by intragastric administration of I ml absolute ethanol per rat. Rats received zinc sulfate (100 mg/kg/day) for 3 consecutive days 2 hr prior to the administration of absolute ethanol. Acute ethanol exposure caused degenerative morphological changes, a decrease in metallothionein immunreactivity; an increase in lipid peroxidation (LPO) levels, and a decrease in reduced glutathione (GSH) levels in gastric mucosa. On the other hand, zinc sulfate administration to ethanol-treated rats caused a significant reduction in the histological damage, an increase in metallothionein immunreactivity, a decrease in LPO levels, and an increase in GSH levels in gastric mucosa. As a result, the present study indicates that zinc sulfate has a protective effect against ethanol-induced acute gastric damage. In addition, we might say that the zinc given as exogenous protection against acute gastric damage has a protective effect both by stimulation of metallothionein synthesis and through GSH as well as having antioxidative potential

Zinc Prevents Ethanol-Induced Oxidative Damage in Lingual Tissues of Rats.

The current study was designed to investigate the effects of zinc sulfate on cell proliferation, metallothionein (MT) immunoreactivity and antioxidant system against acute ethanol-induced oxidative damage in tongue tissues of rats. Wistar albino male rats, 2.5 to 3.0 months, were divided into four groups: Group I (n = 8), intact control rats; group II (n = 8), control animals given only zinc sulfate (100 mg/kg/day, for 3 consecutive days); group III (n = 14), animals given 1 mL absolute ethanol; group IV (n = 11), animals given zinc sulfate and absolute ethanol at the same dose and time. Animals were sacrificed under anesthesia 2 h after ethanol administration or 4 h after the last zinc sulfate treatment. Ethanol administration caused a marked decrease in the number of MT immunopositive cells and the proliferating cells in the lingual epithelium. A statistically significant decline in reduced glutathione levels, catalase activity and superoxide dismutase activities was also observed, whereas a significant elevation of lipid peroxidation levels and lactate dehydrogenase activities was detected in the ethanol group. In contrast, these changes were reversed by administration of zinc sulfate to ethanol-treated rats. In conclusion, it shows that zinc sulfate has therapeutic effects on acute ethanol-induced oxidative damage in the tongue tissues of rats

The effects of vitamins and selenium mixture or ranitidine against small intestinal injury induced by indomethacin in adult rats.

This study was aimed at investigating morphological and biochemical efficacies of antioxidants on indomethacin-induced small intestinal damage in rats. Group I: control animals (negative control) given only placebo, Group II: (positive control) are animals orally given combination of antioxidants [vitamin C (Vit C), vitamin E (Vit E), beta-carotene and sodium selenite (Se)] daily for 3 days, Group III: Rats were given only indomethacin, Group IV: animals were given of antioxidants combination for 3 days, last dose was given 2 hr before the administration of indomethacin. Group V: Animals receiving ranitidine for 3 days (second positive control). Group VI: Animals received ranitidine for 3 days, last dose was given 2 hr before to indomethacin administration. Indomethacin caused degenerative morphological and biochemical changes, which were reversed on antioxidants administration. As a result, we propose that antioxidants combination would be therapeutically beneficial for treating indomethacin-induced lesions of small intestine. Practical applications Indomethacin is a widely preferred nonsteroidal anti-inflammatory drug (NSAID) but its side effects on gastrointestinal system are well known. Indomethacin also causes production of reactive oxygen species. Antioxidants and selenium has protective effects. According to the results of this study, antioxidants and selenium can be used as a food supplement for preventing NSAID-induced side effects and toxicity