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

Cyclic Dodecapeptide Induces Cell Death Through Membrane-Peptide Interactions in Breast Cancer Cells

Antimicrobial peptides (AMPS) are present in many organisms ranging from insects to mammals. They have a selectivity as cationic and amphiphilic alpha-helical peptide molecules and might interact with tumor cell membranes. In this study, it was aimed to investigate the anticancer effects of cyclic dodecapeptide (CDP), which is an AMP on MCF-7 and MDA-MB 231 cells from breast cancer cell lines for the first time. Anticancer activity and mechanism of action of CDP were investigated via cancer cell viability assay, cell cytotoxic assay, acridine orange/ethidium bromide dual fluorescence dying assay and scanning electron microscope technique, solid phase heparan sulfate and chondroitin sulfate binding assay, and peptide binding assay. CDP decreases cell viability and induces the death of breast cancer cells by impairing the membrane integrity and causes necrotic cell death by forming pores in the membranes. CDP binds to the negatively charged glycosaminoglycans and shows more affinity against breast cancer cells than fibroblast cells. As a result, the anticancer activity of CDP presented for the first time against breast cancer cells and it has a therapeutic value due to its selective toxicity

Combination of selenium and three naturally occurring antioxidants administration protects D-galactosamine-induced liver injury in rats

D-Galactosamine (D-GaIN) is a highly selective hepatotoxin that causes liver injury similar to human viral hepatitis via depletion of uridine nucleotides, which subsequently diminishes synthesis of RNA and proteins. The aim of this study was to investigate the role of selenium, ascorbic acid, beta-carotene, and alpha-tocopherol on D-GaIN-induced liver injury of rats by morphological and immunohistochemical means. In this study, Sprague-Dawley female rats were divided into four groups. Group I consists of rats injected physiologic saline solution intraperitoneally. Group II consists of rats given selenium (0.2 mg/kg per day), ascorbic acid (100 mg/kg per day), beta-carotene (15 mg/kg per day), and alpha-tocopherol (100 mg/kg per day) for 3 days via gavage method. Group III consists of the single dose of D-GaIN (500 mg/kg)-injected animals. Group IV are the D-GaIN-injected animals given the same antioxidant combination. In situ terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling (TUNEL) assay was applied to determine apoptosis for paraffin sections of the liver samples. Moreover, caspase-3 and proliferating cell nuclear antigen antibody were applied for paraffin sections. In the group given D-GaIN, apoptotic cells with TUNEL assays and caspase-3 activity, which are liver injury markers induced by D-GaIN, the hepatocyte proliferation with cell proliferation assay increased. However, selenium and other three antioxidants combination clearly suppressed an increase in apoptotic cells with TUNEL assay and caspase-3 activity. In addition, it suppressed D-GaIN-induced cell proliferation in the liver. As a result, these results indicate that selenium and three naturally occurring antioxidants shows a protective effect against liver injury induced by D-GaIN. These results suggest that supplementation with the combination of selenium, ascorbic acid, beta-carotene, and alpha-tocopherol may help prevent the development of liver injury

The potential role of combined antioxidant treatment on pancreas of STZ-diabetic mice

In diabetes, cells and tissues are damaged due to the imbalance between production of free radicals and removal of them. The effective biologic antioxidants for oxidative stress such as alpha-lipoic acid, vitamin E and selenium are effective in diminishing oxidative damage such as membrane lipid peroxidation. The experiment aimed to investigate the oxidative stress occurring in mitochondrial and cytoplasmic fraction of pancreatic tissues in streptozotocin-diabetic mice and the possible effects of alpha-lipoic acid + vitamin E + selenium combination on oxidative damage and antioxidative system by using microscopic and biochemical methods

Effects of vitamin E, vitamin C, and selenium on gastric fundus in cadmium toxicity in male rats

Cadmium (Cd) is a highly toxic metal. It has an indirect role in the generation of various free radicals. Antioxidants such as vitamin E, vitamin C, and selenium are important for preventing the damage caused by reactive oxygen species. This study was undertaken to examine the effect of acute cadmium and/or antioxidants on serum lipid metabolism, tissue glutathione, and lipid peroxidation (LPO) levels, and ghrelin and metallothionein production in the gastric fundus mucosa of rats. Cd (2 mg/kg/day CdCl2) was administered to rats for 8 days, intraperitoneally. Vitamin E (250 mg /kg/day) + vitamin C (250 mg/kg/day) + sodium selenate (0.25 mg /kg/day) were administered to rats orally at the same time. The animals were treated by antioxidants 1 h prior to treatment with Cd every day. Gastric tissue homogenates were used for protein and glutathione and LPO levels. Phospholipid and total lipid levels were determined in serum. Gastric fundus sections examined for histopathological changes and by immunohistochemistry for expression of ghrelin and metallothionein. In the group treated with Cd, degenerative changes such as discontinuity in the surface epithelium were observed. The degenerative changes induced by Cd were decreased in the group given vitamin E + vitamin C + selenium. There was no significant change in ghrelin-and metallothionein-immunoreactive cells in fundus mucosa. Stomach glutathione levels insignificantly decreased in the Cd groups, but in the Cd group given antioxidant, stomach glutathione levels were significantly increased. Serum phospholipid and total lipid levels were significantly increased in the Cd groups. On the other hand, treatment with antioxidants reversed these effects. These results indicate that antioxidants partly prevent the toxicity of Cd in rat gastric fundus