Synthesis, characterization, and antibacterial effect of St. John's wort oil loaded chitosan hydrogel.

Hydrogels prepared with natural and synthetic polymers were found to be applicable for the development of resistance against some Gram positive and negative bacterial species. Numerous studies have shown that chitosan polymers can be advantageous to be used in medicine due to their high antibacterial activity. In this study, biocompatible yellow cantorone oil doped hydrogels (chitosan/poly(vinyl alcohol) based) with antimicrobial properties were synthesized. The structural, morphological, swelling and mechanical properties of these biocompatible hydrogels prepared by double crosslinking were investigated and characterized. FTIR spectroscopy showed the appearance of new imine and acetal bonds due to both covalent cross-linking. In vitro cytotoxicity evaluation revealed that hydrogels showed weak cytotoxic effect. In the antimicrobial evaluation, it was determined that the hydrogel containing only chitosan showed better antimicrobial effect against Escherichia coli, Pseudomonas auriginosa, Staphylococcus aureus and Enterococcus faecalis bacteria than the one containing St. John's Wort oil. The antibacterial effect of polyvinyl alcohol/chitosan hydrogel was low. In our wound healing study, chitosan hydrogel loaded with yellow St. John's Wort oil was more effective in reducing wound size.

Effects of Arum dioscoridis Extract on Hepatic Toxicity Caused by Thioacetamide in Rats.

BACKGROUND: The aim of this study was to investigate the prophylactic and therapeutic effects of Arum dioscoridis (tirsik) plant extract against thioacetamide-induced experimental liver toxicity. METHODS: In this study, 35 male Wistar-Albino rats, of 12-14 weeks old, weighing between 200 and 270 g, were used. Rats were divided into 5 groups of 7 each. The first group was determined as the control group, the second group as the hepatotoxicity group, the third group as the prophylaxis group, the fourth group as the intraperitoneal treatment group, and the fifth group as the oral treatment group. Hepatotoxicity was achieved with a single intraperitoneal dose of 350 mg/kg of thioacetamide (TAA). On the seventh day, the rats were sacrificed under general anesthesia. Their blood was taken and liver enzymes were studied. Malondialdehyde (MDA), glutathyon peroxi dase (GPx), catalase (CAT), superoxit dismutase (SOD) enzymes were studied from liver tissues. In addition, liver tissues were evaluated histopathologically. RESULTS: With Arum dioscoridis treatment and prophylaxis, improvements in all parameters and increases in tissue antioxidant levels were detected. CONCLUSION: It was determined that Arum dioscoridis plant extract has prophylactic and therapeutic effects on liver toxicity. In cases of acute liver injury and hepatotoxicity, we suggest the potential application of Arum dioscoridis for effective and inexpensive treatment.

Investigation of the Effects of Octreotide Agent on Oxidative Stress, 8-Hydroxy Deoxyguanosine in Experimental Hepatic Carcinogenesis Rat Model.

INTRODUCTION: 2-AAF and DEN are well-known liver toxicants commonly used to stimulate tumors in laboratory animals. AIM: The aim of this study was to investigate the effect of octreotide on DEN-induced and 2-AAF-supplemented hepatocarcinogenesis in Wistar albino rats. MATERIALS AND METHODS: In this study, 64 Wistar albino rats were divided into 8 groups. DEN (175 mg/kg) initiated and 2-AAF (20 mg/kg) promoted liver carcinogenesis in rats. The tumor growth inhibitor octreotide (300 µg/kg) was used. Rats were sacrificed at the end of experiment and their liver tissues were taken for the study. SOD, GSH-Px, CAT activities, NO and MDA levels were measured spectrophotometrically. Also, Hsp70 and 8-OHdG was measured by the ELISA method. RESULTS: In group 7, MDA, 8-OHdG, and Hsp70 levels were significantly increased. In addition, SOD, GSH-Px activity was significantly reduced in this group. MDA, 8-OHdG and Hsp70 levels were significantly reduced in Group 8, which received octreotide for treatment. CONCLUSION: DEN and 2-AAF cause very serious liver damage. Octreotide protects the liver from carcinogenesis, increases the activity of cellular antioxidant enzymes and helps reduce DNA damage. Therefore, octreotide may be an inhibitor in tumor cells and may reduce oxidative stress.

The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state.

Remarkable interest has risen in the idea that oxidative/nitrosative stress is mediated in the etiology of numerous human diseases. Oxidative/Nitrosative stress is the result of an disequilibrium in oxidant/antioxidant which reveals from continuous increase of Reactive Oxygen and Reactive Nitrogen Species production. The aim of this review is to emphasize with current information the importance of antioxidants which play the role in cellular responce against oxidative/nitrosative stress, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue. Products of lipid peroxidation have commonly been used as biomarkers of oxidative/nitrosative stress damage. Lipid peroxidation generates a variety of relatively stable decomposition end products, mainly α, ß-unsaturated reactive aldehydes, such as malondialdehyde, 4-hydroxy-2-nonenal, 2-propenal (acrolein) and isoprostanes, which can be measured in plasma and urine as an indirect index of oxidative/nitrosative stress. Antioxidants are exogenous or endogenous molecules that mitigate any form of oxidative/nitrosative stress or its consequences. They may act from directly scavenging free radicals to increasing antioxidative defences. Antioxidant deficiencies can develop as a result of decreased antioxidant intake, synthesis of endogenous enzymes or increased antioxidant utilization. Antioxidant supplementation has become an increasingly popular practice to maintain optimal body function. However, antoxidants exhibit pro-oxidant activity depending on the specific set of conditions. Of particular importance are their dosage and redox conditions in the cell.

Vitamin B complex and vitamin B12 levels after peripheral nerve injury.

The aim of the present study was to evaluate whether tissue levels of vitamin B complex and vitamin B12 were altered after crush-induced peripheral nerve injury in an experimental rat model. A total of 80 male Wistar rats were randomized into one control (n = 8) and six study groups (1, 6, 12, 24 hours, 3, and 7 days after experimental nerve injury; n = 12 for each group). Crush-induced peripheral nerve injury was performed on the sciatic nerves of rats in six study groups. Tissue samples from the sites of peripheral nerve injury were obtained at 1, 6, 12, 24 hours, 3 and 7 days after experimental nerve injury. Enzyme-linked immunosorbent assay results showed that tissue levels of vitamin B complex and vitamin B12 in the injured sciatic nerve were significantly greater at 1 and 12 hours after experimental nerve injury, while they were significantly lower at 7 days than in control group. Tissue level of vitamin B12 in the injured sciatic nerve was significantly lower at 1, 6, 12 and 24 hours than in the control group. These results suggest that tissue levels of vitamin B complex and vitamin B12 vary with progression of crush-induced peripheral nerve injury, and supplementation of these vitamins in the acute period may be beneficial for acceleration of nerve regeneration.

Selenium has a protective effect on ischemia/reperfusion injury in a rat ovary model: biochemical and histopathologic evaluation.

BACKGROUND/PURPOSE: The aim of the study was to evaluate the effects of selenium (Se) on ischemia/reperfusion (I/R) injury in rat ovaries. METHODS: Thirty-five female Sprague-Dawley rats were randomly divided into 5 groups (n = 7): sham (S), I/R1, I/R2, Se1, and Se2. In the I/R1 and Se1 groups, 4 hours of ischemia was followed by 6 hours of reperfusion, and in the I/R2 and Se2 groups, 4 hours of ischemia was followed by 12 hours of reperfusion. In the Se groups, 30 minutes before reperfusion, a single dose of 0.2 mg/kg Se was administered intraperitoneally. The ovarian tissue levels of malondialdehyde (MDA) and nitric oxide (NO), and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured biochemically. Tissue damage to ovarian tissue was scored by histopathologic examination. RESULTS: The I/R groups had significantly higher MDA levels and lower CAT, SOD, and GPx activities than the sham group (P < .05). Although NO levels were significantly higher in the I/R1 group than in the sham group (P < .05), the NO levels in the I/R2 and sham groups were similar. Selenium pretreatment significantly lowered tissue MDA and NO levels and increased tissue SOD and GPx activities in the Se groups, compared with those in the I/R groups (P < .05). Catalase activities were significantly higher in the Se2 group than in the I/R2 group (P < .05). Catalase activities were higher in the Se1 group than in the I/R1 group, but the difference was not statistically significant. Treatment with Se significantly decreased the ovarian tissue damage scores in the Se2 group compared with those in the I/R2 group (P < .05). CONCLUSION: Selenium is effective in preventing tissue damage induced by I/R in rat ovaries.

Effects of L-carnitine on oxidant/antioxidant status in acetic acid-induced colitis.

Recently, the role of oxidative stress in the pathogenesis of ulcerative colitis has been investigated. This study was designed to evaluate the possible beneficial effects of L-carnitine on tissue injury and oxidative stress in acetic acid-induced colitis in rats. Acetic acid administration induced severe damage macroscopically and histopathologically in colon and significantly increased the levels of malondialdehyde and myeloperoxidase in colonic tissue. Supplementation of L-carnitine to acetic acid-treated rats did not prove to induce any improvements in macroscopic scores, while L-carnitine administration improved histopathologic scores and significantly decreased malondialdehyde and myeloperoxidase levels in treatment groups. Acetic acid administration significantly decreased reduced glutathione, superoxide dismutase, and catalase levels in colonic homogenate. Supplementation of L-carnitine prevented the depletion of reduced glutathione levels but significantly increased superoxide dismutase levels. On the other hand, no significant change in catalase activity was observed. In conclusion, these results may reflect that L-carnitine could be beneficial as a complementary agent in treatment of ulcerative colitis.

Beneficial effects of N-acetylcysteine on acetic acid-induced colitis in rats.

Ulcerative colitis is a chronic recurrent inflammatory bowel disease in which oxidative stress has been implicated. The aim of the present study was to evaluate possible protective effects of N-acetylcysteine against acetic acid-induced colitis in a rat model. Rats were administered intrarectal saline (control group) or acetic acid (colitis model group). Rats with acetic acid-induced colitis were treated by intraperitoneal or intrarectal administration of N-acetylcysteine (500 mg/kg) (treated group). Another series of rats were pre-treated by intraperitoneal or intrarectal administration of N-acetylcysteine, then administered intrarectal acetic acid (pre-treated group). The degree of tissue injuries was assessed by macroscopical and histopathological scores of the colonic mucosa. Malondialdehyde, myeloperoxidase, reduced glutathione, superoxide dismutase, and catalase levels were measured in tissue extracts of the dissected colon. Administration of N-acetylcysteine intraperitoneally or intrarectally ameliorated macroscopic score alterations produced by acetic acid in treated groups. In addition, microscopical improvement was observed in all N-acetylcysteine-treated rats compared to untreated animals with colitis. In the colonic tissues of the acetic acid-induced colitis, myeloperoxidase activity and malondialdehyde levels were elevated, while the reduced glutathione levels and superoxide dismutase and catalase activities were decreased. However, intraperitoneal or intrarectal treatment with N-acetylcysteine reversed these parameters, compared to the untreated colitis group. Notably, intrarectal administration of N-acetylcysteine elevated the reduced glutathione levels more markedly compared to the other treatment groups. Superoxide dismutase levels were increased in intraperitoneally or intrarectally N-acetylcysteine-treated groups significantly compared to the control, colitis and pre-treated groups. But there was no significant increase in catalase activity. In conclusion, N-acetylcysteine could be beneficial as a complementary agent in treatment of ulcerative colitis.

The role of urtica dioica (urticaceae) in the prevention of oxidative stress caused by tourniquet application in rats.

Tourniquets are used in extremity surgery and provide a relatively bloodless field, thereby minimizing blood loss and helping identify the vital structures. However, they may cause an ischemia-reperfusion injury with potentially harmful local and systemic consequences. Many therapeutic effects such as diuretic, natriuretic, hypotensive, anti-rheumatic, anti-prostatic, and in-vitro anti-oxidant effects of the Urtica dioica (UD) have been determined. In the present study, we aimed to investigate the potential role of UD plant for prevention of oxidative stress in muscle tissues generated by tourniquet application in rats. Wistar rats were used in this study. The UD extract or 1.15% KCl aqueous solution, in which UD leaf samples were homogenized, was given to each group of eight rats once a day for 5 days through an intraesophageal canule. No treatment was applied to untreated group. Tourniquets were applied to the left posterior limb of rats for 1 or 2 h followed by a reperfusion period of 1 h. After the ischemia and reperfusion, the rats were killed with a high dose of anesthetic drug, and malonyldialdehyde (MDA) levels were measured in their tibialis anterior muscles. Basal MDA levels were obtained from tibialis anterior muscles of 8 control rats, which were not exposed to ischemia. MDA levels were lower in the UD-treated rats than those in untreated and KCl-treated rats after either 1 or 2 h of ischemia and 1 h reperfusion. These results indicate that UD has a potential antioxidant effect on ischemic muscle tissues.

Effects of antioxidant therapy on leukocyte myeloperoxidase and Cu/Zn-superoxide dismutase and plasma malondialdehyde levels in experimental colitis.

The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model. The mean polymorphonuclear leukocyte MPO and Cu/Zn-SOD activity was significantly higher in the colitis group than in the control group. Both NAC and LCAR pretreatment markedly decreased MPO and Cu/Zn-SOD activity compared to colitis group. AA administration significantly increased the levels of plasma MDA in comparison with controls. However, NAC and LCAR administration to the AA-treated rats significantly reduced the MDA levels compared to colitis group. In conclusion NAC and LCAR could be beneficial agents in restoring the circulating proinflammatory mediators.