The effects of morus nigra on the alveolar bone loss in experimentally-induced periodontitis.

PURPOSE: The aim of this study is to evalute the anti-inflammatory effects of morus migra on experimentally-induced periodontitis in rats. MATERIALS AND METHODS: Twenty-four Wistar-albino rats were randomly divided into three groups: control group (C, n=8), experimental periodontitis (PER, n=8), experimental periodontitis and treated with Morus nigra (MN+PER, n=8) (50 mg/kg per day for 21 days). After 21 days, the rats were sacrificed, and alveolar bones were evaluated histopathologically and histometrically analyzed to obtain level of alveolar bone loss. The detection of RANKL and OPG were immunohistochemically performed. Serum and tissue levels of MMP-8 and MMP-13 were also analyzed. RESULTS: Morus nigra treatment decreased tissue MMP-8 and MMP-13 levels and there were significant differences in the case of tissue levels of MMP-8 and MMP-13 between groups PER and MN+PER (p=0.035, p=0.041). There were no significant differences among all the groups serum levels of MMP-8 and MMP-13 (p=0.067, p=0.082). In the histometric evaluation, alveolar bone loss was greater in the PER group compared to C and MN groups (p=0.035). Immuno-histochemical staining of RANKL activities were found significantly lower (p=0.037) and OPG activities were found significantly higher in MN+PER group when compared to PER group (p=0.021). CONCLUSION: The present study reveals that systemic administration of Morus nigra significantly inhibited the regional alveolar bone resorption and contributes to periodontal healing in the rat experimental-periodontitis models.

The investigation of effect of alpha lipoic acid against damage on neonatal rat lung to maternal tobacco smoke exposure.

This study was carried out to determine the changes in the lungs of the rat pups exposed to tobacco smoke during pregnancy period and to investigate the protective effects of alpha lipoic acid, which is administered during pregnancy, on these changes. Spraque-Dawley female rats were divided into four groups: control, tobacco smoke (TS), tobacco smoke + alpha lipoic acid (TS + ALA) and alpha lipoic acid (ALA). The rats in control group were untreated. Rats were exposed to TS twice a day for one hour starting from eight weeks before mating and during pregnancy. 20 mg / kg of ALA was administered to rats. On 7th and 21st days 7 of the pups from each group were decapitated. Histological, morphometric, biochemical and quantitative real-time RT-PCR analyzes were performed. Histopathological and biochemical changes were observed in TS group. While a significant decrease was observed both in SP-A and VEGF immunoreactivities and mRNA levels, caspase-3 immunoreactivity and TUNEL positive cells were increased in TS group. It is suggested that prenatal TS exposure leads to morphological and histopathological changes on lung development by causing oxidative damage in lungs of neonatal rats and the maternal use of ALA can provide a limited protective effect on the neonatal lung development against this oxidative stress originating from TS. Although pregnant women are increasingly aware on health risks of smoking, environmental tobacco smoke exposure is still a widespread problem. For this reason, it is thought that this damage can be partially reduced by some antioxidant supplements in pregnancy.

Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation.

In this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (H2O2)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 µmol/L H2O2 caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 µmol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, H2O2 decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-κß, TNF-α, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-κß, TNF-α, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the H2O2 treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by H2O2. H2O2 also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.

Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats.

Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose intake on health and their prevention should take greater consideration. Caffeic Acid Phenethyl Ester (CAPE) has beneficial effects on metabolic syndrome and vascular function which is important in the prevention of cardiovascular disease. However, there are no known studies about the effect of CAPE on fructose-induced vascular dysfunction. In this study, we examined the effect of CAPE on vascular dysfunction due to high fructose corn syrup (HFCS). HFCS (6 weeks, 30% fed with drinking water) caused vascular dysfunction, but treatment with CAPE (50 micromol/kg i.p. for the last two weeks) effectively restored this problem. Additionally, hypertension in HFCS-fed rats was also decreased in CAPE supplemented rats. CAPE supplements lowered HFCS consumption-induced raise in blood glucose, homocysteine, and cholesterol levels. The aorta tissue endothelial nitric oxide synthase (eNOS) production was decreased in rats given HFCS and in contrast CAPE supplementation efficiently increased its production. The presented results showed that HFCS-induced cardiovascular abnormalities could be prevented by CAPE treatment.

Change in Free Radical and Antioxidant Enzyme Levels in the Patients Undergoing Open Heart Surgery with Cardiopulmonary Bypass.

Objective. The purpose of this study is to determine the changes in oxidative damage and antioxidant parameters in open heart surgeries with cardiopulmonary bypass (CPB) in preoperative and early postoperative periods. Methods. A total of three consecutive arterial blood samples were obtained from the patients in the study group, in preoperative, early postoperative, and postoperative periods, respectively. Oxidative damage indicator (MDA) and antioxidant indicators (GPx, GSH, CAT, and SOD) were examined. Results. A statistically significant increase was observed in MDA level in postoperative period compared to preoperative and early postoperative periods. GSH levels and CAT activities increased significantly in early postoperative and postoperative periods. Analyses revealed an increase in GPx and SOD enzyme activities only in the postoperative period. Conclusion. Even though the increase in MDA level was suppressed by the increased GSH level and CAT activity like in early postoperative period, efficiency can be brought for the increases in insufficient significant antioxidant parameters in postoperative period by administering antioxidant supplements to the patients and thus the increase in MDA in postoperative period can be significantly suppressed.

Effect of taurine on brain 8-hydroxydeoxyguanosine and 3-nitrotyrosine levels in endotoxemia.

Taurine is a sulfur-containing ß-amino acid that is found in milimolar concentrations in most mammalian tissues and plasma. It was shown to have cytoprotective effects in many in vitro and in vivo studies and these actions are often attributed to an antioxidant mechanism. In this study, we aimed to investigate the effect of acute taurine administration on endotoxin-induced oxidative and nitrosative stress in brain. Fourty adult male guinea pigs were divided into four groups: control, taurine, endotoxemia, and endotoxemia + taurine. Taurine (300 mg/kg), lipopolysaccharide (LPS, 4 mg/kg), or taurine plus LPS was administered intraperitoneally. After 6 h of incubation, when highest blood levels of taurine and endotoxin were attained, the animals were killed and brain tissue samples were collected. 3-Nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHdG) and taurine levels were measured using high-performance liquid chromatography methods. LPS administration significantly increased 3-NT, 8-OHdG levels, and dramatically reduced taurine concentrations in brain tissue compared to control group. The groups in which taurine was administered alone or with LPS, contradiction to well-known antioxidant effect, taurine caused elevated concentrations of 3-NT and 8-OHdG compared to both control and endotoxemia groups. In conclusion, endotoxemia leads to tyrosine nitration and DNA base modification that can be assessed by 3-NT and 8-OHdG, respectively. Taurine did not exhibit any antioxidant effect; moreover, it may contribute to neuronal damage at this dose. Thus, we can suggest that lower dose of taurine administration may be benefial for neuronal protection or adversely taurine administration may have toxic effect at all doses.

Effects of taurine on nitric oxide and 3-nitrotyrosine levels in spleen during endotoxemia.

Taurine (2-aminoethanesulfonic acid) is a free sulfur-containing ß-amino acid which has antioxidant, antiinflammatory and detoxificant properties. In the present study, the role of endotoxemia on peroxynitrite formation via 3-nitrotyrosine (3-NT) detection, and the possible antioxidant effect of taurine in lipopolysaccharide (LPS)-treated guinea pigs were aimed. 40 adult male guinea pigs were divided into four groups; control, endotoxemia, taurine and taurine+endotoxemia. Animals were administered taurine (300 mg/kg), LPS (4 mg/kg) or taurine plus LPS intraperitoneally. After 6 h of incubation, when highest blood levels of taurine and endotoxin were attained, the animals were sacrificed and spleen samples were collected. The amounts of 3-nitrotyrosine and taurine were measured by HPLC, and reactive nitrogen oxide species (NOx) which are stable end products of nitric oxide was measured spectrophotometrically in spleen tissues. LPS administration significantly decreased the concentration of taurine whilst increased levels of 3-NT and NOx compared with control group. It was determined that taurine treatment decreased the levels of 3-nitrotyrosine and NOx in taurine+endotoxemia group. The group in which taurine was administered alone, contradiction to well-known antioxidant effect, taurine caused elevated concentration of 3-NT and NOx. This data suggest that taurine protects spleen against oxidative damage in endotoxemic conditions. However, the effect of taurine is different when it is administered alone. In conclusion, taurine may act as an antioxidant during endotoxemia, and as a prooxidant in healthy subjects at this dose.

The relationship between taurine and 3-nitrotyrosine level of hepatocytes in experimental endotoxemia.

It has been proposed that taurine may function as an oxidant in a dose-dependent manner in vivo and in vitro. The present study was carried out to investigate the relationship between taurine concentration and 3-nitrotyrosine level, a stable marker of peroxynitrite action, in hepatocytes of guinea pig in endotoxemia before and after taurine administration. The levels of taurine and 3-nitrotyrosine were measured by HPLC method. In the present study, taurine was low concentration in hepatocytes exposed to endotoxemia. In taurine plus endotoxin treated animals, HPLC analysis showed higher taurine level compared with animals only supplemented with taurine. But 3-nitrotyrosine levels were same in both taurine alone and taurine plus endotoxin groups. In conclusion, taurine is able to prevent the damaging effect of peroxynitrite, at concentration measured in hepatocytes, in our experimental conditions.