Investigation of Propolis' Effect on Thiobarbituric Acid Reactive Substances and Anti-Oxidant Enzyme Levels of Hippocampus in Diabetic Rats Induced by Streptozotocin.

BACKGROUND: Propolis is an organic resinous viscous substance collected from flower bud and plant sprig by bees. Propolis has a potential treatment agent for oxidative damage caused by diabetes in hippocampus due to its flavonoid and phenolic content. AIM: In this study effect of propolis on thiobarbituric acid reactive substances and anti-oxidative enzyme levels of hippocampus in diabetic rats induced by streptozotocin was investigated. MATERIALS AND METHODS: The study involved measuring levels of SOD, CAT, GSH-Px and TBARs in hippocampus tissue of STZ-induced diabetic rats (Adult Male Sprague Dawley rats) after applying propolis for one month. The subjects of the study were composed of 51 rats randomly assigned to four groups (Control, STZ, P+STZ and STZ+P). For analysis of data, Kruskal Wallis Test was utilized. RESULTS: The findings of the study showed that there were no significant difference in the levels of TBARS, SOD, CAT and GSH-Px of hippocampus across the groups. CONCLUSION: Propolis application in four-week duration does not have effect on TBARS, SOD, CAT and GSH-Px levels of hippocampus of diabetic rats. These findings mean that more time for observing oxidative harms on hippocampus is needed.

Influence of dihydropyridine calcium antagonist nitrendipine on benzo(a)pyrene-induced oxidative stress.

The aim of this study was to investigate the influence of nitrendipine (NIT), a dihydropyridine derived calcium channel antagonist, on polycyclic aromatic hydrocarbon benzo(a)pyrene (BAP)-induced oxidative stress. Male Sprague Dawley rats (155-220 g) were divided into four groups: Control (corn oil, i.p.); BAP (200 mg/kg, i.p.), BAP + NIT (200 mg/kg, i.p. + 50 mg/kg, i.p.), and NIT (50 mg/kg, i.p.) groups. Twenty-four hours after the injection of BAP, the rats were sacrificed and blood samples, liver, lung, and brain tissues were removed to determine serum alanine transaminase (ALT), aspartate transferase (AST), and gamma-glutamyltransferase (GGT) activities and tissue thiobarbituric acid reactive substances (TBARS), glutathione (GSH), and superoxide dismutase (SOD) levels. BAP significantly elevated serum ALT and TBARS levels in all tissues. However, NIT pre-treatment protected against increasing TBARS levels in lung and brain tissues. In addition, NIT pre-treatment significantly increased SOD levels in lung and liver tissues, as well as GSH levels in the lungs, compared to the BAP group. Thus, in conclusion, further studies are required to confirm the protective effects of calcium channel blockers, especially in liver tissue.

Effects of Acute Moderate and Strenuous Exercise Bouts on IL-17 Production and Inflammatory Response in Trained Rats.

In this study, we aimed to compare the effects of a single bout of acute moderate and strenuous running exercise on the production of interleukin-17 (IL-17), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra) and inflammatory response of skeletal muscles in regularly trained rats. Eight week old rats were trained by treadmill running 5 days per week for 13 weeks at the durations of 30 min (moderate) and 60 min (strenuous). Two days after the last training session, the animals were subjected to a single bout of moderate or strenuous exercise and serum samples were analyzed for IL-17, IL-6, IL-1ra levels and myeloperoxidase (MPO) activity of gastrocnemius muscle were determined. IL-17 level significantly increased in strenuous exercise group when compared to that of sedentary controls (p < 0.01), On the other hand, only in the moderate exercise group, there was a negative correlation between IL-6 and IL-17 levels (r = - 0.857 and p = 0.014). In conclusion, acute single bout of strenuous exercise increased IL-17 production in trained rats and, this cytokine may be involved in inflammatory process of skeletal muscles. Key pointsA single bout of acute strenuous running exercise markedly elevated IL-17 production.This preliminary result should be supported by forthcoming studies that investigate the role of IL-17 in acute inflammatory process of skeletal muscle.

Effects of benzo(a)pyrene and ethanol on oxidative stress of brain, lung tissues and lung morphology in rats.

Ethanol and benzo(a)pyrene cause lipid peroxidation either by producing the reactive oxygen species or decreasing the activities of antioxidant enzymes that lead to cellular damage and cellular dysfunction. In this study, we investigated both physiological and histological changes in lung and physiological changes in brain after the administration of benzo(a)pyrene and ethanol both separately and together. Male Sprague Dawley rats were divided into four groups, each containing seven rats as follows: Group I (control), group II (benzo(a)pyrene, [B(a)P]), group III ([B(a)P] + ethanol (EtOH)) and group IV (EtOH). Superoxide dismutase (SOD) activity, levels of glutathione(GSH), malondialdehyde (MDA) as well as histological examinations were evaluated to demonstrate the damages in lung and brain tissues following the administration of [B(a)P] and EtOH. SOD activities of lung and brain tissues in group II and group III decreased significantly, compared to that in group I and group IV, respectively. GSH levels of both the lung and brain tissues in the experimental groups were lower when compared to the control group. MDA levels of lung tissues in group II and III were significantly higher than that in the control group. Moreover, MDA levels in the brain tissues of all the experimental groups were higher than that in the control group, but these values were only significantly higher in group II and IV. In the second study group, [B(a)P] administration resulted in lung damage. On the other hand, lung tissue of the third experimental group showed moderate damage, and lung tissues of the fourth group was less severely damaged. [B(a)P] and EtOH administration alone or together caused changes in the GSH, MDA levels and SOD enzyme activity in the lung and brain tissues. We also noted that [B(a)P] and EtOH caused different degrees of histological changes.

Protection from renal ischemia reperfusion injury by an endothelin-A receptor antagonist BQ-123 in relation to nitric oxide production.

The aim of this study was to investigate whether the protective effect of endothelin-A (ET(A)) receptor antagonist BQ-123 against renal ischemia reperfusion (I/R) injury is related to nitric oxide (NO) production. Sprague-Dawley rats were divided into six groups: control, I/R, N sup omega nitro-L-arginine methyl ester (L-NAME), BQ, BQ+L-NAME, BQ+L-NAME+L-Arg groups. After urethane anesthesia, 30min renal ischemia and 2h reperfusion were performed in all groups except control group. Mean arterial pressures (MAP) during reperfusion in all L-NAME-treated groups were higher than during pre-ischemia and ischemia, however, MAP at 60th and 120th minute of reperfusion in control and BQ groups were lower than during ischemia. MAP of L-NAME-treated groups were significantly higher than the other groups during reperfusion period. The I/R caused lipid peroxidation and protein oxidation, however, BQ-123 treatment prevented oxidant injury. The inhibition of NO production prevented effect of BQ-123 treatment. Also, BQ-123 treatment caused an increase in superoxide dismutase and catalase activities. Both BQ-123 and L-NAME treatments prevented high xanthine oxidase activity. BQ-123 prevented risen myeloperoxidase activity and L-NAME reversed this effect of BQ-123 just like the addition of L-arginine to the treatment altered the effect of L-NAME. The plasma BUN was affected as increasing manner from L-NAME treatments; on the other hand, plasma Cr and Na concentrations were affected as decreasing manner from BQ-123 treatments. ET(A) receptor antagonist BQ-123 may be revealed a protective agent against renal I/R injury with a possible secondary pathway via its antioxidant effects. We suggest that BQ-123 may mediate the protective effect via a NO-dependent mechanism.

Protective role of aminoguanidine on gentamicin-induced acute renal failure in rats.

The toxicity of aminoglycosides including gentamicin (GEN), the most widely used drug in this category, is believed to be related to the generation of reactive oxygen species (ROS) in the kidney. Aminoguanidine (AG) is known as an effective antioxidant and its free radical scavenger effects may protect GEN-induced acute renal failure (ARF). Therefore, this study was focused on investigating the possible protective effect of AG against GEN-induced nephrotoxicity in an in vivo rat model. We investigated the effects of AG on GEN-induced changes in renal tissue malondialdehyde (MDA) levels; nitric oxide (NO) generation; glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities; glutathione (GSH) content; serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined using light microscopy. GEN administration to control group rats increased renal MDA and NO levels but decreased GSH-Px, SOD, CAT activities and GSH content. AG administration with GEN injection resulted in significantly decreased MDA, NO generation and increased GSH-Px, SOD, CAT activities and GSH content when compared with GEN alone. Serum levels of Cr and BUN significantly increased as a result of nephrotoxicity. Also, AG significantly decreased Cr and BUN levels. Morphological changes in the kidney, including tubular necrosis, intracellular edema, glomerular and basement membrane alterations were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of AG reduced the GEN-induced kidney damage. We propose that AG acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level.

Effects of melatonin or acetylsalicylic acid on gastric oxidative stress after bile duct ligation in rats.

BACKGROUND: Antioxidant enzyme activities decrease after bile duct ligation. The aim of this study was to assess the effect of melatonin and acetylsalicylic acid on antioxidant enzyme activities in gastric oxidative stress induced by bile duct ligation. METHODS: Sixty-four animals were divided into eight groups of eight rats each. Male Sprague-Dawley rats were subjected to either a sham operation or common bile duct ligation (BDL) before treatment with melatonin (MEL) or acetylsalicylic acid (ASA). Gastric superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and malondialdehyde (MDA) and nitric oxide (NO) levels were determined by spectrophotometers and evaluated. RESULTS: Our results indicated that BDL caused a significant increase in lipid peroxidation, whereas coadministration of MEL with ASA significantly decreased MDA and NO levels in BDL rats. Moreover, coadministration of MEL and ASA increased antioxidant enzyme activities after the BDL, and these increases were statistically significant for CAT and GPx. On the other hand, the increase in SOD activity was not significant. CONCLUSIONS: Melatonin administration, either alone or together with acetylsalicylic acid, decreases lipid peroxidation and increases antioxidant enzyme activities in gastric tissues of rats after bile duct ligation. ASA administration, however, either alone or with a vehicle, increases lipid peroxidation and decreases antioxidant enzyme activities.

Protective effect of low dose of melatonin against cholestatic oxidative stress after common bile duct ligation in rats.

AIM: To investigate the role of oxidative injury and the effect of exogenous melatonin administration on liver damage induced by bile duct ligation (BDL), and second, to evaluate the role of nitric oxide (NO), a free oxygen radical, in oxidative injury. METHODS: Thirty-two Sprague-Dawley rats were assigned to four groups: sham operation (SO), BDL, BDL+melatonin, and BDL+vehicle. Cholestasis was achieved by double ligature of the common bile duct. Melatonin was injected intraperitoneally 500 microg/(kg.d) for 8 d. Hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA), and reduced GSH. Total nitrite (NOX) concentrations were determined in hepatic homogenates. Histopathological examination was performed using a histological scoring system. RESULTS: The histopathological changes including portal inflammation, necrosis, apoptosis, focal inflammation and fibrosis were severe in the BDL and BDL+vehicle groups. There were numerous large areas of coagulation necrosis. Histological Activity Index scores of these groups were significantly higher than that of the SO group. Treatment with melatonin reduced these alterations significantly. The degree of necro-inflammation and fibrosis showed significant difference between the BDL and BDL+melatonin groups. BDL was accompanied by a significant increase in MDA and NOX, and a significant decrease in GSH levels. Mean+/-SE values of MDA, GSH and NOX levels of SO group were 147.47+/-6.69, 0.88+/-0.33 micromol/g and 180.70+/-6.58 nm/g, respectively. The values of BDL group were 200.14+/-21.30, 0.65+/-0.02 micromol/g, and 400.46+/-48.89 nm/g, respectively, whereas the values of BDL+melatonin group were 115.93+/-6.8, 0.74+/-0.02 micromol/g, and 290.38+/-32.32 nm/g, respectively. Melatonin treatment was associated with a significant recovery of MDA, GSH and NOX levels. CONCLUSION: We have concluded that oxidative stress is associated with the pathogenesis of cholestatic liver damage and NO contributes to oxidative damage. Melatonin, even at low dose, is an efficient agent in reducing negative parameters of cholestasis.

Renal antioxidant status in rats with hypertension induced by N sup omega nitro-L-arginine methyl ester.

Nitric oxide (NO) has a role in the etiopathogenesis of hypertension. Relaxation of vascular smooth muscles is failed when NO production is reduced leading to increased vascular peripheral resistance. N sup omega nitro-L-arginine methyl ester (L-NAME) is one of the inhibitors of NO production. The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Rats were divided into three groups: control group and study groups treated with 100 or 500 mg/l L-NAME in drinking water for 15 days. The activities of catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and NO were studied in the renal tissue after hypertension induction. Arterial blood pressure was increased in both L- NAME groups. CAT activity of 500-mg L-NAME group was higher than control. GSH-Px activity of 500-mg L-NAME group was decreased compared with 100-mg ones. NO level was lower in 500-mg L-NAME group than control. MDA levels in both L-NAME groups were decreased compared with control. In conclusion, hypertension was induced with oral L-NAME treatment. Increased CAT activity was compensated with decreased GSH-Px activity in 500-mg L-NAME group. Both study groups were protected from lipid peroxidation with NO inhibition.