Mehmet Emin Büyükokuroğlu

Antihyperglycemic and antioxidative potential of Matricaria chamomilla L. in streptozotocin-induced diabetic rats

Plants with antidiabetic activities provide important sources for the development of new drugs in the treatment of diabetes mellitus. In the present study, we investigated possible antihyperglycemic and antioxidative activities of the aerial part of the Matricaria chamomilla L. ethanolic extract (MCE) in streptozotocin (STZ; 70xa0mg/kg, i.p.)-induced diabetic rats. The following groups were assigned; sham (did not receive any substance), STZxa0+xa0distilled water (control), STZxa0+xa05xa0mg/kg glibenclamide, STZxa0+xa020xa0mg/kg MCE, STZxa0+xa050xa0mg/kg MCE, STZxa0+xa0100xa0mg/kg MCE. Diabetic rats were treated for 14 days by gavage. Postprandial blood glucose levels, malondialdehyde, reduced glutathione (GSH), nitrate, nitrite, ascorbic acid, retinol, β-carotene, superoxide dismutase, and catalase levels were measured, and immunohistochemical studies were performed in all of the groups. The obtained data showed that STZ resulted in oxidative stress and affected the antioxidant status. Treatment with different doses of MCE significantly reduced postprandial hyperglycemia and oxidative stress, and augmented the antioxidant system. In histological investigations, MCE treatment protected the majority of the pancreatic islet cells, with respect to the control group. As a result, MCE exhibited significant antihyperglycemic effect and protected β-cells in STZ-diabetic rats, in a dose-dependent manner, and diminished the hyperglycemia-related oxidative stress.

Protective potential of Royal Jelly against carbon tetrachloride induced-toxicity and changes in the serum sialic acid levels.

Royal Jelly (RJ) is used in the Turkish folk medicine for the treatment of number of disorders. The present study describes the hepatoprotective and antioxidant activities of the RJ against carbon tetrachloride (CCl(4))-induced acute liver damage. Sprague-Dawley rats were used for the experiment. CCl(4) (0.8 ml/kg; s.c.) and RJ (50, 100, 200mg/kg; orally) were given every other day, for 20 days. Malondialdehyde, reduced glutathione in whole blood and tissues; ceruloplasmin, sialic acid, ascorbic acid, retinol, β-carotene and liver enzymes levels in serum were measured. Additionally, histopathological alterations in the liver were examined. RJ exerted the significant protective effect on liver damage as well as on oxidative stress induced by CCl(4), resulting in reduced lipid peroxidation and improved endogenous antioxidant defence systems. It also reduced the elevated levels of liver enzymes. Histopathological study further confirmed the hepatoprotective effect of RJ, when compared with the CCl(4) treated control groups. In conclusion, present study reveals biological evidence that supports the use of RJ in the treatment of chemical-induced hepatotoxicity.

Antioxidative role of melatonin in organophosphate toxicity in rats

Previous studies revealed that oxidative stress could be an important component of the mechanism of organophosphate (OP) compound toxicity. The aim of the present study was to investigate both prophylactic and therapeutic effects of melatonin against fenthion-induced oxidative stress in rats. Therefore, we determined the changes in the levels of reduced glutathione (GSH) and malondialdehyde (MDA) in the whole blood, brain, pectoral muscle, liver, lung, heart, kidney, pancreas, and jejunum. Also, the changes in the levels of serum nitrite and nitrate, ascorbic acid, retinal, b-carotene, and ceruloplasmin were measured. In addition, activities of enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in erythrocyte of normal and experimental animals were measured. It was found that fenthion administration increased the levels of MDA in all tissues and decreased or increased the levels of GSH in some tissues. In comparison to nitrate, nitrite and ascorbic acid levels in the serum of experimental groups, there was no significant difference between groups. However, fenthion toxicity led to decrease in retinol and β-carotene levels; melatonin administration significantly prevented this decrease. Serum ceruloplasmin level was increased due to fenthion administration, but prophylactic and therapeutic melatonin administration inhibited the increase in ceruloplasmin level of serum. There was no significant change in SOD levels in melatonin-administered groups. Melatonin modulates the fenthion-induced changes in the activities of GPx and CAT. In conclusion, the results of the current study revealed that OP toxicity, induced by fenthion, activated oxidant systems in all antioxidant systems in some tissues. Melatonin administration led to a marked increase in antioxidant activity and inhibited lipid peroxidation in most of tissues.

Nimodipine can improve cerebral metabolism and outcome in patients with severe head trauma

In the present study, the effect of nimodipine was investigated in a patient with severe head trauma. Nimodipine was administered into the peripheral vein to prevent secondary neuronal damages in patients. The five patients in control group were treated according to the standard procedures without nimodipine. Other five patients in nimodipine group were treated with standard procedures plus nimodipine. Cerebral perfusion pressure (CPP), intracranial pressure (ICP), jugular venous oxygen saturation (SjvO2), jugular lactate and glucose levels were measured. Additionally, all patients were evaluated with Glascow outcome score (GOS) before discharge. It was found that CPP (p<0.05) and SjvO2 (p<0.05) were significantly higher; but, ICP (p<0.001), jugular lactate (p<0.05) and jugular glucose (p<0.05) were lower in nimodipine than that of control groups. Again, GOS values were significantly higher in nimodipine than that of control groups (p<0.05). Results of this study revealed that nimodipine can improve cerebral metabolism and outcome in patient with severe head trauma. Thus, nimodipine may be considered as a protective agent against severe head trauma related neuronal injuries.

Dantrolene can reduce secondary damage after spinal cord injury

The aim of this experimental study was to investigate the possible protective effects of dantrolene on traumatic spinal cord injury (SCI). Twenty-four New Zealand rabbits were divided into three groups: Sham (no drug or operation, nxa0=xa08), Control (SCIxa0+xa01xa0mL saline intraperitoneally (i.p.), nxa0=xa08), and DNT (SCIxa0+xa010xa0mg/kg dantrolene in 1xa0mL, i.p., nxa0=xa08). Laminectomy was performed at T10 and balloon catheter was applied extradurally. Four and 24xa0h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. After 4xa0h SCI, all animals in control or DNT-treated groups became paraparesic. Significant improvement was observed in DNT-treated group, 24xa0h after SCI, with respect to control. Traumatic SCI led to an increase in the lipid peroxidation and a decrease in enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. DNT treatment prevented lipid peroxidation and augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, DNT treatment significantly decreased the apoptotic cell number induced by SCI. In conclusion, experimental results observed in this study suggest that treatment with dantrolene possess potential benefits for traumatic SCI.

Protective effect of Matricaria chamomilla on ethanol-induced acute gastric mucosal injury in rats.

The antiulcerogenic and antioxidant properties of Matricaria chamomilla L. (Compositae) hydroalcoholic extract (MCE) on ethanol-induced gastric mucosal injury were investigated in rats. After the induction of gastric mucosal injury, all groups were sacrificed; the gastric ulcer index was calculated, and malondialdehyde (MDA) and reduced glutathione (GSH) in whole blood and gastric tissue, and serum ascorbic acid, retinol, and β-carotene levels were measured in all groups. Pretreatment with MCE at some doses significantly reduced gastric lesions. Again, some doses of MCE significantly reduced the MDA, and significantly increased GSH levels in gastric tissue or whole blood. Serum β-carotene and retinol levels were significantly higher in the 200u2009mg/kg MCE-administered group with respect to control. As a result, MCE clearly has a protective effect against ethanol-induced gastric mucosal lesions, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in antioxidant activity.

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twenty-two New Zealand rabbits were divided into three groups: sham (no drug or operation, nxa0=xa06), Control [SCIxa0+xa0single dose of 1xa0mL saline intraperitoneally (i.p), after trauma; nxa0=xa08] and DEX (SCIxa0+xa01xa0μg/kg dexmedetomidine in 1xa0mL, i.p, after trauma, nxa0=xa08). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24xa0h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4xa0h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24xa0h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.

Royal jelly can diminish secondary neuronal damage after experimental spinal cord injury in rabbits.

The aim of this experimental study was to investigate the neuroprotective effect of Royal jelly (RJ) on traumatic spinal cord injury (SCI). Twenty-one New Zealand male rabbits, weighing between 2.5 and 3.0 kg were divided into three groups: Sham (no drug or operation, n = 7), Control (laminectomy+single dose of 1 ml/kg saline orally, after trauma; n = 7) and RJ (laminectomy+100mg/kg RJ, orally, after trauma, n = 7). Laminectomy was perfor med at T10 and balloon catheter was applied extradurally for traumatic SCI. Four and 24h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. Four hours after SCI, all animals in control or RJ treated groups became paraparesic. Significant improvement was observed in RJ treated group, 24h after SCI, with respect to control. Traumatic SCI led to increase in the lipid peroxidation and decrease enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. RJ treatment mostly prevented lipid peroxidation and also augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, RJ treatment significantly decreased the apoptotic cell number induced by SCI.

Antioxidant Enzyme and Element Status in Heroin Addiction or Heroin Withdrawal in Rats: Effect of Melatonin and Vitamin E Plus Se

Heroin use, withdrawal syndrome, and heroin-related deaths are still the most serious public health problems. Antioxidants and bio-elements are essential for metabolism in living organisms. To our knowledge, there are no data about the effect of antioxidant therapy on the levels of bio-elements and antioxidant enzymes in the naloxone (NX)-induced heroin withdrawal syndrome. Therefore, in the present study for the first time, we have investigated the role of antioxidant therapy, melatonin, and vitamin E plus Se, on the trace and major elements and antioxidant enzymes in the heroin addiction or heroin withdrawal in rats. Glutathione peroxidase levels were increased and catalase levels were decreased in the all study groups when compared to the sham group. The level of superoxide dismutase (SOD) in the fixed dose of heroin (FDH) given group was lower; however, in the variable doses of heroin (VDH) given group SOD level was higher. Furthermore, in withdrawal syndrome, Fe, Mg, Mn, and Ti levels were diminished and Al, Ca, and Cu levels were increased in the FDH+NX group. Moreover, Mg, Mn, and Se levels were also diminished and Al level was increased in the VDH+NX group. In conclusion, our results obviously indicated that heroin effected both bio-element status and antioxidant enzyme activities and, exogenous melatonin or vE+Se therapy might relieve on the element and antioxidant enzyme the destructive activity caused by heroin.

Tissue trace and major element levels in organophosphate insecticide fenthion (Lebaycid) toxicity in rats: prophylactic and therapeutic effect of exogenous melatonin.

Organophosphate compounds are very toxic chemicals and used in widespread applications. The present study was designed to examine the role of exogenous melatonin against organophosphate toxicity in tissues (brain, heart, jejunum, kidney, liver, lung, muscle and pancreas) trace and major element levels of rats. Trace and major element concentrations in the tissues were measured in the sham group, the control group, prophylaxis with the melatonin group and therapy with the melatonin group (TM) by inductively coupled plasma-optical emission spectroscopy. Statistically significant differences among the experimental groups were detected for some tissue trace and major element concentrations. In the brain tissue, the Al, Mn and Se concentrations in the sham group were significantly higher than those in the control group (p<0.05). In the heart tissue, the Cu, Mn and Se concentrations in the sham group were significantly increased than those in the control group (p<0.05). In the kidney tissue, trace and major element concentrations in the TM group were significantly lower than those in the sham group (Fe and Mn; p<0.05, Cu, Mo, Ni, Ti, V and Zn; p<0.01). In the liver, Mg, Al, Zn and Ca concentrations in the TM group were significantly higher than those in the fenthion-treated control group (p<0.01). In the muscle tissue, element concentrations in the TM group were significantly lower when compared with the sham groups (Ca and Si; p<0.01). The Al, Cr, Mo, Ni, Si and Zn element concentrations were markedly decreased in the control group as compared with the TM group in the pancreas tissue (p<0.01). In conclusion, according to the results of the present study the major findings are that the fenthion-treated rats tissue element levels were effected and the melatonin may normalize the altered levels of some trace and major elements of the tissues in organophosphate toxicity.