Sadik Buyukbas

Neuroprotective effects of Nigella sativa on experimental spinal cord injury in rats

The aim of this study was to investigate the possible beneficial effects of Nigella sativa (NS) in comparison to methylprednisolone on experimental spinal cord injury (SCI) in rats. SCI was performed by placing an aneurysm clip extradurally at the level of T11-12. Rats were neurologically tested over 24 h after trauma and spinal cord tissue samples were harvested for both biochemical and histopathological evaluation. The neurological scores of rats were not found to be different in SCI groups. SCI significantly increased the spinal cord tissue malondialdehyde (MDA) and protein carbonyl (PC) levels, however SCI decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities compared to the control. Methylprednisolone and NS treatment decreased tissue MDA and PC levels and prevented inhibition of SOD, GSH-Px and CAT enzymes in the tissues. The most significant results were obtained when NS was given. In SCI and placebo groups, the neurons of spinal cord tissue became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in methylprednisolone and NS-treated groups were well protected, however, not as well as the neurons of the control group. The number of neurons in the spinal cord tissue of the SCI and placebo groups was significantly less than the control, laminectomy, methylprednisolone and NS-treated groups. In conclusion, NS treatment might be beneficial in spinal cord tissue damage, and therefore shows potential for clinical implications.

The influence of dexmedetomidine on ischemic rat hippocampus

In our study, we evaluated the neuroprotective effects of dexmedetomidine on oxidant-antioxidant systems, pro-inflammatory cytokine TNF-alpha and number of apoptotic neurons on hippocampus and dentate gyrus after transient global cerebral I/R injury. Eighteen rats divided into 3 groups, equally. Group I rats were used as shams. For group II and III rats, they were prepared for transient global cerebral ischemia using a four-vessel-occlusion model. 5 mL/kg/h 0.9% sodium chloride was infused to the Group II and 3 microg/kg/h/5 ml dexmedetomidine was infused to the Group III for 2 h after I/R injury. The levels of MDA and NO and activities of SOD and CAT were measured in the left hippocampus tissue. The levels of TNF-alpha concentration were measured in the plasma. The number of apoptotic neurons was counted by TUNNEL method in histological samples of right hippocampus tissue. MDA and NO levels increased in Group II compared with Group I rats (p=0.002, p=0.002, respectively). In group III, MDA and NO levels decreased as compared to Group II (p=0.015, p=0.002, respectively). SOD and CAT activities increased in Group III as compared to Group II rats (p=0.002, p=0.002, respectively). The decrease in TNF-alpha levels of group III was significant as compared to group II (p=0.016). The number of apoptotic neurons in group III was lower than Group II rats. Our study showed that dexmedetomidine has a neuroprotective effect on hippocampus and dentate gyrus of rats after transient global cerebral I/R injury.

The neuroprotective effect of dexmedetomidine in the hippocampus of rabbits after subarachnoid hemorrhage.

BACKGROUND Subarachnoid hemorrhage is a serious condition, often accompanied by cerebral vasospasm, which may lead to brain ischemia and neurologic deterioration. We evaluated if dexmedetomidine has neuroprotective effects in the hippocampus of vasospastic SAH rabbits or not. MATERIALS AND METHODS Eighteen New Zealand rabbits were taken. An experimental SAH model was formed by injecting 0.9 mL of autologous arterial blood per 1 kg of body weight to the cisterna magna of 12 rabbits. Craniotomy was performed in the control group (n = 6) except performing experimental SAH. Rabbits in the SAH-alone (n = 6) group were infused with 5 mL.kg(-1).h(-1) 0.9% sodium chloride, and rabbits (n = 6) in the SAH-dexmedetomidine group were infused with 5 microg.kg(-1).h(-1) dexmedetomidine for 2 hours, 48 hours after SAH was established. Rabbits of all groups were sacrificed via penthotal 24 hours after dexmedetomidine administration. Brains were removed immediately, and hippocampal tissues were blocked from the right hemisphere for histopathologic study. In addition to this, hippocampal tissues of left hemispheres were dissected for biochemical analyses to evaluate MDA levels, activity of XO, and SOD. RESULTS The histopathologic study showed that dexmedetomidine may have a neuroprotective effect in SAH-induced hippocampal injuries. The biochemical parameters support the neuroprotective effect of dexmedetomidine (P < .05). CONCLUSION Our study showed that dexmedetomidine may have a neuroprotective effect in the hippocampus of vasospastic SAH rabbits.

Antifibrotic Effects of Aldosterone Receptor Blocker (Spironolactone) in Patients with Chronic Kidney Disease

Aims. Proteinuria and transforming growth factor β (TGF-β) are parameters that can lead to glomerulosclerosis and tubulointerstitial fibrosis. All components of the renin-angiotensin-aldosterone system (RAAS) activate the TGF-β. Aldosterone may not be inhibited with angiotensin-converting enzyme inhibitors (ACEIs) and/or angiotensin receptor blockers (ARBs) due to aldosterone escape. We aimed to evaluate the effect of spironolactone on parameters leading to fibrosis. Methods. This prospective study included 30 non-diabetic chronic kidney disease (CKD) patients treated with ACEIs and/or ARBs. The patients were divided into two groups that are similar in terms of demographic parameters. 25 mg of spironolactone was added to group 1 (n = 15) for six months, though it was not administered to group 2 (n = 15). Creatinine (U-Cr), protein (U-Prot), and TGF-β1 (U- TGF-β1) were measured in spot urine sample in the beginning of study and six months later. Results. Twenty-four patients completed the study. There were no significant changes in mean blood pressure, glomerular filtration rate, creatinine, albumin, and plasma aldosterone concentrations during the observation period in either group. U-Prot/U-Cr (mg/mg Cr) was reduced from 2.43 ± 4.85 at baseline to 1.66 ± 3.51 at sixth month (p = 0.003) in group 1. In addition, U-TGF-β1/U-Cr (ng/mg Cr) was also reduced from 22.50 ± 6.65 at baseline to 17.78 ± 10.94 at sixth month (p = 0.041) in the same group. U-TGF-β1/U-Cr and U-Prot/U-Cr ratios after the sixth month were not found significant compared with baseline values in group 2. Conclusion. Spironolactone reduced both proteinuria and urinary TGF-β1 excretion in CKD patients. We consider that spironolactone would be beneficial to prevent progression of renal fibrosis in CKD.

The serum levels of resistin in ankylosing spondylitis patients: a pilot study

Resistin is a recently described adipokine which is a member of cysteine-rich secretory protein family. Although it has been primarily defined in human adipocytes, it has been identified that its level was higher in mononuclear leukocytes, macrophages, spleen, and bone marrow cells. Because ankylosing spondylitis is an inflammatory disease, it is suspected that upregulation of proinflammatory cytokines is effective in its immunopathogenesis. The aim of our study is to determine the serum resistin levels in patients with AS and to research the relationship with disease activity markers. A total of 30 patients with AS and 30 healthy controls were included in this study. Serum resistin concentrations, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Bath AS Disease Activity Index (BASDAI) were evaluated. In results resistin levels in ankylosing spondylitis group were significantly higher than in control group. But, there was no correlation between resistin and ESR, CRP, BASDAI. In conclusion, higher serum resistin levels in patients with AS compared to healthy subjects give clues that resistin could have a role in the pathogenesis of AS.

Protective effect of aprotinin on ischemia–reperfusion injury in rat ovary

Aim:  We investigated the effects of aprotinin on reperfusion injury in a controlled experimental rat torsion–detorsion model.

Effects of Coenzyme Q10 Supplementation on Plasma Adiponectin, Interleukin-6, and Tumor Necrosis Factor-α Levels in Men

The aim of the study was to determine the effects of coenzyme Q10 supplementation on plasma adiponectin, interleukin (IL)-6, and tumor necrosis factor (TNF )-alpha levels in sedentary men. Fourteen healthy, nonsmoking, sedentary men participated in the study. The protocol was approved by the Ethical Committee of our institution. This study was a randomized, double-blind, crossover trial. Blood samples were collected from all participants before coenzyme Q10 or placebo supplementation. The participants were randomly allocated to two groups. Seven participants received oral coenzyme Q10 (100 mg/day) supplementation, and seven participants received placebo (glucose) for 8 weeks. At the end of the 8 weeks, a second blood sampling was performed. After a 4-week washout period, placebo was given to the participants who used coenzyme Q10 the first time, and vice versa, and blood sampling was repeated. Plasma was stored at -80 degrees C until the time of analysis for adiponectin, IL-6, and TNF-alpha. Both CoQ10 and placebo supplementation did not affect plasma adiponectin and TNF-alpha levels. IL-6 level increased with coenzyme Q10 supplementation, but this increase did not differ from that seen with placebo supplementation. Coenzyme Q10 supplementation did not affect plasma adiponectin, IL-6, and TNF-alpha levels in sedentary men.

The protective effect of α‐lipoic acid in experimental ovarian ischaemia‐reperfusion injury

Background:  We investigated the effect of α‐lipoic acid (LA) on reperfusion injury in a rat ovarian torsion–detorsion model. The changes in tissue and plasma levels of malondialdehyde (MDA), end‐product of lipid peroxidation, superoxide dismutase (SOD), xanthine oxidase (XO) and nitric oxide (NO), were determined. Ovarian histopathological findings were scored and compared among groups.

Effects of grape seed polyphenols on oxidative damage in liver tissue of acutely and chronically exercised rats.

The objective of the present study was to investigate the effects of grape seed extract (GSE) supplementation on oxidative stress and antioxidant defense markers in liver tissue of acutely and chronically exercised rats. Rats were randomly assigned to six groups: Control (C), Control Chronic Exercise (CE), Control Acute Exercise (AE), GSE‐supplemented Control (GC), GSE‐supplemented Chronic Exercise(GCE) and GSE‐supplemented Acute Exercise (GAE). Rats in the chronic exercise groups were subjected to a six‐week treadmill running and in the acute exercise groups performed an exhaustive running. Rats in the GSE supplemented groups received GSE (100 mg.kg−1.day−1) in drinking water for 6 weeks. Liver tissues of the rats were taken for the analysis of malondialdehyde (MDA), nitric oxide (NO) levels and total antioxidant activity (AOA) and xanthine oxidase (XO) activities. MDA levels decreased with GSE supplementation in control groups but increased in acute and chronic exercise groups compared to their non‐supplemented control. NO levels increased with GSE supplementation. XO activities were higher in AE group compared to the CE group. AOA decreased with GSE supplementation. In conclusion, while acute exercise triggers oxidative stress, chronic exercise has protective role against oxidative stress. GSE has a limited antioxidant effect on exercise‐induced oxidative stress in liver tissue. Copyright

Relationship Between Iron-Deficiency Anemia and Periodontal Status in Female Patients

BACKGROUND The aim of this study was to evaluate the periodontal status of patients with iron-deficiency anemia (IDA) and the correlation of changes in serum and gingival crevicular fluid (GCF) ferritin levels after periodontal therapy. METHODS Nineteen female patients with anemic hematologic values were classified as group A, and 20 healthy females with normal hematologic values were classified as group B. After group A was recruited, group B was enrolled with patients who had similar gingival indices as group A. At baseline and the 3-month follow-up visit, clinical periodontal indices and hematologic parameters were recorded, and GCF samples were taken. All patients received an oral hygiene-improvement session followed by scaling, and sites with >4-mm probing depths received root planing. At the 3-month follow-up visit, all measurements and analyses were repeated. RESULTS During the follow-up period, all clinical indices decreased in both groups (P <0.05), but the gingival index in group A did not change. The GCF ferritin concentration showed statistically significant decreases (P <0.05), but total amounts of ferritin in GCF did not change. No significant correlation was found between serum and GCF ferritin levels. CONCLUSION The findings of this study showed that changes in serum ferritin levels did not correlate with the GCF ferritin levels, and IDA was not a direct risk factor for periodontal diseases.