Onder Sahin

The protective effect of fish n-3 fatty acids on cerebral ischemia in rat hippocampus

Reactive oxygen species (ROS) have been implicated in the pathogenesis of cerebral injury after ischemia-reperfusion (I/R). Fish n-3 essential fatty acids (EFA), contain eicosapentaenoic acids (EPA) and docosahexoenoic acids (DHA), exhibit antioxidant properties. DHA is an important component of brain membrane phospholipids and is necessary for the continuity of neuronal functions. EPA prevents platelet aggregation and inhibits the conversion of arachidonic acid into thromboxane A(2) and prostaglandins. They have been suggested to be protective agents against neurological and neuropsychiatric disorders. In this study, the neuroprotective effects of fish n-3 EFA on oxidant-antioxidant systems and number of apoptotic neurons of the hippocampal formation (HF) subjected to cerebral I/R injury was investigated in Sprague-Dawley rats. Six rats were used as control (Group I). Cerebral ischemia was produced by occlusion of both the common carotid arteries combined with hypotension for 45 min, followed by reperfusion for 30 min, in rats either on a standard diet (Group II) or a standard diet plus fish n-3 EFA (Marincap((R)), 0.4 g/kg/day, by gavage) for 14 days (Group III). At the end of procedures, the rats were sacrificed and their brains were removed immediately. The levels of malonedialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in left HF. In addition, the number of apoptotic neurons was counted by terminal transferase dUTP nick end labelling (TUNEL) assay in histological samples of the right HF. We found that SOD activities and MDA levels increased in Group III rats compared with Group II rats. On the other hand, CAT activities and NO levels were found to be decreased in Group III rats compared with Group II rats. Additionally, the number of apoptotic neurons was lower in Group III in comparison with Group II rats. The present findings suggest that fish n-3 EFA could decrease the oxidative status and apoptotic changes in ischemic rat hippocampal formation. Dietary supplementation of n-3 EFA may be beneficial to preserve or ameliorate ischemic cerebral vascular disease.

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.

Expression of cyclooxygenase-2 and matrix metalloproteinase-2 in adenomyosis and endometrial polyps and its correlation with angiogenesis.

This study investigates the expression of cyclooxgenase (COX)-2 and matrix metalloproteinase (MMP)-2 in patients with adenomyosis or endometrial polyps and their possible relation to microvascular density in these lesions. The subjects were 25 patients with adenomyosis, 30 patients with endometrial polyps, and 20 female controls. The expression of COX-2, MMP-2, and CD34 was studied immunohistochemically. Microvesseldensity (MVD) was calculated by the counting of CD34-positive vascular endothelial cells. The quantity and intensity of COX-2 expression in endometrium did not vary during the menstrual cycle in the control group and in patients with endometrial polyps. In patients with adenomyosis, it was higher in the secretory phase. MMP-2 expression in stromal cells in adenomyotic foci and endometrial polyps were higher than in normal endometrium. In the proliferative phase, MVD in adenomyosis foci was higher than in normal endometrium and endometrial polyps. In the secretory phase, MVD in adenomyotic foci and endometrial polyps was higher than in normal endometrium. Overexpression of stromal MMP-2 may play a role in the development of adenomyosis and endometrial polyps. Aberrant COX-2 expression in eutopic endometrium during the luteal phase may be associated with the pathogenesis of adenomyosis; however, expression of COX-2 does not seem to play a role in the development of endometrial polyps. MVD was high in both lesions, but there was no significant correlation between MVD and the expression of MMP-2 or COX-2. Mechanisms other than COX-2 and MMP-2 may contribute to the promotion of angiogenesis in these lesions.

The protective effect of fish n-3 fatty acids on cerebral ischemia in rat prefrontal cortex

This study presents neuroprotective effects of fish n-3 EFA on the prefrontal cortex after cerebral ischemia and reperfusion. Eighteen rats divided into three groups. Group A rats were used as control. Cerebral ischemia and reperfusion was produced in rats either on a standard diet (Group B) or a standard diet plus fish n-3 EFA for 14 days (Group C). The malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were measured and the number of apoptotic neurons was counted. The levels of MDA and activities of SOD increased in Group B rats as compared to Group A rats, and decreased in Group C rats as compared to Group B rats. The activities of CAT increased in Group C as compared to Group B rats. The number of apoptotic neurons in the prefrontal cortex was lower in Group C as compared to Group B rats.

The neuroprotective effect of fish n-3 fatty acids in the hippocampus of diabetic rats

Abstract Introduction: Diabetes mellitus may lead to functional and structural changes in the brain. Fish oil is a rich source of n-3 essential fatty acids (EFA) such as eicosapentaenoic and docosahexoenoic acids. We examined the neuroprotective effects of fish n-3 EFA in the hippocampus of diabetic rats. Materials and methods: Nineteen adult male rats were divided into three groups. Group I (control; n = 6) was fed a normal rat diet. Group II (diabetic; n = 6) was fed a normal rat diet and streptozotocin (STZ) was administered to induce diabetes mellitus. Group III (n-3 + diabetic; n = 7) was fed a normal rat diet and fish n-3 EFA (Marincap®, 0.4 g/kg/day) for 8 weeks and STZ was administered to induce diabetes mellitus. The levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in the left hippocampus after the animals were sacrificed. The right hemisphere was completely blocked. The sections were stained with Cresyl Violet and apoptotic neurons were counted in the hippocampus. Results: The levels of MDA and activities of SOD and CAT increased in diabetic rats compared to control rats. However, the levels of MDA and activities of SOD and CAT decreased in n-3 + diabetic rats compared to diabetic rats. Also, the number of apoptotic neurons increased in diabetic rats compared to control rats and decreased in n-3 + diabetic rats compared to diabetic rats. Conclusions: Fish n-3 EFA reduces oxidative stress and induces apoptotic changes in the hippocampus of STZ-diabetic rats. The addition of fish n-3 EFA to diets may be useful to prevent functional and structural changes to cerebral centers due to diabetes mellitus.

Lithium-induced lung toxicity in rats: the effect of caffeic acid phenethyl ester (CAPE)

Aims: We aimed to evaluate the effects of caffeic acid phenethyl ester (CAPE) on lithium (Li)‐induced lung toxicity. Methods: Twenty‐two adult male Wistar albino rats weighing between 280 and 300 g were used. The rats were randomly divided into three groups: control, Li and Li+CAPE groups. Li and CAPE were co‐administered intraperitoneally twice daily for 4 weeks. Control rats were given 0.9% NaCl during the same period. All the rats were allowed to feed ad libitum until midnight after they had received the proposed treatment. Results: In the Li group, peribronchial and intraparenchymal lymphocyte and macrophage infiltration were observed. Atypical type II pneumocytes, alveolar destruction and emphysematous changes were also detected. Lymphocyte and macrophage infiltration was significantly decreased in the Li+CAPE group compared with the Li group. Alveolar destruction, emphysematous changes and intraparenchymal mononuclear cell infiltration were also recovered to a level close to the control group. Malondialdehyde (MDA) levels were increased in the Li group compared with the control group. CAPE administration decreased the MDA levels in the Li+CAPE group. Conclusions: CAPE was found to associate with histopathological changes recovery in the lungs and oxidative stress due to Li treatment.

Caffeic acid phenethyl ester reduces mortality and sepsis-induced lung injury in rats.

Objective: Sepsis and ensuing multiorgan failure continue to be the major causes of mortality in intensive care units. Nuclear factor (NF)‐[kappa]B activation is supposed to be one of the targets in the treatment of sepsis. We studied the effectiveness of caffeic phenethyl ester (CAPE), a known NF‐[kappa]B inhibitor, in cecal ligation and puncture (CLP)‐induced sepsis and lung injury. Design: Randomized, controlled animal study. Setting: Research laboratory of an academic institution. Subjects: Female Sprague‐Dawley rats. Interventions: CLP was performed in all rats except the rats in control and sham+CAPE groups. CAPE was administered to rats at the time of operation in sham+CAPE and CAPE+sepsis0 groups. CAPE was administered to rats in the CAPE+sepsis12 group 12 hrs after CLP. Eight rats from each group were killed 24 hrs after CLP. Blood was taken for assessment of interleukin‐1, interleukin‐6, interleukin‐10, and tumor necrosis factor‐[alpha]; the right lung was removed for histopathologic examination and the left lung for biochemical examination. Apoptosis, inducible nitric oxide synthase, heat shock protein 70, malondialdehyde, catalase, superoxide dismutase, and glutathione peroxidase were studied. The rest of the rats were observed for mortality. Measurements and Main Results: Mortality was significantly decreased in groups that received CAPE compared with the sepsis group. All cytokine levels were similar to control levels only in the CAPE+sepsis12 group. Apoptosis, inducible nitric oxide synthase, and heat shock protein 70 evaluation were significantly changed between all groups in the following order: control < sham+CAPE< CAPE+sepsis12 < CAPE+sepsis0 < sepsis. Malondialdehyde and catalase were increased in the sepsis group. Conclusions: CAPE reduced mortality in sepsis and improved histopathologic variables best when it was administered after the onset of sepsis.

Bone wax as a cause of foreign body reaction after lumbar disc surgery: a case report.

This report describes a 45-year-old patient who was admitted to the hospital with complaints of low-back pain, lower extremity weakness, and difficulty in walking for the previous 6 mo. The patient’s history revealed 2 lumbar-disc surgeries that were performed 1 y earlier. The patient underwent surgery at our hospital because of clinical symptoms and radiologic findings on magnetic resonance imaging. During the operation, 1×1×1 cm of bone wax that was compressing the dural sac and spinal root was extirpated from the surgical area. Bone wax use should be limited in spinal surgery because of the potential for compression and chronic inflammation.

Effects of melatonin on the oxidant/antioxidant status and lung histopathology in rabbits exposed to cigarette smoke

Objectives and background:  To evaluate the effects of cigarette smoking on the histopathology and the oxidant/antioxidant status of the lungs and to test the potential antioxidant benefits of melatonin on these induced changes.