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Objective: The most common type of epilepsy affecting about 50 million people worldwide is temporal lobe epilepsy (TLE). Chemical and electrical kindling methods in animals can be used to form the TLE model. In this study, it was aimed to investigate neurogenesis by immunofluorescence methods in the hippocampus of adult Wistar rats, which were applied chemical kindling. Methods: Adult male Wistar albino rats weighing 250-300 gr were injected PTZ (35 mg/kg) subcutaneously every other day to produce chemical kindling (Wistar kindling 7th day group n=6; 14th day group n=6). Sham-operated control groups were injected physiological saline solution subcutaneously (Wistar shamoperated 7th day group n=6; 14th day group n=6). Animals having grade 5 seizures five times were considered to be kindled. Intracardiac perfusion was performed under deep anesthesia on the 7th and 14th days after the last grade 5 seizure. Then, the animals were decapitated and brain tissues were removed and incubated at 4°C overnight within the same fixative. The tissues were frozen at -80ºC and 5 μm sections were obtained with a cryomicrotome. Immunofluorescence methods were used to show doublecortin (DCX) positive newly formed neurons and glial fibrillary acidic protein (GFAP) positive cells. Sections were then examined under fluorescence microscope. Results: DCX positive cells were observed in the subgranular zone of gyrus dentatus in the control and kindling groups. An increase in GFAP positive cells in the kindling groups, compared to the control groups, was observed. Conclusion: The findings of the present study indicate the existence of neurogenesis in the control and kindled adult Wistar rats. The increase in GFAP positive cells in the kindling groups suggests astrogliosis. [ABSTRACT FROM AUTHOR]

Trauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control (n = 16), trauma (n = 16) and dexpanthenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol- and lucigenin-enhanced chemiluminescence (CL), malondialdehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated (p < 0.05–0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen (p < 0.05–0.001) and MDA levels were decreased (p < 0.05). Decreased SOD and CAT activities (p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group (p < 0.05–0.001). in the dexpanthenol group there was relatively less neuronal damage observed microscopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. [ABSTRACT FROM AUTHOR]

Objective: Traumatic brain injury (TBI) is one of the most common preventable causes of mortality and morbidity. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophysiological mechanisms underlying neuronal loss after TBI. Mildronate is demonstrated to be beneficial in various experimental models of ischemic diseases via anti-inflammatory, antioxidant, and neuroprotective mechanisms. This study aimed to investigate possible antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of mildronate in a rat model of TBI.Methods: A total of 46 male rats were divided into three groups of control, saline-treated TBI, and mildronate-treated TBI. Both TBI groups were subjected to closed-head contusive weight-drop injuries followed by treatment with saline or mildronate (100 mg/kg) administered intraperitoneally. The forebrain was removed 24 h after trauma induction, the activities of myeloperoxidase (MPO) and caspase-3, levels of superoxide dismutase (SOD), luminol- and lucigenin-enhanced chemiluminescence were measured, and histomorphological evaluation of cerebral tissues was performed.Results: Increased MPO and caspase-3 activities in the vehicle-treated TBI group (p < 0.001) were suppressed in the mildronate-treated TBI group (p < 0.001). Similarly, increase in luminol and lucigenin levels (p < 0.001 and p < 0.01, respectively) in the vehicle-treated TBI group were decreased in the mildronate-treated TBI group (p < 0.001). Concomitantly, in the vehicle-treated TBI group, TBI-induced decrease in SOD activity (p < 0.01) was reversed with mildronate treatment (p < 0.05). On histopathological examination, TBI-induced damage in the cerebral cortex was lesser in the mildronate-treated TBI group than that in other groups.Conclusion: This study revealed for the first time that mildronate, exhibits neuroprotective effects against TBI because of its anti-inflammatory, antiapoptotic, and antioxidant activities. [ABSTRACT FROM AUTHOR]

Reactive oxygen metabolites play important roles in ischemia/reperfusion (I/R) injury in several organ systems. Riboflavin has been shown to exert antioxidant and/or anti-inflammatory activities in several experimental models. The aim of this study was to investigate the role of riboflavin against I/R injury in the rat kidney. Wistar albino rats 200-300 g weighing were divided into 3 groups. One week after unilateral nephrectomy, the IR procedure was applied to the rats. To induce I/R injury renal pedicle was clamped for 45 minutes and then rats were allowed reperfusion for 6 hours. Riboflavin (25 mg/kg, orally) or vehicle was administered for one week as pretreatment. After decapitation, kidney tissue samples were taken for the evaluation of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and 8-hydroxydeoxyguanosine (8-OHdG), a specific marker of oxidative DNA damage. Furthermore, myeloperoxidase (MPO) and caspase-3 activities were also examined together with histological analysis. Ischemia/reperfusion induced significant increases in MDA and 8-OHdG levels and MPO and caspase- 3 activities, and decrese in GSH levels. In the riboflavin treatment these indices were found to be reversed back to control levels. The present data demonstrated that riboflavin, through its antioxidant effect, attenuates I/R induced acute renal injury in rats. [ABSTRACT FROM AUTHOR]

Objective: Purinergic 2X7 receptor (P2X7R) activation is known to be involved in pathogenesis of depression. Our aims were to investigate P2X7R-activated inflammasome pathways in parallel with induction of depression and to test the antidepressant-like effects of the selective P2X7R antagonist Brilliant Blue G (BBG) in a rat model of chronic unpredictable mild stress (CUMS). Methods: Male Wistar albino rats were divided into control, CUMS, CUMS+BBG25 (25 mg/kg/day) and CUMS+BBG50 (50 mg/kg/day) groups (n=10 for each group). Various stressors were applied to rats for 6 weeks to establish the CUMS model and daily BBG treatment was started at the end of 3rd week. Sucrose preference test and forced swim test (FST) were performed to assess antidepressant-like effects. Brain samples were obtained for real-time polymerase chain reaction and immunohistochemistry analysis. Results: In FST, duration of immobility was reduced in the CUMS+BBG50 group. Also, BBG treatment significantly enhanced sucrose preference. While NLRP3 gene expression levels were unchanged in rats exposed to the CUMS protocol, expression levels of other inflammasome pathway factors NLRP1, caspase-1, ASC, NF-κB, IL-1β, IL-6 and P2X7R were increased. BBG treatment reduced expression levels of these factors. Likewise, Iba-1 and GFAP immunoreactivities were enhanced by the CUMS protocol and this action was reversed by BBG treatment. Conclusion: Chronic administration of BBG in CUMS model results in antidepressant-like activity in a dose dependent manner. Molecular and histological results show that these effects might be at least partially related to the suppression of inflammasome-related neuroinflammatory responses and suggest involvement of NLRP1 in depression. [ABSTRACT FROM AUTHOR]

Objective: Traumatic brain injury (TBI) is associated with high mortality and morbidity. Trauma-induced primary damage is followed by apoptosis, lipid peroxidation and oxidative stress that lead to secondary damage, causing exacerbation of TBI. In various inflammation models, dexpanthenol was shown to protect tissues against oxidative damage. It was aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI model. Methods: Wistar albino male rats were randomly assigned to control (n = 8), TBI+dexpanthenol (500 mg/kg; n = 10) and TBI+vehicle (n = 10) groups. TBI was performed under anesthesia (ketamine+xylazine) by dropping a 300 g weight from 70- cm height on the skull of rats, which were injected intraperitoneally with vehicle or dexpanthenol immediately after trauma. At 24th h of trauma, rats were decapitated. Malondialdehyde (MDA) -indicative of lipid peroxidation-, myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) levels and catalase (CAT) activities and levels of luminol- and lucigenimmediated chemiluminescence (CL), -indicating presence of reactive oxygen species- were measured in brain tissues. Following transcardiac parafolmadehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. The data was evaluated by one-way ANOVA. Results: In the vehicle-treated TBI group, MPO level, caspase- 3 activity and luminol-lucigenin CL levels were elevated (p<0.05-0.001), while in the dexpanthenol-treated TBI group these increases were suppressed (p<0.05-0,001) and MDA levels were decreased (p<0.05). Decreased SOD and CAT activities (p<0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol-treated TBI group (p<0.05- 0.001). Neuronal damage observed microscopically in the cortices of TBI was relatively less in the dexpanthenol-treated group. Conclusion: Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and thereby alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. [ABSTRACT FROM AUTHOR]

Objective: Oxidative stress following traumatic brain injury (TBI) leads to further deterioration of brain damage. Mildronate, known for its vasodilator and anticonvulsant effects, has been shown to be useful in a variety of experimental models and ischemic diseases. In this study, it was aimed to investigate possible antioxidant and neuroprotective effects of mildronate in a rat TBI model. Methods: Under ketamine anesthesia, TBI (n=20) was induced by dropping a metal weight (300 g) from a height of 70 cm on the skull of male Wistar albino rats. Half of the rats was treated intraperitoneally with vehicle, while the other half was treated with mildronate (100 mg/kg) immediately after TBI. Control group (n=8) was not exposed to any trauma. Twenty-four hours after TBI, transcardial paraformaldehyde perfusion was performed and brain injury was graded histopathologically following hematoxylin-eosin staining. Activities of myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) and catalase (CAT), and levels of luminol- and lucigenin-enhanced chemiluminescence (CL) were measured in brain tissues. The data were evaluated by one-way ANOVA. Results: In the mildronate-treated group, the damage in the cerebral cortex that has occurred due to TBI was lighter compared to that of the vehicle-treated TBI group. Antioxidant SOD activity, which was found to be decreased in the brain tissues of the vehicle-treated TBI group (p<0.01), was increased in the group that has received mildronate treatment (p<0.05). Higher levels of CL, increased MPO and caspase-3 activities (p<0.01- 0.001) in the vehicle-treated TBI group were found to be suppressed in the mildronate-treated group (p<0.05-0.001). Conclusion: Suppression of oxidative damage and apoptosis in brain tissues of rats in mildronate-treated TBI group, and alleviation of brain damage by stimulating antioxidant systems suggest that mildronate should be further evaluated for its possible therapeutic effect in traumatic brain injury. [ABSTRACT FROM AUTHOR]