RESUMEN
Background@#Chronic exposure to silica is related with the provocation of an inflammatory response and oxidative stress mechanism. Vitamin D has multiple benefits in biological activities particularly respiratory system disease.MethodIn this research, 20 male Wistar rats were randomly allocated into four groups (5 rats /group) as follow: Group1 received saline as (negative control) group. The group 2 received a single IT instillation of silica (positive control) group; the group 3 was co-administrated with single IT silica and Vitamin D (20 mg/kg/day) daily for a period of 90 days. The rats of group 4 received Vitamin D daily for a period of 90 days. @*Results@#Silica significantly increased serum and lung total Oxidant Status (TOS). Meanwhile, silica reduced serum and lung total antioxidant capacity (TAC), GSH and tumor necrosis factor-α (TNF-a). Vitamin D treatment meaningfully reversed oxidative stress, antioxidants status and inflammatory response. Also, Vitamin D improved histopathological changes caused by silica. @*Conclusion@#These findings indicate that Vitamin D exerts protective effects against silica-induced lung injury. It seems that Vitamin D has potential use as a therapeutic object for silica induced lung injure.
RESUMEN
@#Introduction: Intracerebroventricular administration of streptozotocin (icv-STZ) induced apoptosis changes in neurons similar to Alzheimer's disease. The serotonergic system via its receptor involved in survival of neurons. The present study examined the ability of selective 5-HT1A receptor antagonist (NAD-299) and 5-HT2A receptor agonist (TCB-2) to attenuate the apoptosis caused by the icv-STZ in the rat. Methods: The icv-STZ (3 mg/kg, 10 μL, twice) induced neuronal loss in the hippocampus of adult male rats. Animals were divided into naive control, sham-operated, STZ+saline (1 μL, icv), STZ+NAD-299 (5 μg/μL, icv), STZ+TCB-2 (5 μg/μL, icv), and STZ+NAD-299+TCB-2 (5 μg/μL of any agent, icv) groups. Following the 35 days’ treatment period, neuronal apoptosis was detected using the Tunnel. Cells with morphological features of apoptotic cell were contended by microscopy. Results: TCB-2 and NAD-299 administration decreased number of apoptotic neurons in the treatment group compared with the STZ group. Combined treatment of STZ rat with NAD+TCB more decreased number of apoptotic cells in compare to TCB-2 or NAD-299 treated STZ groups. Conclusion: Treatment with 5-HT1A receptor antagonist or 5-HT2A receptor agonist diminished apoptosis. The beneficial effect of 5HT1A receptor inhibition was potentiated with activation of 5-HT2A receptor in prevention of apoptosis in hippocampus.
RESUMEN
Introduction: Lead [Pb] is a neurotoxin that its different effects on the central nervous system are well-known. Previous studies have reported the potent effects of vitamin C on memory.The present study was undertaken to evaluate the protective effects of vitamin C against leadinduced amnesia
Methods: Male Wistar rats were divided into 4 groups: the control [saline], negative control [lead], positive control [Vitamin C, 150 mg per kg], and experimental [Lead+Vitamin C]. To induce lead toxicity, the rats received water containing 0.2% Pb instead of regular water for 1 month. Passive avoidance learning was assessed by Shuttle Box 2 months later. Retention was tested 24 hours after training
Results: The results showed that lead causes impairment in acquisition and retrieval processes of passive avoidance learning and memory. However, vitamin C administration reinforced passive avoidance learning and memory. All results were significant [P<0.001]
Conclusion: Vitamin C administration in rats counteracts the negative effect of lead on spatial learning and memory
RESUMEN
Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ventricular zone neurons are vulnerable to ischemia that can impair memory and learning functions. Although neurogenesis normally occurs in the dentate gyrus [DG] of the hippocampus and sub-ventricular zone [SVZ] following brain damage, this response is unable to compensate for severely damaged areas. This study aims to assess both neurogenesis and the neuroprotective effects of transforming growth factor-alpha [TGF-alpha] on the hippocampus and SVZ following ischemia-reperfusion. In this experimental study, a total of 48 male Wistar rats were divided into the following groups: surgical [n=12], phosphate buffered saline [PBS] treated vehicle shams [n=12], ischemia [n=12] and treatment [n=12] groups. Ischemia was induced by common carotid occlusion for 30 minutes followed by reperfusion, and TGF-alpha was then injected into the right lateral ventricle. Spatial memory was assessed using Morris water maze [MWM]. Nestin and Bcl-2 family protein expressions were studied by immunohistochemistry [IHC] and Western blot methods, respectively. Finally, data were analyzed using Statistical Package for the Social Sciences [SPSS, SPSS Inc., Chicago, USA] version 16 and one-way analysis of variance [ANOVA]. TGF-alpha injection significantly increased nestin expression in both the hippocampal DG and SVZ areas. TGF-alpha treatment caused a significant decrease in Bax expression and an increase in Bcl-2 anti-apoptotic protein expression in the hippocampus. Our results showed a significant increase in the number of pyramidal neurons. Memory also improved significantly following TGF-alpha treatment. Our findings proved that TGF-alpha reduced ischemic injury and played a neuroprotective role in the pathogenesis of ischemic injury
Asunto(s)
Animales de Laboratorio , Trastornos de la Memoria , Memoria , Neurogénesis , Daño por Reperfusión , Hipocampo , Ratas WistarRESUMEN
3,4-methylenedioxymethamphetamine [MDMA] is an illicit, recreational drug that causes cellular death and neurotoxicity. This study evaluates the effects of different doses of MDMA on the expression of apoptosis-related proteins and genes in the hippocampus of adult rats. In this experimental study, a total of 20 male Sprague Dawley rats [200-250 g] were treated with MDMA [0, 5, 10, 20 mg/kg i.p. twice daily] for 7 days. Seven days after the last administration of MDMA, the rats were killed. Bax and Bcl-2 genes in addition to protein expressions were detected by western blot and reverse transcription polymerase chain reaction [RT-PCR].Results were analyzed using one-way ANOVA and p = 0.05 was considered statistically significant. Our results showed that MDMA caused dose dependent up-regulation of Bax and down-regulation of Bcl-2 in the hippocampus. There was a significant alteration in bcl-2 and bax genes density. Changes in apoptosis-related proteins and respective genes relating to Bax and Bcl-2 might be involved in the molecular mechanism of MDMA-induced apoptosis
Asunto(s)
Animales de Laboratorio , Genes bcl-2 , Expresión Génica , Ratas Sprague-Dawley , Apoptosis , HipocampoRESUMEN
The spice Zingiber officinale or ginger possesses antioxidant activity and neuroprotective effects. The effects of this traditional herbal medicine on 3,4-methylenedioxymethamphetamine [MDMA] induced neurotoxicity have not yet been studied. The present study considers the effects of Zingiber officinale on MDMA-induced spatial memory impairment and apoptosis in the hippocampus of male rats. In this experimental study, 21 adult male Sprague Dawley rats [200-250 g] were classified into three groups [control, MDMA, and MDMA plus ginger]. The groups were intraperitoneally administered 10 mg/kg MDMA, 10 mg/kg MDMA plus 100 mg/kg ginger extract, or 1 cc/kg normal saline as the control solution for one week [n=7 per group]. Learning memory was assessed by Morris water maze [MWM] after the last administration. Finally, the brains were removed to study the cell number in the cornu ammonis [CA1] hippocampus by light microscope, Bcl-2 by immunoblotting, and Bax expression by reverse transcription polymerase chain reaction [RT-PCR]. Data was analyzed using SPSS 16 software and a one-way ANOVA test. Escape latency and traveled distances decreased significantly in the MDMA plus ginger group relative to the MDMA group [p<0.001]. Cell number increased in the MDMA plus ginger group in comparison to the MDMA group. Down-regulation of Bcl-2 and up-regulation of Bax were observed in the MDMA plus ginger group in comparison to the MDMA group [p<0.05]. Our findings suggest that ginger consumption may lead to an improvement of MDMA-induced neurotoxicity
Asunto(s)
Animales de Laboratorio , Apoptosis , Encéfalo/patología , Memoria Espacial , N-Metil-3,4-metilenodioxianfetamina/farmacología , Hipocampo , Ratas Sprague-DawleyRESUMEN
3-4, methylenedioxymethamphetamine [MDMA] causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein [NAC] as an antioxidant on MDMA-induced apoptosis. 21 Sprague dawley male rats [200-250mg] were treated with MDMA [2x0,5mg/kg] or MDMA plus NAC [100mg/kg IP for 7 day]. After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method. The results of this study showed that MDMA causes up-regulation of Bax and down-regulation of Bcl-2 and NAC administration attenuated MDMA-induced apoptosis. The present study suggests that NAC treatment may improve MDMA-induced neurotoxicity.