The Effects of Resveratrol on Silica-Induced Lung Oxidative Stress and Inflammation in Rat

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.

Protective Effects of 5-HT1A Receptor Inhibition and 5-HT2A Receptor Stimulation Against Streptozotocin-Induced Apoptosis in the Hippocampus

@#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.

Vitamin C can alter lead-induced passive avoidance learning impairment in rats

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

Transforming growth factor -alpha improves memory impairment and neurogenesis following ischemia reperfusion

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

Evaluation of Bcl-2 family gene expression in hippocampus of 3, 4-methylenedioxymethamphetamine treated rats

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

Zingiber officinale alters 3,4-methylenedioxymeth amphetamine-induced neurotoxicity in rat brain

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

Protective effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-induced Neurotoxicity in Cerebellum of male rats

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.