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Inflammation can cause memory impairment. In the present study, the effect of carvacrol on brain tissue inflammation and oxidative stress as well as learning and memory in lipopolysaccharide (LPS)-challenged rats was evaluated. The animals were grouped and treated: (1) control which received vehicle instead of LPS and carvacrol, (2) LPS (1 mg/kg; i.p. 120 min before behavioral tests), and (3-5) in these groups, 25, 50, or 100 mg/kg of carvacrol (i.p.) was administered 30 min prior to LPS. In a Morris water maze test, compared to LPS group, administration of all three doses of carvacrol shortened the elapsed time and the traveled distance to find the platform, while it prolonged the traveled time in the target area. In a passive avoidance test, administration of all 25, 50, and 100 mg/kg carvacrol significantly increased the latency at the 3 h, 24 h, 48 h, and 72 h after the shock compared to the LPS group. Interleukin (IL)-6, malondialdehyde (MDA), and NO (nitric oxide) metabolites were increased in the brain by LPS injection, while thiol, superoxide dismutase (SOD), and catalase (CAT) were decreased. Pretreatment with carvacrol reduced IL-6, NO metabolites, and MDA, while it improved thiol content, CAT, and SOD. The results indicated that carvacrol protected from learning and memory impairment and the brain tissue inflammation and oxidative stress in LPS-challenged rats.

We investigated the effects of feeding vitamin C (Vit C) during neonatal and juvenile growth on learning and memory of rats. Rats after delivery were randomly divided into four groups and treated. Group 1, control group, received normal drinking water. Groups 2-4 received Vit C 10, 100, and 500 mg/kg, respectively, from the first day. After 8 weeks, 10 male offspring of each group were randomly selected and tested in the Morris water maze (MWM) and passive avoidance (PA) tests. Finally, the brains were removed for biochemical measurement. In MWM, 10-500 mg/kg Vit C reduced the latency and traveled distance and increased time spent in the target quadrant. In PA, 10 and 100 mg/kg of Vit C increased the latency; 10-500 mg/kg of Vit C decreased the malondialdehyde (MDA) in the brain tissues and increased thiol and catalase (CAT) activity compared to the control group. We showed that feeding rats Vit C during neonatal and juvenile growth has positive effects on learning and memory.

The effects of vitamin E (Vit E) on brain derived neurotrophic factor (BDNF) and brain tissues oxidative damage as well as on learning and memory impairments in juvenile hypothyroid rats were examined. The rats were grouped as: (1) Control; (2) Propylthiouracil (PTU); (3) PTU-Vit E and (4) Vit E. PTU was added to their drinking water (0.05%) during 6 weeks. Vit E (20 mg/kg) was daily injected (IP). Morris water maze (MWM) and passive avoidance (PA) were carried out. The animals were deeply anesthetized and the brain tissues were removed for biochemical measurements. PTU increased the escape latency and traveled path in MWM (P < 0.001). It also shortened the latency to enter the dark compartment of PA as well as the time spent in the target quadrant in probe trial of MWM (P < 0.01-P < 0.001). All the effects of PTU were reversed by Vit E (P < 0.01-P < 0.001). PTU administration attenuated thiol and BDNF content as well as the activities of superoxide dismutase (SOD) and catalase (CAT) in the brain tissues while increased molondialdehyde (MDA). Moreover, Vit E improved BDNF, thiol, SOD and CAT while diminished MDA. The results of the present study showed that Vit E improved BDNF and prevented from brain tissues oxidative damage as well as learning and memory impairments in juvenile hypothyroid rats.

Aim: Renin-angiotensin system has a role in inflammation and also involves in learning and memory. In the present study, the effects of captopril on lipopolysaccharide (LPS) induced learning and memory impairments, hippocampal cytokine levels and brain tissues oxidative damage was investigated., Materials and Methods: The rats were divided and treated : [1] saline (Control), [2] LPS (1mg/kg), [3-5] 10, 50 or 100mg/kg captopril 30min before LPS. The treatment was started since six days before the behavioral experiments and continued during the behavioral tests (LPS injection two h before each behavioral experiment)., Results: Administration of LPS prolonged the escape latency and traveled path to find the platform in Morris water maze (MWM) test (P<0.01-P<0.001) while, shortened the latency to enter the dark compartment in passive avoidance (PA) test (P<0.001). Pretreatment by all doses of captopril improved performances of the rats in MWM (P<0.05-P<0.001) and also prolonged the latency to enter the dark in PA test (P<0.001). LPS also increased IL-6, TNF-α, malondialdehyde (MDA) and nitric oxide(NO) metabolites in the hippocampal tissues (P<0.05-P<0.001) which were prevented by captopril (P<0.05-P<0.001). The thiol, superoxide dismutase(SOD) and catalase(CAT) in the hippocampus of LPS group were lower than the control (P<0.001) while, they were enhanced when the aniamls were pretraeted by captopril (P<0.01-P<0.001)., Conclusion: The results of present study showed that captopril improved the LPS-induced learning and memory impairments in rats which were accompanied with attenuating hippocampal cytokine levels and improving the brain tissues oxidative damage criteria., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Inflammation and oxidative stress have important roles in memory impairment. The effect of 7-nitroindazole (7NI) on lipopolysaccharide (LPS)-induced memory impairment was investigated. Rats were used, divided into four groups that were treated as follows: (1) control (saline); (2) LPS; (3) 7NI-LPS; and (4) 7NI before passive avoidance (PA). In the LPS group, the latency for entering the dark compartment was shorter than in the controls (p < 0.01 and p < 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p < 0.01 and p < 0.001). Malondialdehyde (MDA) and nitric oxide (NO) metabolite concentrations in the brain tissues of the LPS group were higher than in the controls (p < 0.001 and p < 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p < 0.001 and p < 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p < 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p < 0.001). It is suggested that brain tissue oxidative damage and NO elevation have a role in the deleterious effects of LPS on memory retention that are preventable using 7NI.

The effect of olibanum administered during lactation to methimazole-treated dams on the learning of offspring was evaluated. The animals were treated for 60 days from the first day of lactation period: group 1--tap water, group 2-0.03% methimazole and groups 3 and 4-0.03% methimazole with 0.25% or 0.125% olibanum, respectively. The serum thyroxin level in the offspring of group 2 was significantly lower than that of group 1. However, there was no difference compared to groups 3 and 4. In a Morris water maze, the distance and time latency to reach the platform in offspring of group 2 was significantly higher than groups 1, 3 and 4. In probe trial, the time spent in target quadrant (Q₁) by offspring of group 2 was lower than groups 1, 3 and 4. It is suggested that impaired learning and memory in the offspring of hypothyroid rats may be prevented by olibanum.

Aim: The effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist pioglitazone on the brain tissues oxidative damage and learning and memory impairment in the juvenile hypothyroid rats was evaluated. Main methods: Rats were classified as: (1) Control; (2) Propylthiouracil (PTU); (3) PTU-Pio 10 and (4) PTU-Pio 20. PTU was given in drinking water (0.05%) during 6 weeks. Pioglitazone (10 or 20 mg/kg) was daily injected intraperitoneally. Passive avoidance (PA) and Morris water maze (MMW) were conducted. Later, the animals were sacrificed and the brain tissues were removed for biochemical measurements. Key funding: The results indicated that in the MWM escape latency as well as traveled path increased in the PTU group as compared to the control group. Also, the time spent in the target quadrant in the probe test of MWM and step-through latency in the PA test were decreased in the PTU group as compared to the control group. Pioglitazone reversed all the negative behavioral effects of hypothyroidism. Administration of PTU attenuated thiol and superoxide dismutase (SOD), and catalase (CAT) activities in the brain tissues, whereas increased malondialdehyde (MDA) and nitric oxide (NO) metabolites. PPARγ agonist improved thiol, SOD and CAT, while diminished MDA concentration. Significance: Our finding in the present study indicated that PPARγ agonist pioglitazone prevented the brain tissues from oxidative damage and learning and memory impairments in juvenile hypothyroid rats. [ABSTRACT FROM AUTHOR]

Objective(s): The aim of current study was to evaluate improving effects of pioglitazone as an agonist of peroxisome proliferator-activated receptor gamma (PPARγ), on brain-derived neurotrophic factor (BDNF) and cytokines as well as tissue oxidative damage criteria in the hippocampus in a rat model of lipopolysaccharide (LPS) induced memory impairment. Materials and Methods: The rats were classified and treated as follows (10 rats per group): (1) vehicle, (2) vehicle before LPS (1 mg/kg, 120 min before memory tests), (3-5) pioglitazone 10, 20 or 30 mg/kg 30 min before LPS. Finally, the hippocampal tissues were collected for biomedical analyses. Results: In the Morris water maze test, the LPS group, had a longer latency to find the platform while they spent a shorter time in the target quadrant in the probe trial. In the passive avoidance test, the animals of the LPS group had shorter delay times to enter the dark compartment than those of the control group. Treatment with 20 and 30 mg of pioglitazone corrected these parameters. In the hippocampus of LPS group interleukin-6, tumor necrosis factor-α, nitric oxide metabolites, and malondialdehyde were higher while thiol, BDNF, and IL-10 concentrations and the activities of catalase (CAT) and superoxide dismutase (SOD) were lower than the control group. Treatment by both doses of 20 and 30 mg of pioglitazone corrected the biochemical parameters in the hippocampus. Conclusion: The current findings revealed that pioglitazone protected the rats from learning and memory impairment induced by LPS. The effects were associated with improvement of cytokines, oxidative stress criteria, and BDNF. [ABSTRACT FROM AUTHOR]

In this study, the effects of Nigella Sativa (NS) hydro-alcoholic extract on lipopolysaccharide (LPS)- induced learning and memory impairments, hippocampal cytokine levels, and brain tissues oxidative damage were investigated in rats. The rats were grouped and treated: (1) control (saline), (2) LPS (1 mg/ kg i.p.), and (3-5) 100, 200, or 400 mg/kg NS hydro-alcoholic extract 30 min before LPS injection. The treatment was started since 6 days before the behavioral experiments and continued during the behavioral tests (LPS injection 2 h before each behavioral experiment). Finally, the brains were removed for biochemical assessments. In Morris water maze (MWM) test, LPS increased the escape latency and traveled path compared to control group, whereas all doses of NS hydro-alcoholic extract decreased them compared to LPS group. In passive avoidance (PA) test, the latency to enter the dark compartment in LPS group was shorter than control group while in all treated groups it was longer than LPS group. LPS increased tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), malondialdehyde (MDA), and nitric oxide (NO) metabolites, and decreased thiol content, superoxide dismutase (SOD), and catalase (CAT) in the hippocampal tissues compared to control group while NS hydro-alcoholic extract decreased MDA and NO metabolites and increased thiol content, SOD, and CAT compared to LPS group. Findings of the current study indicated that the hydro-alcoholic extract of NS improved the LPS-induced learning and memory impairments induced by LPS in rats by improving hippocampal cytokine levels and brain tissues oxidative damage. [ABSTRACT FROM AUTHOR]

Objectives: It has been shown that hypothyroidism-induced oxidative damage in brain tissue is involved in its adverse effects on learning and memory.Nigella sativa(N. sativa) has been suggested to have antioxidant and neuroprotective effects. The objective of this study was to investigate the effects of hydroalcoholic extract ofN. sativaon hypothyroidism-associated learning and memory impairment during neonatal and juvenile growth in rats. Methods: Thirty pregnant rats were kept in separate cages. After delivery, the mothers and their offspring were randomly divided into six groups including: (1) control, (2) PTU (propylthiouracil), (3) PTU-NS 100, (4) PTU-NS 200, (5) PTU-NS 400, and (6) PTU-Vit C (vitamin C). All dams except the control group received 0.005% PTU in their drinking water during lactation. Besides PTU, dams in groups 3, 4, 5, and 6 received 100, 200, and 400 mg/kgN. sativaextract, or 100 mg/kg Vit C, respectively. After lactation period, pups continued to receive same experimental treatment for the first 8 weeks of their life. Then, 10 male offspring of each group were randomly selected and assessed for the learning and memory abilities by using Morris water maze (MWM) and passive avoidance (PA) tests. Blood samples were collected for thyroxine assessment, animals were euthanized, and the brain tissues were removed and analyzed for total thiol groups and malondialdehyde (MDA) concentrations. Results: PTU exposure significantly increased the time latency in MWM test, while reduced the time spent in target quadrant, and decreased the latency for entering the dark compartment in PA test. These effects were associated with significant reduction in serum thyroxine levels and brain levels of thiol groups, and significant elevation in hippocampal MDA. Administration of 400 mg/kgN. sativaextract and 100 mg/kg Vit C reduced the time latency, while increased the time spent in target quadrant compared to the PTU group in MWM test. Treatment by 100–400 mg/kg ofN. sativaextract and also Vit C significantly increased the time latency for entering the dark compartment in PA test. The serum thyroxine concentrations of the animals treated by all doses of theN. sativaextract as well as by Vit C were higher than that of the PTU group. Two hundred and four hundred milligrams/kilogram of NS extract and 100 mg/kg Vit C decreased the MDA concentration in hippocampal tissues, while increased thiol contents compared to the PTU group. Discussion: The results of this study demonstrate that the hydroalcoholic extract ofN. sativahave protective effects on hypothyroidism-associated learning and memory impairment during neonatal and juvenile growth in rats. The effects were comparable to Vit C and might be due to the protective effects ofN. sativaextract against brain tissues’ oxidative damage. [ABSTRACT FROM PUBLISHER]

Regarding the therapeutic properties of Nigella sativa (NS), the effects of the plant hydro - alcoholic extract on learning, memory and brain tissues oxidative damage were investigated in penthylenetetrazole (PTZ) - induced repeated seizures. There were 4 experimental groups including: 1- control group; received saline, 2- PTZ group ; received saline and PTZ (50 mg/Kg, i.p) , 3-PTZ- NS 200 and 4- PTZ- NS 400 ; received 200 and 400 mg/Kg of NS extract respectively, before PTZ injection in 5 consecutive days. Seizure scores were lower in PTZ - NS 200 and 400, furthermore the seizure onset latencies were higher in these groups than PTZ group (P<0.05 and P<0.01 ). In Morris water maze, the time spent in target quadrant by PTZ group was lower than control group (P<0.05); while, 400 mg/Kg of the extract increased it (P<0.01). In the passive avoidance test, delay time to enter the dark by PTZ group was lower than control at 1 and 24 hours after training (P<0.01- P<0.001); while, 400 mg/Kg of the extract increased it (P<0.05). The total thiol concentration in hippocampal and cortical tissues of PTZ group was reduced while, MDA concentration was higher than control (p<0.05 - p<0.001). Administration of the extract increased the total thiol and decreased the MDA concentrations (p<0.01- p<0.001). It is concluded that the hydro-alcoholic extract of NS possess beneficial effects on learning and memory impairments in repeated seizures model which is accompanied by antioxidant effects in the brain. [ABSTRACT FROM AUTHOR]