O déficit de memória induzido por lipossacarídeos em ratos é prevenido por nitroindazol

Inflamação e estresse oxidativo tem importante papel no déficit de memória. O efeito do 7-nitroindazol (7NI) no déficit de memória induzido por lipossacarídeos (LPS) foi investigado. Foram utilizados ratos que foram divididos em quatro grupos e tratados da seguinte maneira: (1) controles (solução salina); (2) LPS; (3) 7NI-LPS; e (4) 7NI antes da esquiva passiva (PA). No grupo LPS, a latência para entrar no compartimento escuro foi mais curta que nos controles (p < 0,01 e p < 0,001); enquanto no grupo 7NI-LPS, a latência foi maior que aquela do grupo LPS (p < 0,01 e p < 0,001). Concentrações de malondialdeído (MDA) e metabólitos do ácido nítrico (NO) no tecido cerebral do grupo LPS foram maiores que aquelas dos controles (p < 0,001 e p < 0,05); enquanto no grupo 7NI-LPS, as concentrações foram menores do que no grupo LPS (p < 0,001 e p < 0,05, respectivamente). O conteúdo cerebral de tiol no grupo LPS foi menos do que nos controles (p < 0,001); enquanto no grupo 7NI-LPS, este conteúdo foi maior que no grupo LPS (p < 0,001). Sugere-se que o dano oxidativo cerebral e o aumento de NO tenham um papel nos efeitos deteriorativos dos LPS na memória de retenção, e que isto possa ser prevenido com o uso de 7NI.

aprendizado; memória; lipopolissacarídeo; 7NI

Autoria

Akbar Anaeigoudari

Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;Mashhad University of Medical SciencesIranMashhad, IranNeurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;

Mohammad Naser Shafei

Mohammad Soukhtanloo

Department of Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;Mashhad University of Medical SciencesIranMashhad, IranDepartment of Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;

Hamid Reza Sadeghnia

Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;Mashhad University of Medical SciencesIranMashhad, IranPharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran;

Parham Reisi

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran;Isfahan University of Medical SciencesIranIsfahan, IranDepartment of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran;

Farimah Beheshti

Reza Mohebbati

Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.Mashhad University of Medical SciencesIranMashhad, IranNeurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Seyed Mojtaba Mousavi

Mahmoud Hosseini

Correspondence: Mahmoud Hosseini; Neurocognitive Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Mashhad 9177948564, Islamic Republic of Iran; E-mail:hosseinim@mums.ac.ir

Conflict of interest: There is no conflict of interest to declare.

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Figuras | Fórmulas

Figuras (7)
Fórmulas (2)

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Figure 1
Comparison of latency for entering to the dark compartment before and at the 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI, 30 minutes before saline and LPS respectively. The control group received saline. **p < 0.01, *** p < 0.001 compared to control group. ++ p < 0.01, +++ p < 0.001 compared to LPS group.

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Figure 2
Comparison of the total time spent in dark component at 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI,30 minutes before saline and LPS. The control group received saline. ** p < 0.01, *** p < 0.001 compared to control group. + p < 0.05, ++ p < 0.01, +++ p < 0.001 compared to LPS group.

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Figure 3
Comparison of the total time spent in light component at 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI, 30 minutes before saline and LPS respectively. The control group received saline. *** p < 0.001 compared to control group. + p < 0.05, ++ p < 0.01, +++ p <0.001 compared to LPS group.

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Figure 4
Comparison of the MDA concentrations in cortical tissues of four groups. Data are presented as Mean ± SEM (n = 9-10 in each group). *** p < 0.01 compared to control group. +++ p < 0.001 compared to LPS group.

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Figure 5
Comparison of the total thiol concentrations in cortical tissues of four groups. Data are presented as Mean ± SEM (n= 9-10 in each group). *** p < 0.01 compared to control group. +++ p < 0.001 compared to LPS group.

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Figure 6
Comparison of the SOD level in cortical tissues between four groups. Data are shown as Mean ± SEM (n = 9-10 in each group). There is no significant difference between groups.

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Figure 7
Comparison of the nitric oxide metabolites level in cortical tissues between four groups. Data are shown as Mean ± SEM (n= 5-6 in each group) * p < 0.05 compared to control group. + p < 0.05 compared to LPS group.

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Figure 1 Comparison of latency for entering to the dark compartment before and at the 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI, 30 minutes before saline and LPS respectively. The control group received saline. p < 0.01, * p < 0.001 compared to control group. ++ p < 0.01, +++ p < 0.001 compared to LPS group.

Figure 2 Comparison of the total time spent in dark component at 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI,30 minutes before saline and LPS. The control group received saline. p < 0.01, * p < 0.001 compared to control group. + p < 0.05, ++ p < 0.01, +++ p < 0.001 compared to LPS group.

Figure 3 Comparison of the total time spent in light component at 3, 24, 48 and 72 hours after receiving the shock in the experimental groups. Data are presented as Mean ± SEM (n = 9-10 in each group). The animals of LPS and 7NI-LPS groups were treated by 1 mg/kg LPS, 2 h before the retention phase in passive avoidance test. The animals of 7NI and 7NI-LPS groups received 30 mg/kg 7NI, 30 minutes before saline and LPS respectively. The control group received saline. *** p < 0.001 compared to control group. + p < 0.05, ++ p < 0.01, +++ p <0.001 compared to LPS group.

Figure 4 Comparison of the MDA concentrations in cortical tissues of four groups. Data are presented as Mean ± SEM (n = 9-10 in each group). *** p < 0.01 compared to control group. +++ p < 0.001 compared to LPS group.

Figure 5 Comparison of the total thiol concentrations in cortical tissues of four groups. Data are presented as Mean ± SEM (n= 9-10 in each group). *** p < 0.01 compared to control group. +++ p < 0.001 compared to LPS group.

Figure 6 Comparison of the SOD level in cortical tissues between four groups. Data are shown as Mean ± SEM (n = 9-10 in each group). There is no significant difference between groups.

Figure 7 Comparison of the nitric oxide metabolites level in cortical tissues between four groups. Data are shown as Mean ± SEM (n= 5-6 in each group) * p < 0.05 compared to control group. + p < 0.05 compared to LPS group.

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O déficit de memória induzido por lipossacarídeos em ratos é prevenido por nitroindazol

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[1] Correspondence: Mahmoud Hosseini; Neurocognitive Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Mashhad 9177948564, Islamic Republic of Iran; E-mail:hosseinim@mums.ac.ir