scholarly journals Prevention of Memory Impairment and Neurotrophic Factors Increased by Lithium in Wistar Rats Submitted to Pneumococcal Meningitis Model

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Lutiana R. Simões ◽  
Roberta R. E. S. Abreu ◽  
Jaqueline S. Generoso ◽  
Jéssica A. Goularte ◽  
Allan Collodel ◽  
...  
Keyword(s):  
Group Treatment ◽  
Neurotrophic Factor ◽  
Memory Impairment ◽  
Pneumococcal Meningitis ◽  
Mood Stabilizer ◽  
Inhibitory Avoidance ◽  
Saline Control ◽  
Artificial Cerebrospinal Fluid ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

The aim of this study was to investigate the effects of lithium on brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and glial cell line-derived neurotrophic factor (GDNF) expression in the hippocampus and on memory in experimental pneumococcal meningitis. The mood-stabilizer lithium is known as a neuroprotective agent with many effects on the brain. In this study, animals received either artificial cerebrospinal fluid or Streptococcus pneumoniae suspension at a concentration of 5 × 109 CFU/mL. Eighteen hours after induction, all animals received ceftriaxone. The animals received saline or lithium (47.5 mg/kg) or tamoxifen (1 mg/kg) as adjuvant treatment, and they were separated into six groups: control/saline, control/lithium, control/tamoxifen, meningitis/saline, meningitis/lithium, and meningitis/tamoxifen. Ten days after meningitis induction, animals were subjected to open-field habituation and the step-down inhibitory avoidance tasks. Immediately after these tasks, the animals were killed and their hippocampus was removed to evaluate the expression of BDNF, NGF, and GDNF. In the meningitis group, treatment with lithium and tamoxifen resulted in improvement in memory. Meningitis group showed decreased expression of BDNF and GDNF in the hippocampus while lithium reestablished the neurotrophin expression. Lithium was able to prevent memory impairment and reestablishes hippocampal neurotrophin expression in experimental pneumococcal meningitis.

scholarly journals Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

Sodium Butyrate Prevents Memory Impairment by Re-establishing BDNF and GDNF Expression in Experimental Pneumococcal Meningitis

2014 ◽  
Vol 52 (1) ◽  
pp. 734-740 ◽  
Author(s):  
Tatiana Barichello ◽  
Jaqueline S. Generoso ◽  
Lutiana R. Simões ◽  
Cristiano Julio Faller ◽  
Renan A. Ceretta ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Memory Impairment ◽  
Pneumococcal Meningitis ◽  
Experimental Pneumococcal Meningitis

scholarly journals Brain-derived neurotrophic factor (BDNF)

2019 ◽  
pp. 83-88
Author(s):  
А.А. Пальцын
Keyword(s):  
Emotional Disorders ◽  
Neurotrophic Factor ◽  
Memory Impairment ◽  
Emotional State ◽  
Hypotensive Effect ◽  
Brain Derived Neurotrophic Factor ◽  
Carbohydrate And Lipid Metabolism ◽  
Treatment Of Hypertension ◽  
The Brain ◽  
State Stress

Сегодня нейротрофический фактор мозга (BDNF) - вещество очень популярное. Большой интерес к белку объясняется его участием в важнейших для жизни и здоровья процессах: нервной регуляции, углеводном и липидном обмене, адаптации к физическим нагрузкам. Вещество участвует в регуляции эффективности профилактических и лечебных процедур, эмоционального состояния, стрессоустойчивости, нейропластичности, нейрогенеза. BDNF - главный регулятор действия самого универсального и, часто, самого эффективного лечебного средства - физических нагрузок. Следовательно, он становится веществом первостепенного значения в одной из самых актуальных проблем современной медицины - профилактике и лечении гипертонической болезни. Кроме гипотензивного действия, доказана эффективность BDNF при обусловленных гипертонией когнитивных нарушениях, шизофрении, дефектах памяти, эмоциональных расстройствах. Today, the brain-derived neurotrophic factor (BDNF) is a very popular substance. The high interest to this protein is due to its participation in key processes for life and health, including nervous regulation, carbohydrate and lipid metabolism, and exercise capacity. BDNF regulates preventive and therapeutic efficacy of exercise, emotional state, stress resistance, neuroplasticity, and neurogenesis. BDNF determines the action of the most universal and often the most effective therapeutic means, physical exercise. Therefore, BDNF appears to be the substance of primary importance for a burning issue of current medicine, prevention and treatment of hypertension. In addition to its hypotensive effect, BDNF has proved to be beneficial in hypertension-induced cognitive decline, schizophrenia, memory impairment, and emotional disorders.

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