@article {2387, title = {Changes in Blood Brain-Derived Neurotrophic Factor (BDNF) Levels in Experimental Animals with Traumatic Brain Injury after Magnesium Sulfate Administration: An Experimental Study}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {October 2024}, pages = {1086-1089}, type = {Research Article}, chapter = {1086}, abstract = {

Background: Traumatic brain injury (TBI) results in notable impairments in neurological function and is associated with poor outcomes. Various processes occur at the cellular level, one of which is neuroinflammation. Brain-derived neurotrophic factor (BDNF) is a neurotrophin protein produced by the brain that circulates in plasma post-injury. It has functions such as anti-apoptosis, anti-neurotoxicity, and antiinflammatory effects. Therapeutic approaches aimed at modulating or synergizing BDNF are anticipated to reduce inflammation and enhance outcomes in TBI patients. Magnesium sulfate administration is known for its anti-inflammatory and neuroprotective effects. Methods: This study employed a true experimental post-test-only group design. The subjects, male Wistar rats (Rattus norvegicus), were subjected to weight-drop-induced TBI and divided into three distinct groups: a control group (Group A), a TBI group without therapy (Group B), and a therapy group (Group C). Group B received TBI without magnesium sulfate administration, while Group C received TBI with magnesium sulfate administered at 250 μm/kg BW. BDNF levels in blood plasma were assessed at the conclusion of therapy utilizing ELISA. ANOVA was used to conclude the inquiry after all groups underwent a Shapiro-Wilk test. Results: Plasma BDNF levels were significantly lower in the TBI rat models treated with magnesium sulfate at 250 μm/kg BW within 4 hours after injury than in the untreated group (p = 0.005). Compared to the untreated group, the magnesium sulfate-treated group had reduced plasma BDNF levels. Conclusions: Administration of MgSO4 to the TBI treatment group resulted in decreased BDNF levels compared to the untreated group.

}, keywords = {BDNF, Magnesium sulfate, Neuroinflammation, Traumatic Brain Injury}, doi = {10.5530/pj.2024.16.176}, author = {Aditya Brahmantio Sujaka and Prananda Surya Airlangga and Tedy Apriawan and Muhammad Arifin Parenrengi} } @article {2002, title = {The Antidepressant Effect of Fluoxetine and Mozart K448 Combination Therapy on Hippocampal Serotonin and BDNF Levels}, journal = {Pharmacognosy Journal}, volume = {15}, year = {2023}, month = {April 2023}, pages = {325-328}, type = {Original Article }, chapter = {325}, abstract = {

Despite the use of fluoxetine as a first-line therapy, some patients do not show a good therapeutic effect. Effective antidepressant therapy will reverse the low serotonin and BDNF levels found in depression. Mozart K. 448 was reported to yield a good therapeutic effect for depression. Based on findings, the combination of Mozart K. 448 and fluoxetine as a therapy for depression is very rare. Therefore, this study aimed to determine the effect of the combined therapy of fluoxetine and Mozart K. 448 on hippocampal serotonin and BDNF levels in an animal model of depression under CUMS conditions. In this study, the animal model of depression was administered three different treatments, i.e. fluoxetine, Mozart, or fluoxetine-Mozart combined therapy, respectively. Hippocampal serotonin and BDNF levels were assessed after 21 days of treatment. Statistical analysis was then carried out using T-test or Mann-Whitney test and ANOVA or Kruskal-Wallis. The fluoxetine-Mozart group has higher BDNF levels, but lower serotonin levels compared to other groups with values of 1,694{\textpm}0.215 and 44,533{\textpm}3,275, respectively.

}, keywords = {BDNF, Fluoxetine, Hippocampus, Mozart, Serotonin}, doi = {10.5530/pj.2023.15.48}, author = {Lisa Pangemanan and Irwanto Irwanto and Margarita M. Maramis} }