@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 {2204, title = {Effects of Cerebrospinal Fluid Drainage on Pro-Inflammatory and Anti-Inflammatory Cytokines Expression in the Subventricular Zone of Kaolin-Induced Hydrocephalic Rats}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {February 2024}, pages = {20-27}, type = {Original Article}, chapter = {20}, abstract = {

Background: To determine the neuroprotective effect of CSF drainage by analyzing its impact on the expression and the ratio of pro- and anti-inflammatory cytokines in the subventricular zone in kaolininduced hydrocephalic rats. Method: Sprague-Dawley rats of 23 weeks of age (n=36) were used in this study. The rats were randomly divided into normal control, hydrocephalus, and CSF drainage-treated groups. Hydrocephalus was obtained by injecting 0,05 cc of 20\% kaolin suspension into the cisterna magna. The CSF drainage-treated group had ventricular tapping seven days after kaolin induction. The rats were sacrificed 7, 14, or 21 days after kaolin induction. The brain was removed and prepared for immunohistochemistry analysis to detect IL-1β, IL-6, TNF-α, and IL-10 cytokines expression. Results: Immunohistochemistry analysis revealed that the expression of pro-inflammatory cytokines was significantly increased in hydrocephalus groups than in the control group. In contrast, the expression of anti-inflammatory cytokine was significantly decreased. CSF drainage had a neuroprotective effect by reducing pro-inflammatory cytokine expression and increasing anti-inflammatory cytokine expression. In the hydrocephalus group, the ratios of IL-1β/IL-10, IL-6/IL-10, and TNF-α/IL-10 increased toward a pro-inflammatory status. After CSF drainage, the ratios of IL-1β/IL-10, IL-6/IL-10, and TNF-α/IL-10 shifted toward an anti-inflammatory status. Conclusion: CSF drainage protects the brain from excessive neuroinflammatory processes in kaolin-induced hydrocephalic rats. Additional investigation is warranted to ascertain the use of inflammatory cytokines expression as a valuable biomarker for hydrocephalus. Furthermore, research on anti-inflammatory drug administration in clinical settings is required.

}, keywords = {cerebrospinal fluid drainage, Cytokines, Kaolin-induced hydrocephalus, Neuroinflammation, Neuroprotective, subventricular zone}, doi = {10.5530/pj.2024.16.3}, author = {Muhammad Arifin Parenrengi and Ahmad Data Dariansyah and Wihasto Suryaningtyas and Dyah Fauziah and I Ketut Sudiana and Budi Utomo and Prastiya Indra Gunawan} } @article {1926, title = {Kaempferia galanga L. Extract Administration Attenuate Aquaporin-4 Expression in Traumatic Brain Injury: An Experimental Study in Rats}, journal = {Pharmacognosy Journal}, volume = {14}, year = {2022}, month = {January 2023}, pages = {893-897}, type = {Original Article }, chapter = {893}, abstract = {

Introduction: Traumatic brain injury (TBI) is still a major health problem in the world. It might cause long-term disability that affect socio-economic life and become nation health burden. Post-traumatic cerebral edema might develop and commit to an unfavorable prognosis. Aquaporin 4 (AQP4) is water channel protein and a key regulator of water metabolism in the brain. Although the mechanism of AQP4 in the regulation of post-traumatic brain edema remains controversial, AQP4-lacking mice show better survival and decreased brain edema. Thus, novel strategies that suppress AQP4 become a potential field. We hypothesized that Kaempferia galanga L. may suppress brain expression of AQP4 following TBI and possibly limit the development of cerebral edema due to its neuroinflammation properties. Method: We conducted TBI to experimental rats, then given Kaempferia galanga L. extract at a dose of 600 mg/kg BW and 1200 mg/kg BW. Evaluation intensity of AQP4 expression by immunohistochemistry was performed 24 and 48 hours later to see its therapeutic effect. Results: Administration of Kaempferia galanga L. extract at a dose of 1200 mg/kg BW showed weak expression of AQP4 in all samples, both 24 and 48 hours following traumatic brain injury treatment. Conclusions: Intensity of AQP4 expression in rats{\textquoteright} brain was lower at 24 and 48 hours after TBI in rats receiving Kaempferia galanga L. extract with dose 1200 mg/ kg BW compared to the other groups. Our result indicates that Kaempferia galanga L. might affect the expression of brain AQP4 in a dose-dependent manner.

}, keywords = {Ayuverdic medicine, Neuroinflammation, Neurotrauma, Post-traumatic cerebral edema}, doi = {10.5530/pj.2022.14.185}, author = {Fajar Herbowo Niantiarno and Agus Turchan and Myrna Adianti and Budi Utomo and Muhammad Arifin Parenrengi and Abdul Hafid Bajamal} }