<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Muhammad Chairul</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effectiveness of Radish (Raphanus sativus) Extract In Reducing Tnf-α and Nitrit Oxida levels in Tipe II DM Mice Models with Traumatic Brain Injury</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Diabetes mellitus</style></keyword><keyword><style  face="normal" font="default" size="100%">Nitric oxide</style></keyword><keyword><style  face="normal" font="default" size="100%">Raphanus sativus</style></keyword><keyword><style  face="normal" font="default" size="100%">TNF-α</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword><keyword><style  face="normal" font="default" size="100%">Wistar rats.</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">September 2025</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">17</style></volume><pages><style face="normal" font="default" size="100%">597-601</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;The devastating effects of traumatic brain injury (TBI) are fatal, and there is no effective treatment for primary brain injury, especially in patients with diabetes mellitus (DM). Nitric oxide (NO) is a compound that causes systemic vasodilation; a decrease in NO reduces cerebral blood flow after TBI. There is an increase in TNF-α levels demonstrated by mononuclear cells surrounding the traumatic lesion in the rat brain. &lt;em&gt;Raphanus sativus &lt;/em&gt;(radish) is a root vegetable belonging to the Brassicaceae family, which has anti-diabetic effects by lowering blood glucose levels, reducing lipid peroxidation, and improving brain function, thereby protecting against neurotoxic effects associated with oxidative stress in experimental mouse models. &lt;strong&gt;Objective: &lt;/strong&gt;To evaluate the efficacy of radish extract &lt;em&gt;(Raphanus sativus)&lt;/em&gt; in reducing TNF-α and nitric oxide levels in a rat model of type II diabetes mellitus with traumatic brain injury. Method: This study was an in vivo laboratory experimental study with a post-test only control group design. The study population consisted of 25 Wistar rats, which were then induced with diabetes and subjected to a modified Feeney Model closed head injury. After complete data collection, KGD and ELISA assessments were performed, followed by data analysis. &lt;strong&gt;Results: &lt;/strong&gt;There were significant differences (p&amp;lt;0.05) in serum NO and serum TNF-α levels between the normal group, the 100 mg/kg radish extract group, the 300 mg/kg radish extract group, and the 500 mg/kg radish extract group compared to the negative control group. This indicates that radish extract, starting at a dose of 100 mg/kg, can reduce serum NO and serum TNF-α levels. &lt;strong&gt;Conclusion: &lt;/strong&gt;Radish extract &lt;em&gt;(Raphanus sativus)&lt;/em&gt; is effective in reducing TNF-α and nitric oxide levels in a Wistar rat model of type II DM with traumatic brain injury.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><work-type><style face="normal" font="default" size="100%">Original Article</style></work-type><section><style face="normal" font="default" size="100%">597</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Muhammad Chairul&lt;sup&gt;1*&lt;/sup&gt; &lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Medical Science Faculty of Medicine, Dentistry, and Health Sciences, Universitas Prima Indonesia, Medan, INDONESIA&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Aditya Brahmantio Sujaka</style></author><author><style face="normal" font="default" size="100%">Prananda Surya Airlangga</style></author><author><style face="normal" font="default" size="100%">Tedy Apriawan</style></author><author><style face="normal" font="default" size="100%">Muhammad Arifin Parenrengi</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Changes in Blood Brain-Derived Neurotrophic Factor (BDNF) Levels in Experimental Animals with Traumatic Brain Injury after Magnesium Sulfate Administration: An Experimental Study</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">BDNF</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnesium sulfate</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuroinflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">October 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">1086-1089</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Background:&lt;/strong&gt; 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.&lt;strong&gt; Methods: &lt;/strong&gt;This study employed a true experimental post-test-only group design. The subjects, male Wistar rats (&lt;em&gt;Rattus norvegicus&lt;/em&gt;), 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. &lt;strong&gt;Results: &lt;/strong&gt;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. &lt;strong&gt;Conclusions: &lt;/strong&gt;Administration of MgSO4 to the TBI treatment group resulted in decreased BDNF levels compared to the untreated group.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">1086</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Aditya Brahmantio Sujaka&lt;sup&gt;1&lt;/sup&gt;, Prananda Surya Airlangga&lt;sup&gt;2*&lt;/sup&gt;, Tedy Apriawan&lt;sup&gt;3&lt;/sup&gt; , Muhammad Arifin Parenrengi&lt;sup&gt;4&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Clinical Medicine Study Program, Master’s Degree, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Anesthesiology and Reanimation, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Neurosurgery, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Junjungan Kristianto Manurung</style></author><author><style face="normal" font="default" size="100%">Prananda Surya Airlangga</style></author><author><style face="normal" font="default" size="100%">Hamzah Hamzah</style></author><author><style face="normal" font="default" size="100%">Prihatma Kriswidyatomo</style></author><author><style face="normal" font="default" size="100%">Anggraini Dwi Sensusiati</style></author><author><style face="normal" font="default" size="100%">Budi Utomo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Relationship Between Blood Levels of Ubiquitin Carboxyterminal Hydrolase L1 (UCH-L1) Protein and the Severity of Traumatic Brain Injury Based on the Glasgow Coma Scale and Rotterdam CT Score</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Glasgow Coma Scale</style></keyword><keyword><style  face="normal" font="default" size="100%">Rotterdam CT score</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword><keyword><style  face="normal" font="default" size="100%">UCH-L1</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">695-699</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Objective:&lt;/strong&gt; Traumatic brain injury (TBI) is a leading cause of disability and death worldwide, with an estimated 64-74 million cases annually. The current gold standard for diagnosis is a computed tomography (CT) scan, which has limitations such as access, cost, and radiation risk. Therefore, a simple, accessible, and safe diagnostic modality is needed, one of which is biomarker examination. This study aims to establish the relationship between blood levels of the biomarker ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) and the severity of TBI based on the Glasgow Coma Scale (GCS) and Rotterdam CT score. &lt;strong&gt;Material and Methods: &lt;/strong&gt;This observational analytic study with a cross-sectional design involved 41 samples aged 18-50 years who presented to the Emergency Department of Dr. Soetomo General Hospital, Surabaya, within 3-24 hours of the incident. UCH-L1 levels were measured from blood samples using the ELISA method, and the data on UCH-L1, GCS, and Rotterdam CT scores were analyzed with SPSS 29. &lt;strong&gt;Results:&lt;/strong&gt; The mean UCH-L1 level was 0.522 ± 0.592, with a cutoff value of &amp;gt; 0.2057, indicating moderate to severe TBI if UCH-L1 levels exceeded 0.2057. Spearman's test and correlation coefficient analysis showed a strong relationship between UCH-L1 levels and Rotterdam CT score (p &amp;lt; 0.05), as well as between UCH-L1 levels and TBI severity based on GCS (p &amp;lt; 0.05). The cutoff value for Rotterdam CT score was &amp;gt; 2, indicating moderate to severe TBI if the score exceeded 2. &lt;strong&gt;Conclusion:&lt;/strong&gt; Serum UCH-L1 levels are significantly associated with the severity of TBI based on GCS and Rotterdam CT score.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">695</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;Junjungan Kristianto Manurung&lt;sup&gt;1&lt;/sup&gt;, Prananda Surya Airlangga&lt;sup&gt;1&lt;/sup&gt;*, Hamzah Hamzah&lt;sup&gt;1&lt;/sup&gt;, Prihatma Kriswidyatomo&lt;sup&gt;1&lt;/sup&gt;, Anggraini Dwi Sensusiati&lt;sup&gt;2&lt;/sup&gt;, Budi Utomo&lt;sup&gt;3&lt;/sup&gt;&amp;nbsp;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Anesthesiology and Intensive Care, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Radiology, Faculty of Medicine, Universitas Airlangga – Airlangga University Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;3&lt;/sup&gt;Departement of Public Health &amp;amp; Preventive Medicine, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rian Nofiansyah</style></author><author><style face="normal" font="default" size="100%">Kohar Hari Santoso</style></author><author><style face="normal" font="default" size="100%">Prananda Surya Airlangga</style></author><author><style face="normal" font="default" size="100%">Prihatma Kriswidyatomo</style></author><author><style face="normal" font="default" size="100%">Hamzah</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Relationship Between Cerebrospinal Fluid S100B Levels with Glasgow Coma Scale and Rotterdam CT Score in Traumatic Brain Injury Patients</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Glasgow Coma Scale</style></keyword><keyword><style  face="normal" font="default" size="100%">Rotterdam CT score.</style></keyword><keyword><style  face="normal" font="default" size="100%">S100B</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">503-508</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;!-- x-tinymce/html --&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Background:&lt;/strong&gt; Traumatic brain injury (TBI) stands as one of the foremost reasons for mortality and incapacitation in young adults on a global scale, accounting for nearly half of all injury-related deaths. The severity of TBI can be assessed using various biomarkers, with the SI00B protein being one of them. While many studies have explored the correlation between serum protein levels and various aspects such as neuroimaging findings, clinical scores, and neuropsychological evaluations, there is a notable lack of research examining the correlation with cerebrospinal fluid (CSF) levels. &lt;strong&gt;Methods: &lt;/strong&gt;The research design of this study was prospective and observational, employing analytic methods for analysis. Fifteen TBI patients who met the inclusion and exclusion criteria and were fitted with ICP monitors comprised the study sample. GCS data used is post-resuscitation GCS. Data on SIOOB protein levels were taken from the examination of CSF samples taken when the ICP monitor was installed. Rotterdam CT score variables was taken from the last CT scan performed before the patient was fitted with an ICP monitor. The statistical analysis was conducted utilizing the SPSS version 26 software. &lt;strong&gt;Results: &lt;/strong&gt;Demographic characteristics for this study tended to be more male (73.3%), with ages ranging from 18 to 65 years, and a mean age of 34.60 ± 16.22 years. The majority of injury mechanisms were traffic accidents (80%), and the most common lesion type was ICH. The mean CSF S 100B value of the 15 samples was 2753.689 pg/ ml. The results of the relationship test between S 100B CSF and GCS using the Spearman test obtained a p-value of less than 0.05, indicating a meaningful correlation between S 100B CSF and GCS, with a correlation coefficient or r value of -0.684. The results of the SIOOB CSF relationship test with Rotterdam CT Score obtained a p-value &amp;lt;0.05, with a correlation coefficient or r value of 0.827. &lt;strong&gt;Conclusion: &lt;/strong&gt;Increased levels of S100B in cerebrospinal fluid are associated with decreased GCS and increased Rotterdam CT score in traumatic brain injury patients.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><work-type><style face="normal" font="default" size="100%">Original Article</style></work-type><section><style face="normal" font="default" size="100%">503</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;Rian Nofiansyah&lt;sup&gt;1&lt;/sup&gt;*, Kohar Hari Santoso&lt;sup&gt;2&lt;/sup&gt;, Prananda Surya Airlangga&lt;sup&gt;2&lt;/sup&gt;, Prihatma Kriswidyatomo&lt;sup&gt;2&lt;/sup&gt;, Hamzah&lt;sup&gt;2&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Clinical Medicine Study Program, Master’s Degree, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Anesthesiology and Reanimation, Faculty of Medicine, Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Wibowo Artho Sutrisno</style></author><author><style face="normal" font="default" size="100%">Prananda Surya Airlangga</style></author><author><style face="normal" font="default" size="100%">Citrawati Dyah Kencono Wungu</style></author><author><style face="normal" font="default" size="100%">Prihatma Kriswidyatomo</style></author><author><style face="normal" font="default" size="100%">Hamzah</style></author><author><style face="normal" font="default" size="100%">Bambang Pujo Semedi</style></author><author><style face="normal" font="default" size="100%">Mahmudah</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Role of Neuron Specific Enolase, S100B, Glial Fibrillary Acidic Protein, and Myelin Basic Protein as Prognostic and Survival Values in Traumatic Brain Injury: Systematic Review and Meta-analysis</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Glial Fibriallary Acidic Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Myelin Basic Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuron Specific Enolase</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognostic Value</style></keyword><keyword><style  face="normal" font="default" size="100%">S100B</style></keyword><keyword><style  face="normal" font="default" size="100%">Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">April 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">478-484</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Background: &lt;/strong&gt;The high number of accidents and traumatic brain injuries, especially in the productive age group, causes a lot of morbidity and mortality. A fast and accurate examination method is needed for the diagnosis and treatment of traumatic brain injury. Nerve damage biomarkers such as Neuron Specific Enolase, S100B, Glial Fibrillary Acidic Protein, and Myelin Basic Protein, have been used globally both for research and daily use to determine the severity of traumatic brain injury. &lt;strong&gt;Methods:&lt;/strong&gt; Searches and journal searches were carried out from Science Direct, Scopus, Springer Link, and PubMed, with the keywords &quot;Neuron Specific Enolase&quot;, &quot;S100B&quot;, &quot;Glial Fibrillary Acidic Protein&quot;, &quot;Myelin Basic Protein&quot;, and &quot;Traumatic Brain Injury ”. Screening was carried out using PRISMA 2021 to look for studies that met the criteria and were of sufficient study quality according to the Newcastle-Ottawa Scale. &lt;strong&gt;Results: &lt;/strong&gt;Twenty-three studies were collected and further grouped based on outcomes, both prognostic and survival outcomes. Neuron Specific Enolase, S100B, and Glial Fibrillary Acidic Protein values were higher in poor outcomes (all p values &amp;lt; 0.001) and poor survival (all p values &amp;lt; 0.001) in traumatic brain injury. Myelin Basic Protein was not significant in poor outcome (p = 0.35), but was higher in poor survival (p &amp;lt; 0.001) in traumatic brain injury. &lt;strong&gt;Conclusion:&lt;/strong&gt; Neuron Specific Enolase, S100B, and Glial Fibrillary Acidic Protein, can be used as markers for prognostic and survival value in traumatic brain injury. Myelin Basic Protein can be used as a marker for survival value in traumatic brain injury.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><work-type><style face="normal" font="default" size="100%">Review Article</style></work-type><section><style face="normal" font="default" size="100%">478</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;Wibowo Artho Sutrisno&lt;sup&gt;1&lt;/sup&gt;, Prananda Surya Airlangga&lt;sup&gt;1*&lt;/sup&gt;, Citrawati Dyah Kencono Wungu&lt;sup&gt;2&lt;/sup&gt;, Prihatma Kriswidyatomo&lt;sup&gt;1&lt;/sup&gt;, Hamzah1, Bambang Pujo Semedi&lt;sup&gt;1&lt;/sup&gt;, Mahmudah&lt;sup&gt;3&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Anesthesiology and Reanimation, Faculty of Medicine, Airlangga University - Dr Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Physiology and Medical Biochemistry, Faculty of Medicine, Airlangga University, Surabaya, INDONESIA. 3Department of Community Health, Faculty of Community Health, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Muhammad Fauzan Jauhari</style></author><author><style face="normal" font="default" size="100%">Lucia Yovita Hendrati</style></author><author><style face="normal" font="default" size="100%">Agus Turchan</style></author><author><style face="normal" font="default" size="100%">Asra Al Fauzi</style></author><author><style face="normal" font="default" size="100%">Budi Utomo</style></author><author><style face="normal" font="default" size="100%">Eko Agus Subagio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Impact of Kaempferia galanga L. Extract on Nerve Growth  Factor Expression in A Rat Model of Traumatic Brain Injury</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">kaempferia galanga</style></keyword><keyword><style  face="normal" font="default" size="100%">Nerve Growth Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Traumatic Brain Injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">December 2023</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">1236-1243</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Head injuries contribute significantly to morbidity and mortality globally, and there is need of effective treatment. This study focuses on evaluating NGF (Nerve Growth Factor) expression in a rat model of traumatic brain injury, exploring the potential therapeutic effects of &lt;em&gt;Kaempferia galanga L&lt;/em&gt;. extract. &lt;strong&gt;Methods: &lt;/strong&gt;Male Wistar rats were used in the experiment, and traumatic brain injury was induced using Marmarou's weight drop model. Four groups of rats were studied: a negative control group, a group with traumatic brain injury without &lt;em&gt;Kaempferia galanga L&lt;/em&gt;. extract, and two groups with traumatic brain injury treated with different doses of &lt;em&gt;Kaempferia galanga L.&lt;/em&gt; extract. Rats were divided further based on the time of decapitation, either 24 or 48 hours post-injury. NGF expression was assessed using immunohistochemistry. &lt;strong&gt;Results:&lt;/strong&gt; The study confirmed NGF expression variations among groups, with stronger expression observed 48 hours post-injury in rats receiving 1200 mg/kgbb of &lt;em&gt;Kaempferia galanga L.&lt;/em&gt; extract. This suggests a potential impact of the extract on NGF expression, likely attributed to its anti-inflammatory and antioxidant properties. &lt;strong&gt;Discussion:&lt;/strong&gt; &lt;em&gt;Kaempferia galanga L&lt;/em&gt;. extract has known anti-inflammatory and antioxidant effects, which may contribute to increased NGF expression observed in this study. &lt;strong&gt;Conclusion:&lt;/strong&gt; This study sheds light on the potential benefits of&lt;em&gt; Kaempferia galanga L&lt;/em&gt;. extract in promoting NGF expression and improving outcomes in traumatic brain injury, emphasizing the need for further investigation to translate these findings into clinical practice.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6s</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">1236</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Muhammad Fauzan Jauhari&lt;sup&gt;1&lt;/sup&gt; , Lucia Yovita Hendrati&lt;sup&gt;2 *&lt;/sup&gt;, Agus Turchan&lt;sup&gt;1 &lt;/sup&gt;, Asra Al Fauzi&lt;sup&gt;1&lt;/sup&gt; , Budi Utomo&lt;sup&gt;3&lt;/sup&gt; , Eko Agus Subagio&lt;sup&gt;1&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Neurosurgery, Faculty of Medicine Universitas Airlangga – Dr. Soetomo General Academic Hospital, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Epidemiology, Population Biostatistics and Health promotion, Faculty of Public Health, Universitas Airlangga, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;&lt;strong&gt;3&lt;/strong&gt;&lt;/sup&gt;Department of Public Health and Preventive Medicine, Faculty of Medicine Universitas Airlangga, INDONESIA.&lt;/p&gt;
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