@article {2273, title = {Can Ventilator Settings Influence Lung Damage Biomarkers KL-6 and CRP during One Lung Ventilation?}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {April 2024}, pages = {455-459}, type = {Research Article}, chapter = {455}, abstract = {

Background: Volume-controlled (VCV) or pressure-controlled ventilation (PCV) modes are most often used during OLV. This is a prospective observational analytical study of patients undergoing thoracic surgery with OLV. Method: 40 patients underwent thoracic surgery using one lung ventilation (OLV) from December 2023 to February 2024. All patients received lung protective ventilation (PLV) with a tidal volume of 6 ml/ kgPBW during OLV with PEEP 5-7 cmH2O and were divided into two groups: one with a ventilator in volume-controlled mode (VCV) and the other with pressure-controlled mode (PCV). KL-6, CRP, and p/f ratio were measured before OLV, 2 hours after OLV, and 24 hours after the operation was completed. Respiratory variables during OLV were recorded. Results: KL-6 and CRP levels in PCV and VCV groups were significantly different. There were significant differences in the values of Ppeak (p \<0.001), PEEP (p = 0.008), Cstat (p = 0.004) and driving pressure (p \<0.001) in both groups. The correlation between changes in KL-6 and CRP levels and the P/F ratio were very weak and insignificant. Cytokines play an important role in the inflammatory response in the lungs. Several determining factors of blood flow are gravity, lung disease, surgery, and hypoxic pulmonary vasoconstriction. Duration of OLV may affect the pulmonary inflammatory response and is correlated with the duration of OLV. Conclusion: There is no association found between KL-6 and CRP in PCV and VCV mode during thoracotomy with OLV.

}, keywords = {CRP, KL-6, One lung ventilation, Thoracotomy, Ventilator}, doi = {10.5530/pj.2024.16.72}, author = {Novita Sari and Bambang Pujo Semedi and Prananda Surya Airlangga and Kohar Hari Santoso and Maulydia and Budi Utomo and Christrijogo Sumartono} } @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 {2429, title = {Effect of Cacao Bean Extract as a Paracetamol Adjuvant on Pain Scale and Tumor Necrosis Factor-Alpha in Neuropathic Pain: An Animal Model Study}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {December 2024}, pages = {1336-1341}, type = {Research Article}, chapter = {1336}, abstract = {

Introduction: One treatment for neuropathic pain is paracetamol. Meanwhile, cacao bean extract is a traditional remedy developed for pain management. Objective: Analyzing effect of combining cacao bean extract and paracetamol on pain scale and tumor necrosis factor-alpha (TNF-α) in neuropathic pain. Methods: Subjects were randomized post-test only control group design from 28 mice (Mus musculus) to 4 groups: G0 (control), G1 (paracetamol only), G2 (cacao + paracetamol), and G3 (cacao + {\textonehalf} doses paracetamol). The subject assessed pain scale using von Frey test and TNF-α. The statistical analysis includes paired t-tests, Wilcoxon, one-way ANOVA, Kruskal Wallis, and Pearson correlation tests with p \<0.05. Results: The combination of cacao bean extract and paracetamol resulted in a pain scale of 2.57 {\textpm} 1.10 gf, with significant differences observed among the four groups (p \<0.001). Significant differences in pain scale scores were found in four groups (p \<0.001), including G0 (p = 0.006), G1 (p \<0.001), G2 (p \<0.001), and G3 (p \<0.001). After treatment, the average TNF-α levels was 86.96 {\textpm} 23.73 ng/mL, with significant differences observed among the four groups (p \<0.001). There was a strong correlation between the pain scale and TNF-α levels (p \<0.001). Conclusion: In an animal model of neuropathic pain, using cacao bean extract as a paracetamol adjuvant significantly reduces pain scale (as measured by the von Frey test) and TNF-α levels.

}, keywords = {Cacao, Neuropathic pain, pain scale, Paracetamol, TNF-α}, doi = {10.5530/pj.2024.16.215}, author = {Faiz Muhammad Ammar and Christrijogo Sumartono Waloejo and Herdiani Sulistyo Putri and Kohar Hari Santoso and Prananda Surya Airlangga and Budi Utomo} } @article {2396, title = {Effective Dose of Cocoa as a Preemptive Analgesic and Anti- Inflammatory Agent Assessed through Pain Scale and Tumor Necrosis Factor Alpha (TNF-α) in an Acute Pain Animal Model}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {October 2024}, pages = {1134-1137}, type = {Research Article}, chapter = {1134}, abstract = {

Background: Pain is a significant issue for 40-50\% of hospital patients, with 10-50\% of acute pain cases potentially progressing to chronic pain. Pain-associated inflammation often involves the release of mediators, including Tumor Necrosis Factor Alpha (TNF-α). Cocoa beans contain polyphenols, catechins, anthocyanidins, and proanthocyanidins, compounds believed to possess analgesic properties. This study aims to assess cocoa{\textquoteright}s potential as an oral preemptive analgesic agent in an acute pain mouse model, with an emphasis on its impact on inflammation through TNF-α levels. Methods: This true experimental study involved 24 male white mice split into four groups: a control group (K0) receiving a placebo, a treatment group receiving 15 mg/kg BW oral paracetamol (Kpct), a treatment group receiving 0.5 mg/g BW cocoa (K1), and a treatment group receiving 1 mg/g BW cocoa (K2). Pain response was measured using TNF-α levels and the von Frey test. The Kruskal-Wallis test and One-Way ANOVA were employed for statistical analysis. Results: Cocoa at doses of 0.5 mg/g BW and 1 mg/g BW substantially reduced TNF-α levels (75.82 {\textpm} 7.77 and 70.79 {\textpm} 11.50, respectively) compared to the control and paracetamol groups (98.22 {\textpm} 14.74 and 92.81 {\textpm} 2.64). On the first day, compared to the control group{\textquoteright}s 1.82 {\textpm} 0.78 von Frey values, the cocoa-treated groups{\textquoteright} values (6.20 {\textpm} 2.72 and 7.63 {\textpm} 4.11) were notably higher. There were no notable variations in von Frey values across the groups on the second day. However, a correlation was found between von Frey values on the first and second days. Conclusion: Cocoa can potentially serve as an effective preemptive analgesic agent, reducing pain and inflammation primarily by reducing TNF-α levels. These results provide validity to the use of cocoa as an alternative therapy in acute pain management.

}, keywords = {Cocoa, Pain, Pain Degree Analgesia, TNF-α}, doi = {10.5530/pj.2024.16.185}, author = {Herry Cahya Fathani and Herdiani Sulistyo Putri and Prananda Surya Airlangga and Christrijogo Sumartono Waloejo and Ira Sari Yudaniayanti and Pudji Lestari} } @article {2324, title = {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}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {June 2024}, pages = {695-699}, type = {Research Article}, chapter = {695}, abstract = {

Objective: 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. Material and Methods: 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. Results: The mean UCH-L1 level was 0.522 {\textpm} 0.592, with a cutoff value of \> 0.2057, indicating moderate to severe TBI if UCH-L1 levels exceeded 0.2057. Spearman{\textquoteright}s test and correlation coefficient analysis showed a strong relationship between UCH-L1 levels and Rotterdam CT score (p \< 0.05), as well as between UCH-L1 levels and TBI severity based on GCS (p \< 0.05). The cutoff value for Rotterdam CT score was \> 2, indicating moderate to severe TBI if the score exceeded 2. Conclusion: Serum UCH-L1 levels are significantly associated with the severity of TBI based on GCS and Rotterdam CT score.

}, keywords = {Glasgow Coma Scale, Rotterdam CT score, Traumatic Brain Injury, UCH-L1}, doi = {10.5530/pj.2024.16.111}, author = {Junjungan Kristianto Manurung and Prananda Surya Airlangga and Hamzah Hamzah and Prihatma Kriswidyatomo and Anggraini Dwi Sensusiati and Budi Utomo} } @article {2329, title = {Relationship Between Cerebrospinal Fluid S100B Levels with Glasgow Coma Scale and Rotterdam CT Score in Traumatic Brain Injury Patients}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {June 2024}, pages = {503-508}, type = {Original Article}, chapter = {503}, abstract = {

Background: 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. Methods: 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. Results: 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 {\textpm} 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 \<0.05, with a correlation coefficient or r value of 0.827. Conclusion: Increased levels of S100B in cerebrospinal fluid are associated with decreased GCS and increased Rotterdam CT score in traumatic brain injury patients.

}, keywords = {Glasgow Coma Scale, Rotterdam CT score., S100B, Traumatic Brain Injury}, doi = {10.5530/pj.2024.16.81}, author = {Rian Nofiansyah and Kohar Hari Santoso and Prananda Surya Airlangga and Prihatma Kriswidyatomo and Hamzah} } @article {2277, title = {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}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {April 2024}, pages = {478-484}, type = {Review Article}, chapter = {478}, abstract = {

Background: 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. Methods: Searches and journal searches were carried out from Science Direct, Scopus, Springer Link, and PubMed, with the keywords "Neuron Specific Enolase", "S100B", "Glial Fibrillary Acidic Protein", "Myelin Basic Protein", and "Traumatic Brain Injury {\textquotedblright}. 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. Results: 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 \< 0.001) and poor survival (all p values \< 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 \< 0.001) in traumatic brain injury. Conclusion: 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.

}, keywords = {Glial Fibriallary Acidic Protein, Myelin Basic Protein, Neuron Specific Enolase, Prognostic Value, S100B, Survival, Traumatic Brain Injury}, doi = {10.5530/pj.2024.16.76}, author = {Wibowo Artho Sutrisno and Prananda Surya Airlangga and Citrawati Dyah Kencono Wungu and Prihatma Kriswidyatomo and Hamzah and Bambang Pujo Semedi and Mahmudah} } @article {2448, title = {Successful Practice of Massive Transfusion in Traumatic Amputation of Digit I-V Manus Dextra: A Case Report}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {December 2024}, pages = {1436-1438}, type = {Case Report}, chapter = {1436}, abstract = {

Introduction: Massive blood is the main cause of mortality and morbidity in trauma patients, in which 6 out of 10 cases are reported to die. Case presentation: A 29-year-old man appears to have experienced an amputation of digit I-V manus dextra. Vital signs are in stable condition and the patient is also conscious (GCS of 15) with ASA PS 1. The patient underwent debridement and replantation for 18 hours. Post-first surgery, we found blood seepage in the surgical wound, which for 4 hours showed 2000 mL of blood. The patient experiences decreased consciousness (GCS of 9), hypotension (77/40 mmHg), HR of 130 {\texttimes}/min, and cold extremities. The patient received resuscitation with 1000 mL of crystalloid, 500 mL of colloid, 800 mL of WB, and 400 mL of PRC transfusion. Abnormal laboratory examination revealed Hb 4.6 g/dL, albumin 1.4 g/dL, and prolongation of hemostasis function 2 times. The patient underwent reoperation and was found to have ruptured muscles and veins for which musculorraphy and venorraphy were performed for 16 hours. On the 3rd day, the patient experienced breathing difficulties (RR of 30 {\texttimes}/ min and SO2 of 95\%) and the chest x-ray showed lung edema. The patient was placed on a ventilator using NIV and furosemide 20 mg/8 h. The patient regained consciousness on the 7th day. Discussion: The principle of managing massive bleeding is to stop the bleeding, restore blood circulation volume, and maintain peripheral vascularization. Conclusion: Massive transfusion is a management strategy for preventing death due to hemorrhagic shock.

}, keywords = {Bleeding, Blood massive protocol, Hemorrhagic shock, Trauma}, doi = {10.5530/pj.2024.16.231}, author = {Kashi Ameta Resijiadi Juwono and Maulydia and Prananda Surya Airlangga} } @article {2408, title = {Transient Receptor Potential Vanilloid 1 in Acute Pain: A Literature Review}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {October 2024}, pages = {1196-1201}, type = {Review Article}, chapter = {1196}, abstract = {

Transient Receptor Potential Vanilloid 1 (TRPV1) is a protein that functions as a non-selective channel receptor that is widely expressed in skin tissue, including keratinocytes, peripheral sensory nerve fibers, and immune cells. Several structural features of TRPV1 are involved in heat-induced activation, where stimulation of TRPV1 elicits a burning sensation, reflecting the receptor{\textquoteright}s important role in pain. A TRPV1- mediated signalling pathway that functions as an endogenous pain resolution mechanism by inducing nuclear translocation of β-arrestin2 to minimize desensitization of μ-opioid receptors (MOR). TRPV1 agonists can reduce pain primarily by interfering with pain nerve conduction. Several TRPV1 antagonist drug candidates have failed in clinical trials because by interfering with the detection of the above-mentioned stimuli, they triggered serious side effects such as hyperthermia and painful impaired heat detection. In the case of agonists, systemic administration causes more severe side effects such as respiratory damage. Therefore, only topical preparations with limited effectiveness have been developed. The TRPV1 agonist capsaicin is currently the only one approved for the treatment of muscle, bone, neuropathic pain and migraine, and is only available as a low-concentration cream or as a transdermal patch.

}, keywords = {Agonis TRPV1, Capsaicin, Pain, transient receptor potential vanilloid 1}, doi = {10.5530/pj.2024.16.196}, author = {Dian Retno Mumpuni and Herdiani Sulistyo Putri and Prananda Surya Airlangga and Christrijogo Sumartono Waloejo} } @article {2278, title = {Vitamin D and Wound Recovery: Illuminating the Path to Enhanced Healing in Diabetic Patients}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {April 2024}, pages = {485-491}, type = {Review Article}, chapter = {485}, abstract = {

Wound healing is a highly coordinated biological event as a response to injured skin. It commonly takes 14 days for a wound to be completely healed. However, the duration of wound healing may vary between individuals due to certain factors. One major factor that delays the wound-healing process is Diabetes Mellitus. Delayed wound healing with poor prognosis commonly occurs in diabetic patients. Chronic hyperglycemia may affect macrophage polarisation, which is essential in the wound healing mechanism. The macrophage polarisation enables the pro-inflammatory M1 phenotype to switch to the anti-inflammatory M2 phenotype. Thus, pro-inflammatory M1 phenotype prevails persistently in diabetic wounds, while the anti-inflammatory M2 phenotype remains deficient. It results in significantly elevated levels of pro-inflammatory cytokines triggered by the M1 phenotype. Prolonged wound healing times increase the risk of infection, which can lead to more severe complications. Vitamin D is widely recognized for its essential role in regulating calcium levels and supporting bone health, as well as its positive effects on the immune system. This vitamin has the potential to skew macrophages towards the M2 phenotype and promote a regenerative and anti-inflammatory environment.

}, keywords = {Diabetes mellitus, Macrophage Polarisation, Vitamin D, Wound Healing}, doi = {10.5530/pj.2024.16.77}, author = {Aditya Chrisdianto and Prananda Surya Airlangga and Belindo Wirabuana and Regina Purnama Dewi Iskandar} }