EFFECT OF MANGOSTEEN EXTRACT ON NEUROINFLAMMATION IN RAT MODEL OF ACUTE TRAUMATIC BRAIN INJURY

Objective: Traumatic brain injury (TBI) is one of the major health problems regarding morbidity and mortality, especially in productive ages. Following primary injury, there is a secondary insult, resulting in oxidative stress, neuroinflammation, and cell death. Mangosteen is a powerful natural antioxidant and anti-inflammation that also has neuroprotective property. The aim of this study was to explore the effect of mangosteen extract (ME)on neuroinflammation following TBI. Methods: A total of 30 Sprague-Dawley rats were randomized into three treatments group, i.e., sham-operated controls, closed head injury (CHI), and treatment group. In the treatment group, we gave ME once daily every day after CHI for 7 days. As oxidative process marker, we investigated malondialdehyde (MDA) expression. As neuroinflammation marker, we investigated glial fibrillary acidic protein (GFAP) and CD-68. Results: TBI increased the expression of GFAP and CD-68, but not MDA. There was significant GFAP expression difference between treatment group and CHI group. Regarding the expression of CD-68 and MDA, there was no significant difference between treatment and CHI group. Conclusion: Mangosteen extract supplementation decreased GFAP expression significantly after TBI

Examination of Systole/Diastole Ratio of Umbilical Artery in the third Trimester Gestational Pregnancy and its Correlation with Lactate Acid Level in Fetal Cord

BACKGROUND: Fetal distress is a serious complication of perinatal infants and refers to fetal hypoxia in the uterus and asphyxia immediately after the baby is born. The occurrence of uteroplacental disorders is related to various factors, including maternal and fetal factors. When fetal distress occurs, umbilical cord blood flow and fetal blood flow decrease, which in turn causes fetal circulation and respiratory dysfunction in the womb. Evaluating cord blood flow characteristics with ultrasound can provide a reference for prediction and diagnosis of fetal distress, especially by conducting an ultrasound examination of the Doppler S/D ratio of the umbilical arteries especially at gestational age >30 weeks. OBJECTIVE: The objective of the study was to assess the correlation between umbilical artery SD ratio examinations with lactate acid levels in the umbilical METHODS: This study was an observational analytic study with a cross-sectional study design. The research was conducted in Haji Adam Malik General Hospital Medan and Satellite Hospital. The sample was pregnant women who meet the inclusion and exclusion criteria, we found 38 of pregnant women from January to December 2019. Results: The average age of patients in this study was 30 (5) years, the majority of multiparous patients were 25 (47.2), the average gestational age was 38 (2) weeks. Most births in this study were SC 38 (71.7) with an average S/D ratio in the study of 2.81 (0.52) and a mean lactic acid level of 2.7 (0.4). The average Apgar score in this study was 8/9 as many as 29 (54.7), the average S/D ratio is obtained with the average Apgar score of the patient. From this study, it is known that the higher the Apgar score, the higher the average S/D ratio value in patients. The mean patients with poor Apgar outcomes (5/6) have an S/D ratio of 2.5. From the analysis using ANNOVA also obtained p < 0.28. This shows that there is no significant relationship between Apgar score and S/D ratio. Increasing in lactic acid was found in infant outcomes with an Apgar score of 9/10 with a mean value of 2.9 (0.5). From the ANNOVA analysis, a p = 0.99 was also found. This showed that there was no significant relationship between the levels of lactic acid and Apgar score for infants. Lactic acid has a very weak positive correlation with Apgar score for infants with an R value of 0.274 (p = 0.047), this shows that lactic acid does not have a strong relationship with infant outcomes. CONCLUSION: There was no correlation between umbilical cord S/D ratio and lactic acid with Apgar score. Lactic acid has a very weak positive correlation with the infant Apgar score with an R value of 0.274

Microplastic: Characteristics, exposure pathways, toxicity, and implication for human health

Microplastics particles ranging from 1 µm to 5 mm, have gained attention for their omnipresence in marine environments and potential health risks. Initially recognized in the 1990s, microplastics are classified as primary (designed for microscopic dimensions) or secondary (resulting from degradation). Exposure pathways include ingestion, inhalation, and dermal contact, with sources ranging from food and beverages to personal care products. These particles possess unique properties, facilitating their interaction with organic contaminants and potential bioaccumulation in marine life. Their small size allows them to infiltrate ecosystems, raising concerns about their impacts on human health. Studies suggest associations between microplastic exposure and health issues such as inflammatory bowel disease and neurodevelopmental. Microplastics exhibit toxicity through mechanisms like oxidative stress induction and disruption of neurotransmitter levels. They have been detected in human tissues, including the brain, raising concerns about potential neurological impacts. To comprehend the effects on health over time, additional research is required, including biopersistence and tissue accumulation. Regulatory measures and consumer awareness initiatives are crucial to mitigate microplastic pollution and minimize health risks. Strategies to reduce plastic production, enhance recycling, and develop microplastic removal technologies are vital for protecting both human health and the environment. In summary, microplastics pose significant health risks due to their widespread presence and potential toxicity. Understanding their impacts and implementing effective mitigation strategies are essential for safeguarding human health and environmental integrity

Sustained Tau Phosphorylation and Microglial Activation Following Repetitive Traumatic Brain Injury

BACKGROUND: Repetitive traumatic brain injury (TBI), even without acute sequela, can induce a delayed neurodegenerative with overexpression of phosphorylated tau (p-tau) as hallmark, caused by chronic inflammation mediated in part by microglial activation. AIM: The aim of this study was to examine the dynamics of p-tau accumulation and microglial activation following repetitive TBI. MATERIALS AND METHODS: Thirty Sprague–Dawley rats were randomized into a sham control group and two treatment groups receiving three successive closed-skull impacts (TBI model) from a 40-g mass dropped from a 1-m height on alternating days (days 0, 1, 3, and 7). The first treatment group was sacrificed on the last day of trauma and the second treatment group after 7 days of no trauma. The expression level of p-tau was evaluated by AT-8 antibody immunostaining and microglial activation by anti-CD-68 immunostaining. RESULTS: Immunoexpression of AT-8 was significantly elevated 7 days after TBI compared to the last day of trauma and compared to the sham control group, while CD-68 expression was significantly higher than sham controls on the last day of trauma and remained elevated for 7 days without trauma. CONCLUSION: The study showed that brain trauma can induce p-tau overexpression and microglial activation that is sustained during the non-trauma period

Turmeric Extract Supplementation Reduces Tau Protein Level in Repetitive Traumatic Brain Injury Model

BACKGROUND: Repetitive traumatic brain injury (RTBI) has gained much attention in this decade, especially in contact sports athletes and military personals. This injury is correlated with early neurodegenerative changes that are marked with the increased of tau protein. Turmeric extract (TE) is a well-known anti-inflammation and antioxidant that decreases tau protein expression in neurodegenerative disease. AIM: This study aimed to prove the effect of TE on tau protein level after RTBI. METHODS: Forty Sprague Dawley mice were divided into four groups, i.e. negative sham control group, the control group, and two treatment groups. A weight drop model was used by applying a 40-gram mass that was dropped from a 1-meter height onto the vertex of the head, with a total frequency of 12 times, divided into 4 days (day 0, 1, 3, and 7; 3 traumas on each day). TE was given to all treatment groups with 500 mg/kg BW doses once daily. The first treatment group had TE for seven days along the trauma. The second treatment group had pretreatment TE extract, given from seven days before first trauma and continued along the trauma protocol days. Tau protein level was measured on brain and serum using ELISA method. RESULTS: There was a significant reduction of tau protein level in both treatment groups compared to trauma group, either in serum or brain, but we also found significant differences regarding brain tau level between the treatment and pretreatment group. CONCLUSION: This study might provide evidence of with the role of pretreatment TE in RTBI

The Correlation Between Blood Biomarker and Intracranial Pathologies in Mild Acute Traumatic Brain Injury: a Systematic Review

Systematic Revie

Chemical Composition and Neuroprotective Properties of Indonesian Stingless Bee (<i>Geniotrigona thoracica</i>) Propolis Extract in an In-Vivo Model of Intracerebral Hemorrhage (ICH)

Stroke is the world’s second-leading cause of death. Current treatments for cerebral edema following intracerebral hemorrhage (ICH) mainly involve hyperosmolar fluids, but this approach is often inadequate. Propolis, known for its various beneficial properties, especially antioxidant and anti-inflammatory properties, could potentially act as an adjunctive therapy and help alleviate stroke-associated injuries. The chemical composition of Geniotrigona thoracica propolis extract was analyzed by GC-MS after derivatization for its total phenolic and total flavonoid content. The total phenolic content and total flavonoid content of the propolis extract were 1037.31 ± 24.10 μg GAE/mL and 374.02 ± 3.36 μg QE/mL, respectively. By GC-MS analysis, its major constituents were found to be triterpenoids (22.4% of TIC). Minor compounds, such as phenolic lipids (6.7% of TIC, GC-MS) and diterpenic acids (2.3% of TIC, GC-MS), were also found. Ninety-six Sprague Dawley rats were divided into six groups; namely, the control group, the ICH group, and four ICH groups that received the following therapies: mannitol, propolis extract (daily oral propolis administration after the ICH induction), propolis-M (propolis and mannitol), and propolis-B+A (daily oral propolis administration 7 days prior to and 72 h after the ICH induction). Neurocognitive functions of the rats were analyzed using the rotarod challenge and Morris water maze. In addition, the expression of NF-κB, SUR1-TRPM4, MMP-9, and Aquaporin-4 was analyzed using immunohistochemical methods. A TUNEL assay was used to assess the percentage of apoptotic cells. Mannitol significantly improved cognitive–motor functions in the ICH group, evidenced by improved rotarod and Morris water maze completion times, and lowered SUR-1 and Aquaporin-4 levels. It also significantly decreased cerebral edema by day 3. Similarly, propolis treatments (propolis-A and propolis-B+A) showed comparable improvements in these tests and reduced edema. Moreover, combining propolis with mannitol (propolis-M) further enhanced these effects, particularly in reducing edema and the Virchow-Robin space. These findings highlight the potential of propolis from the Indonesian stingless bee, Geniotrigona thoracica, from the Central Tapanuli region as a neuroprotective, adjunctive therapy