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INDONESIA
The Indonesian Biomedical Journal
Published by The Prodia Education and Research Institute
ISSN : -     EISSN : -     DOI : -
Core Subject : Health, Science,
Biochemistry, Genetics & Molecular Biology Public Health
Arjuna Subject : -
Articles 10 Documents
 1 
Search results for , issue "Vol 17, No 5 (2025)" : 10 Documents clear
Modified High-Fat High-Sucrose Diet Promotes Obesity and Alters Colonic Cytokines Novita, Bernadette Dian; Wedharga, I Gede Putu Adhi; Tjahjono, Yudy; Wijaya, Hendy; Theodora, Imelda; Ervina, Martha; Wilianto, Yufita Ratnasari; Dewi, Sianty; Parengkuan, Irene Lingkan; Herjunianto, Herjunianto; Ghasani, Sabrina Maria; Limantoro, Michael Christian; Jaya, Ferdinand Wiliam
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3807

Abstract

BACKGROUND: Western dietary patterns are often associated with increasing non-communicable diseases, including inflammatory bowel disease (IBD). In experimental models, a high-fat high-sucrose (HFHS) diet is used to mimic metabolic and inflammatory effects of such diets, however the data regarding colonic inflammation in Indonesia remain limited. Therefore, this study was conducted evaluated the impact of HFHS feeding on colonic interleukin (IL)-6, IL-10 expression, and the IL-6/IL-10 ratio.METHODS: Six weeks old male C57BL/6 mice were randomly assigned to a normal fat diet (NFD) or HFHS diet group and fed ad libitum for 8 weeks. Colonic tissues were collected, and IL-6 and IL-10 expression was analyzed by immunohistochemistry.RESULTS: HFHS-fed mice showed significant increases in body weight (increased by 22.44%, p=0.0047) and caloric intake (increased by 125.17%, p=0.0000), confirming obesity induction. Colitis was also evident, with higher histological colitis scores (p=0.0072). However, colonic IL-6 (increased by 9.12%, p=0.1236), IL-10 (increased by 1.49%, p=0.8013), and the IL-6/IL-10 ratio (increased by 7.38%, p=0.4000) showed no significant differences compared to NFD.CONCLUSION: In C57BL/6 mice, an 8-week modified HFHS diet induced obesity, increased caloric intake, and mucosal injury, but did not significantly alter colonic IL-6, IL-10, or their ratio. This suggests preserved mucosal immune homeostasis consistent with an early compensatory phase rather than overt cytokine-driven inflammation. Longer or more intensive exposure may disrupt this balance, highlighting the need for further studies to define the temporal threshold and clarify immune microbiome interactions in colitis progression.KEYWORDS: high-fat high-sucrose diet, colon inflammation, IL-6, IL-10, obesity mice
Impact of GFR Stratification on Tc-99m DTPA Dose Distribution in Target and Non-Target Organs: A MIRD-Based Comparative Study in Renogram Imaging Qalby, Luthfia; Budi, Wahyu Setia; Hidayanto, Eko
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3843

Abstract

BACKGROUND: Renogram using Technetium-99m Diethylene Triamine Pentaacetic Acid (Tc-99m DTPA) is applied to evaluate renal perfusion, glomerular filtration rate (GFR), and urinary excretion. In patients with impaired renal function, delayed tracer elimination may increase accumulation in non-target organs such as the heart and liver, resulting in greater radiation exposure and reduced image quality. Studies examining the relationship between renal function and Tc-99m DTPA dose distribution remain limited, particularly in clinical settings in Indonesia. Therefore, in this study, an organ-level quantitative analysis of Tc-99m DTPA radiopharmaceutical dose distribution and absorbed dose using the Medical Internal Radiation Dose (MIRD) approach based on Single Photon Emission Computed Tomography/Computed Tomography (SPECT/CT) imaging was performed.METHODS: Thirty adult patients undergoing renogram were categorized into low-GFR (<60 mL/min/1.73 m²) and high-GFR (≥60 mL/min/1.73 m²) groups. Each patient received 4–5 mCi of Tc-99m DTPA intravenously. Organ activities were obtained from regions of interest (ROIs) on SPECT/CT images, and organ-level absorbed doses (mGy) were calculated using the MIRD formalism.RESULTS: In the low-GFR group, tracer retention in non-target organs increased, with absorbed doses up to twofold higher in the heart (0.0002–0.0136 mGy) and liver (0.0010–0.0178 mGy) compared to the high-GFR group. Renal absorbed doses ranged from 0.0001–0.0694 mGy, showing no significant difference between the left and right kidneys, while significant differences were observed in the heart and liver.CONCLUSION: GFR significantly affects the radiopharmaceutical dose distribution and absorbed dose of Tc-99m DTPA. Reduced renal function increases radiation exposure in non-target organs, whereas normal function results in a more localized renal dose distribution.KEYWORDS: Tc-99m DTPA, renogram, MIRD, glomerular filtration rate, absorbed dose, SPECT/CT, nuclear medicine
Aluminum Exposure Induces Time-Dependent Cognitive Decline, Anxiety, and Brain Aluminum Accumulation in Rats Ahmad Abdullah, Amirul Hafiz; Anuar, Husna; Rosli, Nur Afiqha; Faizal, Hilal Haiqal; Moothy, Kalaimathy; Fairof, Muhammad Hafiz Zuhdi; Jufri, Nurul Farhana; Masre, Siti Fathiah; Rajab, Nor Fadilah; Ibrahim, Farah Wahida
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3746

Abstract

BACKGROUND: Aluminum, a nonessential element, can accumulate in the brain and has been implicated in neurodegenerative disorders such as Alzheimer’s disease (AD). Although previous studies have examined aluminum neurotoxicity, many focus on a single time point, limiting insight into how aluminum accumulates over time. This study addresses that gap by investigating time-dependent aluminum accumulation and associated neurobehavioral changes in rats at 14, 28, and 42 days.METHODS: Male Wistar rats were administered 200 mg/kg/day aluminum chloride (AlCl3) via oral gavage for 14 (acute), 28 (subacute), and 42 (subchronic) days. Cognitive and anxiety-like behaviors were assessed using the 2-novel object recognition (2NOR) test, spontaneous alternation Y-maze, and open field test (OFT). Brain aluminum levels were quantified using inductively coupled plasma mass spectrometry (ICP-MS).RESULTS: There were impairments in spatial and non-spatial memory and increased anxiety-like behavior across all exposure durations (p<0.05). Non-spatial memory performance decreased by 50.5%, 37.7%, and 56.2% on day-14, -28, and -42, respectively. Spatial memory significantly declined by 34.3% and 43.2% on day-14 and -42, respectively, while the 20.0% decrease at day-28 was not statistically significant. Anxiety-like behavior increased, with center zone entries reduced by 37.6%, 64.9%, and 62.9% across the same time points. Brain aluminum concentrations were significantly elevated in all aluminum-exposed groups compared to controls, with increases of 2,622.6%, 314.7%, and 969.3% on day-14, -28, and -42, respectively (p<0.05). The increase was not strictly proportional to exposure duration, suggesting possible homeostatic regulation. Weight and liver assessments confirmed the subtoxic nature of the exposure.CONCLUSION: Exposure to aluminum for 42 days induces behavioral deficits and increases brain aluminum levels, which may support its potential relevance as a model to study aluminum-induced neurotoxicity.KEYWORDS: aluminum exposure, cognitive function, anxiety, temporal progression, neurobehavioral changes
Quercetin Stabilizes Atherosclerotic Plaques by Reducing Matrix Metalloproteinase-9 Expression and Enhancing M2 Macrophage Activity in Wistar Rats Ermawan, Romi; Pikir, Budi Susetyo; Mulyanto, Mulyanto; Utomo, Budi; Widjiati, Widjiati; Oktaviono, Yudi Her
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3790

Abstract

BACKGROUND: Quercetin has been shown to alleviate and prevent atherosclerosis. However, its role in stabilizing atherosclerotic plaques to prevent plaque rupture remains unclear. Therefore, this study was conducted to investigate the effects of quercetin on stabilizing atherosclerotic plaques.METHODS: Thirty-two Wistar rats were objected to a high-fat diet, along with an endothelial injury procedure conducted during the second week to create atherosclerotic plaque models. After six weeks, the subjects were randomly assigned to five groups consist of two control groups and three treatment groups treated with different quercetin dosages. Following the treatment, all subjects were euthanized to collect the left common carotid artery. The stability of the atherosclerotic plaques was evaluated by measuring the expression of matrix metalloproteinase-9 (MMP-9) using real-time polymerase chain reaction, assessing the activity of M1 and M2 macrophages along with the M1/M2 ratio using an enzyme-linked immunosorbent assay, and determining the maximum intima thickness through histopathological examination.RESULTS: Quercetin significantly reduced the expression of MMP-9, increased the activity of M2 macrophages, and lowered the M1/M2 ratio at doses of 10 and 50 mg/kg. However, there was no effect on M1 macrophage activity or maximum intima thickness. Path analysis indicated that quercetin primarily enhanced atherosclerotic plaque stability by reducing MMP-9 expression (p<0.001) and subsequently enhancing M2 macrophage activity (p=0.002).CONCLUSION: Quercetin administration significantly decreased the expression of MMP-9, enhanced the activity of M2 macrophages, and lowered the M1/M2 ratio at specific doses. These findings emphasize the significance of quercetin in stabilizing atherosclerotic plaques.KEYWORDS: atherosclerotic plaque, quercetin, stability, Wistar rats
Genotype Combination of rs1042044 and rs6458093 in GLP-1R as A Genetic Risk for Osteoporosis in Postmenopausal Iraqi Women Alzubaidi, Ammar Kadhim; Al-Saadi, Farah Abdulwahab; Alagele, Amer Qani
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3768

Abstract

BACKGROUND: Many genetic factors are known to be related to osteoporosis, and currently the role of the glucagon-like peptide-1 receptor (GLP-1R) gene in bone health has been studied intensively. Some variation of this gene, such as rs1042044 and rs6458093, are known to be linked to metabolic diseases and lower bone mineral density, however their specific contribution to osteoporosis remains largely unexplored. Therefore, this study was conducted to investigate the combined genotypic effect of rs1042044 and rs6458093 as a genetic risk factor for osteoporosis in postmenopausal Iraqi women.METHODS: Blood samples from 75 osteoporosis patients and 75 healthy controls, aged 45-85, were collected. DNA was extracted, and a region of GLP-1R gene was amplified by polymerase chain reaction (PCR) and sequenced using the Sanger method to identify polymorphisms. Serum parathyroid hormone (PTH) levels were also measured with chemiluminescent immunoassay (CLIA) methods.RESULTS: Significant differences were observed for age, menopausal age, and PTH levels (p<0.001), but not for Body Mass Index (BMI). While individual SNPs (rs1042044 and rs6458093) showed no significant association with osteoporosis, a specific genotype combination of rs1042044 A and rs6458093 G was found to be a highly significant risk factor for the disease (OR=21.85, p=0.026). Linkage Disequilibrium analysis showed a D' value=0.85 and R²=0.45 between the two SNPs.CONCLUSION: Co-occurrence of the 'A' allele at rs1042044 and the 'G' allele at rs6458093 creates a highly susceptible genetic risk factor for osteoporosis, highlighting a potential novel biomarker for disease risk and providing a benchmark for future studies.KEYWORDS: osteoporosis, postmenopausal, GLP1R, PTH, SNPS
Inositol Hexakisphosphate (InsP₆) Induces Apoptosis via Caspase-Dependent Pathways: Molecular Docking Insights Sandra, Ferry; Ranggaini, Dewi; Halim, Johni; Pakpahan, Alfred; Pratitis, Visi Endah; Lee, Kyung Hoon
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3810

Abstract

BACKGROUND: Inositol hexakisphosphate (InsP₆) exhibits anticancer activity, especially by inducing intrinsic and extrinsic apoptotic pathways. However, there is still no molecular docking evidence that directly examines InsP₆ interactions with either upstream or downstream apoptotic regulators. Therefore, the current study was conducted to investigate the molecular docking of InsP₆ to caspases as upstream/downstream apoptotic regulators.METHODS: Ligands including InsP₆, InsP₅, InsP₄, histone deacetylase inhibitor, and caspase inhibitors were retrieved from PubChem, while target proteins (histone, caspase-8, caspase-2, and caspase-3) were obtained from the Protein Data Bank. Ligand toxicity was predicted using ProTox-3.0, and physicochemical properties were analyzed with SwissADME. Ligand structures were energy-minimized using PyRx with the Universal Force Field, while proteins were prepared by removing water molecules and non-essential heteroatoms in BIOVIA Discovery Studio. Molecular docking was conducted using CB-Dock 2.0, with binding poses selected based on the lowest Vina score, and ligand–protein interactions were visualized in Discovery Studio.RESULTS: Molecular docking results showed that InsP₆ bound strongly to histone, caspase-8, caspase-2, and caspase-3 with affinities comparable to reference inhibitors, forming multiple hydrogen bonds with key active-site residues. InsP₆, InsP₅, and InsP₄ exhibited several similar binding sites to caspase-3, with only minor differences in binding affinity.CONCLUSION: InsP₆ shows strong binding to histone, caspase-8, caspase-2, and caspase-3 based on in silico results, supporting its role in inducing both extrinsic and intrinsic apoptotic pathways. Taken together, InsP₆ could be a potential inducer of apoptosis in cancer cells.KEYWORDS: cancer, apoptosis, InsP₆, InsP₅, InsP₄, caspase, in silico, molecular docking
Long Noncoding RNAs TYMSOS, VASH1-AS1, and LINC01001 Expressions as Biomarkers of β-thalassaemia Severity Among the Malaysian Patients Mohd Yasin, Norafiza; Raman, Nur Fatin Aqilah; Sulaiman, Siti Aishah; Kosnan, Nurhairulamri; Abdul Murad, Nor Azian; Mohd Sahid, Ermi Neiza; Yusoff, Yuslina; Mohd Ibrahim, Hishamshah; Muda, Zulaiha; Esa, Ezalia
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3766

Abstract

BACKGROUND: β-thalassaemia has heterogeneous disease severities ranging from mild to trait, and major. Long noncoding RNAs (lncRNAs) are known to regulate microRNAs (miRNAs) and genes, possibly modifying the disease phenotypes. However, limited data exist on the lncRNAs in β-thalassaemia, and no study has yet addressed this gap in Malaysia. Therefore, this study aimed to identify the expression profile of lncRNAs in β-thalassaemia major and trait among Malaysians.METHODS: Case-control study was conducted in two phases at Tunku Azizah Women and Children's Hospital and the Institute of Medical Research, from September 2019 to November 2021. Total of 141 individuals were recruited, comprising β-thalassemia major (MAJOR, n=11), β-thalassemia trait (TRAIT, n=17), and healthy controls (CON, n=113). All participants were genotyped for thalassaemia and assessed for their haemoglobin and red blood cells (RBC) indices. In the first phase, discovery of lncRNA was performed using microarray, and differential expression of lncRNAs (DEL) in MAJOR, TRAIT, and CON groups was identified. Significant lncRNAs were subjected to lncRNA-miRNA prediction, and gene ontology and biological pathway were analyzed. In validation phase, six potential lncRNAs were further validated via using lncRNA polymerase chain reaction (PCR) custom array.RESULTS: Total of 364 DELs were identified in MAJOR group, and 128 DELs were identified in TRAIT group. Between the MAJOR and TRAIT groups, 100 DELs were dysregulated in MAJOR group. Two molecular networks comprising the lncRNA interactions with miRNAs were identified and associated with traits and major phenotypes, resulting in six potential lncRNAs for validation. Among these six lncRNAs, three lncRNAs (TYMSOS, VASH1-AS1, and LINC01001) were reduced in the MAJOR group (fold change (FC)=-6.67, p=0.026; FC=-8.33, p=0.022; and FC=-8.33, p=0.021, respectively).CONCLUSION: Expressions of TYMSOS, VASH1-AS1, and LINC01001 lncRNAs were altered differently between β-thalassaemia major and trait patients. Therefore these lncRNAs may serve as novel biomarkers for β-thalassaemia disease severity in Malaysian population.KEYWORDS: β-thalassaemia, lncRNAs, miRNAs, severity, major, trait, molecular network
Liposome-based Nanoparticles Encapsulating Vitamin D3 Attenuate IL-6 and TNF-α in a Menopausal Mouse Model Kusuma, Baskara Wiku Adi; Dwiningsih, Sri Ratna; As’adi, Ashon; Wahyuningsih, Sri Puji Astuti
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3796

Abstract

BACKGROUND: Vitamin D3 is an essential regulator of immune function, however its bioavailability is limited. Liposomes as nanocarriers can enhance vitamin D3 absorption and delivery, however the application of liposomal vitamin D3 in postmenopausal remains underexplored, particularly in preclinical models. Estrogen deficiency during menopause promotes immune dysregulation and elevates proinflammatory cytokines, including interleukin (IL)-6 and tumor necrosis factor (TNF)-α. This study was conducted to evaluate the effects of liposomal vitamin D3 supplementation on serum vitamin D3, IL-6, and TNF-α levels in an ovariectomy-induced menopausal mouse model.METHODS: Mice were randomly divided into four groups comprising non-surgical control (N), ovariectomized without treatment (D−), conventional vitamin D3-treated (D+), and liposomal vitamin D3-treated (LD). Treatments were administered daily via oral gavage for two months. Serum vitamin D3, IL-6, and TNF-α levels were measured by enzyme-linked immunosorbent assay (ELISA). IL-6 and TNF-α data were analyzed by ANOVA with Duncan’s post-hoc test, while vitamin D3 data were analyzed using the Brown-Forsythe test with Games-Howell post-hoc test (p<0.01).RESULTS: Ovariectomy significantly decreased vitamin D3 levels and increased IL-6 and TNF-α levels in the D− group. Conventional vitamin D3 supplementation (D+) significantly decreased serum vitamin D3 levels and slightly decreased IL-6 and TNF-α levels. Liposomal vitamin D3 (LD3) significantly increased vitamin D3 levels and decreased TNF-α, only slightly decreasing IL-6. Correlation analysis showed a negative association between serum vitamin D3 levels and both cytokines.CONCLUSION: Administration of vitamin D3 liposomes was able to increase vitamin D3 levels and suppress IL-6 and TNF-α towards normal levels. LD3 offers enhanced bioavailability and anti-inflammatory effects, making it a promising therapeutic strategy for managing menopause-associated inflammation and related systemic disorders.KEYWORDS: menopause, liposomal VD3, inflammation, IL-6, TNF-α
Low Serum Nerve Growth Factor Levels Are Associated with Insulin Resistance, Beta Cell Dysfunction, and Neuropathy Screening Scores in Subjects with Type 2 Diabetes Mellitus Sylvana, Dhini; Lindarto, Dharma; Syafril, Santi
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3750

Abstract

BACKGROUND: Diabetic peripheral neuropathy (DPN) is a common complication of type 2 diabetes mellitus (T2DM), associated with chronic hyperglycemia, insulin resistance, and neuroinflammation. Despite the widespread use of Michigan Neuropathy Screening Instrument (MNSI) for early identification in neuropathy screening, studies assessing its relationship between NGF, insulin resistance, and neuropathy in T2DM patients, particularly in Indonesia, remain limited. Therefore, this study was conducted to evaluate associations between serum NGF, insulin resistance, β-cell function, and MNSI scores in T2DM.METHODS: Seventy-seven T2DM subjects were classified into DPN and non-DPN groups using MNSI. Subjects were excluded if they have comorbidities and conditions potentially affecting metabolic, immune, or organ function. Enzyme-linked immunosorbent assay (ELISA) was used for the measurement of serum NGF, enzymatic hexokinase method for fasting plasma glucose (FPG) and 2-hour postprandial glucose (2HPP), high-performance liquid chromatography (HPLC) for glycated hemoglobin (HbA1c), and chemiluminescent immunoassay for fasting insulin. Homeostatic model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) were then calculated.RESULTS: Most of the study subjects had NGF level of <11 pg/mL. NGF concentrations showed inverse correlations with HOMA-IR (r=–0.263, p=0.021) and HOMA-β (r=–0.316, p=0.005). In the DPN subgroup, NGF demonstrated a stronger negative correlation with HOMA-β (r=–0.425, p=0.009), whereas no significant correlation was found in non-DPN. HbA1c was higher in DPN (p=0.014). No significant associations were observed between NGF and HbA1c, FPG, or 2HPP. NGF was significantly associated with MNSI Part B scores (p=0.032), reflecting objective neuropathic findings, but not with MNSI Part A or total scores.CONCLUSION: Lower NGF levels were significantly associated with insulin resistance and β-cell dysfunction in T2DM. The association with MNSI part B suggests that physical examination findings may reflect NGF-related neuropathic alterations better than symptom-based assessments.KEYWORDS: diabetic peripheral neuropathy, HOMA-IR, HOMA-β, Michigan Neuropathy Screening Instrument, nerve growth factor, T2DM
Design and Stability Evaluation of Active Peptides from Indonesian Echinozoa as Acetylcholinesterase (AChE) Inhibitors for Alzheimer’s Therapy Afifah, Laelatul; Andyra, Vania Uly; Laksitorini, Marlyn Dian; Nuringtyas, Tri Rini
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3837

Abstract

BACKGROUND: Alzheimer’s disease is characterized by cognitive decline resulting from decreased acetylcholine (ACh) levels due to excessive acetylcholinesterase (AChE) activity. Current therapies, such as galantamine, have several side effects. Bioactive peptides derived from marine Echinozoa (sea urchins and sea cucumbers) have emerged as promising therapeutic agents owing to their structural diversity and diverse bioactivities. Previous studies identified peptides from sea cucumbers and sea urchins collected along the southern coast of Gunung Kidul, Yogyakarta (VLCAGDLR, SWIGLK, MNGKKITVRPR, and KTKDLK), which exhibit acetylcholinesterase (AChE) inhibitory activity. However, the therapeutic use of these peptides is challenged by blood–brain barrier (BBB) penetration and stability issues. Therefore, this study was conducted to identify candidate peptides through in silico analysis and to evaluate their stability in phosphate-buffered saline (PBS) as potential AChE inhibitors.METHODS: Molecular docking was conducted to evaluate peptide binding affinity to the active site. The best candidate peptides were synthesized and tested in vitro for AChE inhibition using a colorimetric method. Stability was assessed in PBS by monitoring aggregation through turbidity and Congo Red assays.RESULTS: The sea cucumber peptide SWIGLK showed strong binding affinity (–10.2 kcal/mol) and 12.11% inhibition at 0.19 mM, while the sea urchin peptide KTKDLK exhibited –8.2 kcal/mol and 11.50% inhibition at 0.19 mM. Both peptides remained stable in PBS without aggregation for up to 48 h.CONCLUSION: SWIGLK and KTKDLK demonstrate the most significant AChE inhibitory activity and maintained structural stability, hence supporting their potential as peptide-based candidates for Alzheimer’s therapy.KEYWORDS: Alzheimer, AChE inhibitor, holothuroidea, echinoidea, bioactive peptide, peptide stability

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