Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease
Background: Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disorder characterized by cognitive impairment and behavioral disturbances. Phytochemicals are considered safer alternatives and have shown significant efficacy in inhibiting cholinesterase, scavenging fre...
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Elsevier
2025-02-01
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| Series: | Phytomedicine Plus |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2667031325000132 |
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| author | Arif Malik Mehreen Hassan Sulayman Waquar Muhammad Wasim Anam Naz Faryal M. Awan Muhammad T. Khan Ali I. Khawaja Sumera Zaib Jamshed Iqbal Ayesha Zahid Marvi Marvi Javeid Iqbal Heng Wang Dong-Qing Wei |
| author_facet | Arif Malik Mehreen Hassan Sulayman Waquar Muhammad Wasim Anam Naz Faryal M. Awan Muhammad T. Khan Ali I. Khawaja Sumera Zaib Jamshed Iqbal Ayesha Zahid Marvi Marvi Javeid Iqbal Heng Wang Dong-Qing Wei |
| author_sort | Arif Malik |
| collection | DOAJ |
| description | Background: Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disorder characterized by cognitive impairment and behavioral disturbances. Phytochemicals are considered safer alternatives and have shown significant efficacy in inhibiting cholinesterase, scavenging free radicals, inhibiting amyloid-β neurotoxicity, reducing inflammation, and interacting with neurotransmitters, thereby slowing down the progression of AD. Purpose: EGCG, is an antioxidant/anti-inflammatory that lowers amyloid-b and tau aggregation in AD models and improves cognition at preclinical dosages of 25–100 mg/kg/day and clinical doses of 200–800 mg/ Albeginin, a new flavonoid, reduces neuroinflammation in rats at 10–50 mg/kg/day, equal to 100–200 mg/day in humans. Melanoxetin, a phenolic molecule, chelates toxic metals, lowers ROS, and protects neurons at 15–40 mg/kg/day in animal models and 50–150 mg/day in humans. These chemicals show promise for Alzheimer's treatment. Study design: The study targeted specific AD-related proteins, including acetylcholinesterase (AChE), alpha serine/threonine-protein kinase (AKT-1), β-secretase-1 (BACE-1), cyclooxygenase-2 (COX-2), caspase-3, glycogen synthase kinase-3 (GSK-3), interleukin-6 (IL-6), mitogen-activated protein kinase-2 (MAPK-2), matrix metalloproteins-8 (MMP-8), N-methyl-d-aspartate receptor (NMDAR), Peptidyl arginine deiminase-2 (PAD-2), Presenilin-1 (PSEN-1), mitogen-activated protein kinase-14 (MAPK-14/P38), and tumor necrosis factor-alpha (TNF-α). Methods: Before conducting experimental work, molecular dynamic (MD) simulations were performed to assess the binding affinity of EGCG, albeginin, and melanoxetin against the selected targets. Sprague Dawley rats were injected with colchicine to induce AD, followed by treatment with the selected phytocompounds for three weeks. Results: In silico results indicated strong binding interactions of EGCG, albeginin, and melanoxetin with the target proteins. The rats treated with these phytocompounds showed a significant reduction in oxidative stress, inflammation, Aβ plaque formation, neurofibrillary tangles, and anticholinesterase activity. Conclusion: This is the first comprehensive study on the therapeutic role of EGCG, albeginin, and melanoxetin against AD. These phytocompounds demonstrate potential for better management of AD in the future. |
| format | Article |
| id | doaj-art-86d460fd310444b99e7ba5ff33527022 |
| institution | Kabale University |
| issn | 2667-0313 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
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| series | Phytomedicine Plus |
| spelling | doaj-art-86d460fd310444b99e7ba5ff335270222025-02-10T04:35:22ZengElsevierPhytomedicine Plus2667-03132025-02-0151100740Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's diseaseArif Malik0Mehreen Hassan1Sulayman Waquar2Muhammad Wasim3Anam Naz4Faryal M. Awan5Muhammad T. Khan6Ali I. Khawaja7Sumera Zaib8Jamshed Iqbal9Ayesha Zahid10Marvi Marvi11Javeid Iqbal12Heng Wang13Dong-Qing Wei14School of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, Pakistan; Faculty of Health Sciences, Equator University of Science and Technology (EQUSaT), Masaka, Uganda; Corresponding author at: State Key Laboratory of Microbial Metabolism, Shanghai-Islamabad-Belgrade Joint Innovation Center on Antibacterial Resistances, Joint Laboratory of International Cooperation in Metabolic and Developmental Sciences, Ministry of Education and School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200030, PR China.Department of pharmacology, King Edward Medical University, Lahore, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanDepartment of Medical Lab Technology, University of Haripur, Haripur, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanDepartment of Biochemistry, Faculty of Life Sciences, University of Central Punjab, Lahore, PakistanDepartment of pharmacology, King Edward Medical University, Lahore, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, PakistanDepartment of Pharmacology, Faculty of Pharmacy, University of Baluchistan, Quetta, PakistanSchool of Pain and Regenerative Medicine (SPRM), The University of Lahore-Pakistan. KM Defence Road, Lahore 58810, Pakistan; Faculty of Health Sciences, Equator University of Science and Technology (EQUSaT), Masaka, Uganda; Department of pharmacology, King Edward Medical University, Lahore, Pakistan; Maternal and Children's Health Research Institute, Shunde Women and Children's Hospital, Guangdong Medical University, Foshan, 528300, China; Department of Medical Lab Technology, University of Haripur, Haripur, Pakistan; Department of Biochemistry, Faculty of Life Sciences, University of Central Punjab, Lahore, Pakistan; Department of Pharmacology, Faculty of Pharmacy, University of Baluchistan, Quetta, Pakistan; School of Pharmacy, Minhaj University, Lahore, Pakistan; State Key Laboratory of Microbial Metabolism, School of life sciences and Biotechnology, Shanghai-China, Joint Laboratory of International Cooperation in Metabolic and Developmental Sciences, Ministry of Education, Shanghai Jiao Tong University. Shanghai 200240, China; Peng Cheng Laboratory, Vanke Cloud City Phase I Building 8, Xili Street, Nanshan District, Shenzhen, Guangdong 518055, ChinaState Key Laboratory of Microbial Metabolism, School of life sciences and Biotechnology, Shanghai-China, Joint Laboratory of International Cooperation in Metabolic and Developmental Sciences, Ministry of Education, Shanghai Jiao Tong University. Shanghai 200240, ChinaState Key Laboratory of Microbial Metabolism, School of life sciences and Biotechnology, Shanghai-China, Joint Laboratory of International Cooperation in Metabolic and Developmental Sciences, Ministry of Education, Shanghai Jiao Tong University. Shanghai 200240, China; Peng Cheng Laboratory, Vanke Cloud City Phase I Building 8, Xili Street, Nanshan District, Shenzhen, Guangdong 518055, China; Corresponding author at: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore-Pakistan.Background: Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disorder characterized by cognitive impairment and behavioral disturbances. Phytochemicals are considered safer alternatives and have shown significant efficacy in inhibiting cholinesterase, scavenging free radicals, inhibiting amyloid-β neurotoxicity, reducing inflammation, and interacting with neurotransmitters, thereby slowing down the progression of AD. Purpose: EGCG, is an antioxidant/anti-inflammatory that lowers amyloid-b and tau aggregation in AD models and improves cognition at preclinical dosages of 25–100 mg/kg/day and clinical doses of 200–800 mg/ Albeginin, a new flavonoid, reduces neuroinflammation in rats at 10–50 mg/kg/day, equal to 100–200 mg/day in humans. Melanoxetin, a phenolic molecule, chelates toxic metals, lowers ROS, and protects neurons at 15–40 mg/kg/day in animal models and 50–150 mg/day in humans. These chemicals show promise for Alzheimer's treatment. Study design: The study targeted specific AD-related proteins, including acetylcholinesterase (AChE), alpha serine/threonine-protein kinase (AKT-1), β-secretase-1 (BACE-1), cyclooxygenase-2 (COX-2), caspase-3, glycogen synthase kinase-3 (GSK-3), interleukin-6 (IL-6), mitogen-activated protein kinase-2 (MAPK-2), matrix metalloproteins-8 (MMP-8), N-methyl-d-aspartate receptor (NMDAR), Peptidyl arginine deiminase-2 (PAD-2), Presenilin-1 (PSEN-1), mitogen-activated protein kinase-14 (MAPK-14/P38), and tumor necrosis factor-alpha (TNF-α). Methods: Before conducting experimental work, molecular dynamic (MD) simulations were performed to assess the binding affinity of EGCG, albeginin, and melanoxetin against the selected targets. Sprague Dawley rats were injected with colchicine to induce AD, followed by treatment with the selected phytocompounds for three weeks. Results: In silico results indicated strong binding interactions of EGCG, albeginin, and melanoxetin with the target proteins. The rats treated with these phytocompounds showed a significant reduction in oxidative stress, inflammation, Aβ plaque formation, neurofibrillary tangles, and anticholinesterase activity. Conclusion: This is the first comprehensive study on the therapeutic role of EGCG, albeginin, and melanoxetin against AD. These phytocompounds demonstrate potential for better management of AD in the future.http://www.sciencedirect.com/science/article/pii/S2667031325000132AlzheimerAmyloid plaqueNeurofibrillary tanglesNeuroinflammationPhytocompounds |
| spellingShingle | Arif Malik Mehreen Hassan Sulayman Waquar Muhammad Wasim Anam Naz Faryal M. Awan Muhammad T. Khan Ali I. Khawaja Sumera Zaib Jamshed Iqbal Ayesha Zahid Marvi Marvi Javeid Iqbal Heng Wang Dong-Qing Wei Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease Phytomedicine Plus Alzheimer Amyloid plaque Neurofibrillary tangles Neuroinflammation Phytocompounds |
| title | Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease |
| title_full | Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease |
| title_fullStr | Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease |
| title_full_unstemmed | Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease |
| title_short | Neuroprotective role of epigallocatechin-3-gallate, albeginin and melanoxetin in alzheimer's disease |
| title_sort | neuroprotective role of epigallocatechin 3 gallate albeginin and melanoxetin in alzheimer s disease |
| topic | Alzheimer Amyloid plaque Neurofibrillary tangles Neuroinflammation Phytocompounds |
| url | http://www.sciencedirect.com/science/article/pii/S2667031325000132 |
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