Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice
Abstract Alzheimer’s disease (AD) is characterized by oxidative stress-mediated memory dysfunction and neuronal cell death. This study investigated the effects of an ethanol extract from Bauhinia coccinea (EEBC) on memory impairment and neuronal damage in a memory deficit mouse model. EEBC was admin...
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Nature Portfolio
2025-02-01
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Online Access: | https://doi.org/10.1038/s41598-025-88152-8 |
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author | Eunjin Sohn Bu-Yeo Kim Yu Jin Kim Joo-Hwan Kim Soo-Jin Jeong |
author_facet | Eunjin Sohn Bu-Yeo Kim Yu Jin Kim Joo-Hwan Kim Soo-Jin Jeong |
author_sort | Eunjin Sohn |
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description | Abstract Alzheimer’s disease (AD) is characterized by oxidative stress-mediated memory dysfunction and neuronal cell death. This study investigated the effects of an ethanol extract from Bauhinia coccinea (EEBC) on memory impairment and neuronal damage in a memory deficit mouse model. EEBC was administered to ICR mice at doses of 50, 100, or 200 mg/kg daily for 3 weeks. Cognitive impairment was induced via scopolamine (SCO) injection. Brain tissues were analyzed for acetylcholine (ACh) levels, acetylcholinesterase (AChE) activity, neuronal apoptosis, and antioxidant markers. Behavioral tests showed that SCO injection induced memory loss, whereas EEBC significantly ameliorated SCO-mediated memory impairment. EEBC regulated the cholinergic system by decreasing ACh levels and enhancing AChE activity. Nissl staining and immunohistochemistry for NeuN showed that EEBC exerted neuroprotective effects in SCO-injected mice brains. Moreover, EEBC significantly reduced the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive apoptotic cells increased by SCO treatment. EEBC also reversed the SCO-induced changes in apoptosis-related protein expression in brain tissues. Furthermore, EEBC significantly reduced malondialdehyde levels and activated catalase in SCO-administered brains. Quantitative RNA sequencing showed involvement of lipid metabolism in EEBC memory function regulation. Thus, EEBC is a promising candidate for attenuating AD progression as it targets the cholinergic system and neuronal apoptosis. |
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institution | Kabale University |
issn | 2045-2322 |
language | English |
publishDate | 2025-02-01 |
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spelling | doaj-art-4e361f92cfda4177871870d746bb27002025-02-09T12:29:05ZengNature PortfolioScientific Reports2045-23222025-02-0115111510.1038/s41598-025-88152-8Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in miceEunjin Sohn0Bu-Yeo Kim1Yu Jin Kim2Joo-Hwan Kim3Soo-Jin Jeong4Korean Medicine Convergence Research Division, Korea Institute of Oriental MedicineKorean Medicine Convergence Research Division, Korea Institute of Oriental MedicineKorean Medicine Convergence Research Division, Korea Institute of Oriental MedicineDepartment of Life Science, Gachon UniversityKorean Medicine Convergence Research Division, Korea Institute of Oriental MedicineAbstract Alzheimer’s disease (AD) is characterized by oxidative stress-mediated memory dysfunction and neuronal cell death. This study investigated the effects of an ethanol extract from Bauhinia coccinea (EEBC) on memory impairment and neuronal damage in a memory deficit mouse model. EEBC was administered to ICR mice at doses of 50, 100, or 200 mg/kg daily for 3 weeks. Cognitive impairment was induced via scopolamine (SCO) injection. Brain tissues were analyzed for acetylcholine (ACh) levels, acetylcholinesterase (AChE) activity, neuronal apoptosis, and antioxidant markers. Behavioral tests showed that SCO injection induced memory loss, whereas EEBC significantly ameliorated SCO-mediated memory impairment. EEBC regulated the cholinergic system by decreasing ACh levels and enhancing AChE activity. Nissl staining and immunohistochemistry for NeuN showed that EEBC exerted neuroprotective effects in SCO-injected mice brains. Moreover, EEBC significantly reduced the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive apoptotic cells increased by SCO treatment. EEBC also reversed the SCO-induced changes in apoptosis-related protein expression in brain tissues. Furthermore, EEBC significantly reduced malondialdehyde levels and activated catalase in SCO-administered brains. Quantitative RNA sequencing showed involvement of lipid metabolism in EEBC memory function regulation. Thus, EEBC is a promising candidate for attenuating AD progression as it targets the cholinergic system and neuronal apoptosis.https://doi.org/10.1038/s41598-025-88152-8Alzheimer’s diseaseBauhinia coccineaMemory dysfunctionNeuronal apoptosisAntioxidant activity |
spellingShingle | Eunjin Sohn Bu-Yeo Kim Yu Jin Kim Joo-Hwan Kim Soo-Jin Jeong Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice Scientific Reports Alzheimer’s disease Bauhinia coccinea Memory dysfunction Neuronal apoptosis Antioxidant activity |
title | Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
title_full | Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
title_fullStr | Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
title_full_unstemmed | Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
title_short | Bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
title_sort | bauhinia coccinea extract prevents memory loss induced by scopolamine through activation of antiapoptotic and antioxidant pathways in mice |
topic | Alzheimer’s disease Bauhinia coccinea Memory dysfunction Neuronal apoptosis Antioxidant activity |
url | https://doi.org/10.1038/s41598-025-88152-8 |
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