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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Main Authors: Eunjin Sohn, Bu-Yeo Kim, Yu Jin Kim, Joo-Hwan Kim, Soo-Jin Jeong
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
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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
collection DOAJ
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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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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