Effects of the extract of Ginkgo biloba L. on inflammatory response and mitochondrial dynamics in microglia in Alzheimer’s disease
- 1School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069 China
- 2Department of Pharmacy, Tsinghua University Yuquan Hospital, Tsinghua University, Beijing, 100049 China
- 3Department of Pharmacy, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100020 China
Abstract
Background: Alzheimer’s disease (AD) is a neurodegenerative disorder that lacks disease-modifying therapies. This study investigated the effects of Extract of Ginkgo biloba L. (EGb) on mitochondrial fission machinery and inflammatory responses in an Aβ1−42-stimulated BV2 microglial model.
Methods: The chemical profile of EGb was qualitatively analyzed using HPLC-MS. BV2 microglial cells were exposed to Aβ1−42. Mitochondrial morphology was observed using high-resolution microscopy; DRP1-MFF and DRP1-FIS1 associations were assessed by co-immunoprecipitation (Co-IP); dynamin-related protein 1 (DRP1), mitochondrial fission 1 protein (FIS1) and mitochondrial fission factor (MFF) were evaluated using image-based phenotypic metrics and Western blotting; interleukin-1 beta (IL-1β) levels were measured by ELISA; p38 mitogen-activated protein kinase (p38), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) were assessed via high-content screening; mitochondrial membrane potential (ΔΨm), oxidative stress and apoptosis-associated changes were detected by fluorescence and spectrophotometry.
Results: Fifty-eight compounds, including ginkgolides, flavonoids and phenolic acids, were tentatively identified. EGb alleviated Aβ1−42-induced mitochondrial structural abnormalities, increased MFF expression, and decreased DRP1 and FIS1 expression. Co-IP analysis indicated the association of DRP1 with MFF and FIS1. EGb also reduced IL-1β release and altered the expression levels of p38, JNK, and ERK, while mitigating ΔΨm loss, alleviating oxidative stress-related changes, and partially reducing apoptosis-associated TUNEL staining.
Conclusions: EGb attenuated Aβ1−42-induced injury and modulated mitochondrial fission-related changes in BV2 microglial cells, suggesting a cellular-level protective effect in AD-related microglial dysfunction.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12906-026-05485-1.
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BibTeX
@article{liu2026effects,
title = {{Effects of the extract of Ginkgo biloba L. on inflammatory response and mitochondrial dynamics in microglia in Alzheimer’s disease}},
author = {Xinyi Liu and Dongqi Liu and Yuzhe Gao and Shiqi Yan and Haolong Liu and Xinwei Yang},
journal = {BMC Complementary Medicine and Therapies},
year = {2026},
month = jul,
doi = {10.1186/s12906-026-05485-1},
url = {https://doi.org/10.1186/s12906-026-05485-1},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Effects of the extract of Ginkgo biloba L. on inflammatory response and mitochondrial dynamics in microglia in Alzheimer’s disease
AU - Xinyi Liu
AU - Dongqi Liu
AU - Yuzhe Gao
AU - Shiqi Yan
AU - Haolong Liu
AU - Xinwei Yang
PY - 2026
DA - 2026/07/28
JO - BMC Complementary Medicine and Therapies
DO - 10.1186/s12906-026-05485-1
UR - https://doi.org/10.1186/s12906-026-05485-1
AB - Background: Alzheimer’s disease (AD) is a neurodegenerative disorder that lacks disease-modifying therapies. This study investigated the effects of Extract of Ginkgo biloba L. (EGb) on mitochondrial fission machinery and inflammatory responses in an Aβ1−42-stimulated BV2 microglial model. Methods: The chemical profile of EGb was qualitatively analyzed using HPLC-MS. BV2 microglial cells were exposed to Aβ1−42. Mitochondrial morphology was observed using high-resolution microscopy; DRP1-MFF and DRP1-FIS1 associations were assessed by co-immunoprecipitation (Co-IP); dynamin-related protein 1 (DRP1), mitochondrial fission 1 protein (FIS1) and mitochondrial fission factor (MFF) were evaluated using image-based phenotypic metrics and Western blotting; interleukin-1 beta (IL-1β) levels were measured by ELISA; p38 mitogen-activated protein kinase (p38), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) were assessed via high-content screening; mitochondrial membrane potential (ΔΨm), oxidative stress and apoptosis-associated changes were detected by fluorescence and spectrophotometry. Results: Fifty-eight compounds, including ginkgolides, flavonoids and phenolic acids, were tentatively identified. EGb alleviated Aβ1−42-induced mitochondrial structural abnormalities, increased MFF expression, and decreased DRP1 and FIS1 expression. Co-IP analysis indicated the association of DRP1 with MFF and FIS1. EGb also reduced IL-1β release and altered the expression levels of p38, JNK, and ERK, while mitigating ΔΨm loss, alleviating oxidative stress-related changes, and partially reducing apoptosis-associated TUNEL staining. Conclusions: EGb attenuated Aβ1−42-induced injury and modulated mitochondrial fission-related changes in BV2 microglial cells, suggesting a cellular-level protective effect in AD-related microglial dysfunction. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12906-026-05485-1.
SN - 2662-7671
ER -