Scholarlink

Background <p>Alzheimer’s disease (AD) is a neurodegenerative disorder that lacks disease-modifying therapies. This study investigated the effects of Extract of <i>Ginkgo biloba</i> L. (EGb) on mitochondrial fission machinery and inflammatory responses in an Aβ<sub>1−42</sub>-stimulated BV2 microglial model.</p> Methods <p>The chemical profile of EGb was qualitatively analyzed using HPLC-MS. BV2 microglial cells were exposed to Aβ<sub>1−42</sub>. 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.</p> Results <p>Fifty-eight compounds, including ginkgolides, flavonoids and phenolic acids, were tentatively identified. EGb alleviated Aβ<sub>1−42</sub>-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.</p> Conclusions <p>EGb attenuated Aβ<sub>1−42</sub>-induced injury and modulated mitochondrial fission-related changes in BV2 microglial cells, suggesting a cellular-level protective effect in AD-related microglial dysfunction.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Effects of the extract of Ginkgo biloba L. on inflammatory response and mitochondrial dynamics in microglia in Alzheimer’s disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月28日

查看全文
  • Xinyi Liu,
  • Dongqi Liu,
  • Yuzhe Gao,
  • Shiqi Yan,
  • Haolong Liu,
  • Xinwei Yang

摘要

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.