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Updated: Dec 26, 2025
Viability Assays for Cells in Culture
Published on: January 20, 2014
Protective effects of butein on corticosterone-induced cytotoxicity in Neuro2A cells
Masanori Ohmoto1, Yukina Shibuya1, Shihori Taniguchi1
1Department of Pharmacy Practice and Sciences, Faculty of Pharmaceutical Sciences, Hokuriku University, Japan.
Abstract:
A functional understanding of the relationship between glucocorticoids and neuronal apoptosis induced by the production of reactive oxygen species (ROS) may lead to a novel strategy for the treatment or prevention of depression. Previous reports suggest that butein, a type of flavonoids, may be a potent candidate against depression-related neuronal cell apoptosis caused by oxidative stress; however, the protective effects of butein on damaged corticosterone (CORT)-treated neuronal cells has not been elucidated. In the present study, we examined the protective effect of butein on CORT-induced cytotoxicity and neurite growth during cell differentiation of mouse neuroblastoma Neuro2A (N2A) cells. Moreover, the effect on cultured cells by high concentrations of butein was confirmed. Our results demonstrate that CORT treatment significantly decreases cell viability and induces cell death. CORT was suggested to induce apoptosis via mitochondrial dysfunction and caspase-3 activation; this apoptosis may be attributed to DNA damage by ROS generation, found in this study to be significantly inhibited by pretreatment with butein. We found that CORT produced significant growth suppression of retinoic acid-induced neurite outgrowth in N2A cells; however, butein significantly increased neurite length and induced dose-dependent apoptotic cytotoxicity in N2A cells. This study suggests that low concentration of butein can prevent CORT-induced cytotoxicity in N2A cells, and provides preliminary results supporting some of the beneficial roles of butein in neuroprotection.
Insights
Butein, a flavonoid, protects against corticosterone-induced neuronal cell death and DNA damage by inhibiting reactive oxygen species (ROS). It also promotes neurite growth, suggesting neuroprotective potential for depression treatment.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Glucocorticoids like corticosterone (CORT) can induce neuronal apoptosis via reactive oxygen species (ROS) production, a process implicated in depression.
- Flavonoids, such as butein, show potential in combating oxidative stress and neuronal cell death.
- The specific protective effects of butein against CORT-induced damage in neuronal cells remain largely unelucidated.
Purpose of the Study:
- To investigate the protective effects of butein on corticosterone (CORT)-induced cytotoxicity and neurite growth in mouse neuroblastoma Neuro2A (N2A) cells.
- To determine if butein can mitigate CORT-induced apoptosis, mitochondrial dysfunction, and DNA damage mediated by ROS.
- To assess butein's impact on neurite outgrowth during cell differentiation.
Main Methods:
- Neuro2A cells were treated with CORT to induce cytotoxicity and apoptosis.
- Butein pretreatment was used to evaluate its protective effects against CORT-induced damage.
- Cell viability, apoptosis (caspase-3 activation), ROS generation, and neurite outgrowth were measured.
- The effects of high concentrations of butein on cultured cells were also assessed.
Main Results:
- CORT treatment significantly reduced cell viability and induced apoptosis, associated with mitochondrial dysfunction and caspase-3 activation.
- Butein pretreatment significantly inhibited CORT-induced ROS generation and subsequent DNA damage.
- CORT suppressed neurite outgrowth, while butein significantly enhanced neurite length in a dose-dependent manner.
- High concentrations of butein demonstrated dose-dependent apoptotic cytotoxicity.
Conclusions:
- Low concentrations of butein exhibit neuroprotective effects by preventing CORT-induced cytotoxicity in Neuro2A cells.
- Butein mitigates CORT-induced apoptosis by inhibiting ROS generation and DNA damage.
- Butein supports neuronal health by promoting neurite outgrowth, indicating potential therapeutic applications in neuroprotection and depression treatment.
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