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Knockdown of BCL-3 Attenuates Inflammatory Response in Intracerebral Hemorrhage Through an rBMECs/MGs
Jun Ma1, Hao Yin1, Zhongying Ran1
1Department of Neurosurgery, Guizhou Provincial People's Hospital, PR China.
Insights
BCL-3 plays a key role in intracerebral hemorrhage (ICH) by modulating inflammatory responses in brain microvascular endothelial cells and microglia. Inhibiting BCL-3 shows potential for managing ICH.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Intracerebral hemorrhage (ICH) is a critical condition with high mortality rates.
- The specific mechanisms underlying ICH pathogenesis, particularly the role of BCL-3, require further elucidation.
Purpose of the Study:
- To investigate the role and mechanism of BCL-3 in the inflammatory response following intracerebral hemorrhage.
- To explore BCL-3 as a potential therapeutic target for ICH.
Main Methods:
- Established ICH models in rats using collagenase injection and in vitro using Hemin-treated rat brain microvascular endothelial cells (rBMECs).
- Assessed BCL-3 expression, cell apoptosis, and microglia (MGs) polarization and inflammatory responses.
- Utilized BCL-3 knockdown in both in vitro and in vivo ICH models for functional evaluation.
Main Results:
- BCL-3 expression was upregulated in ICH animal models and Hemin-treated rBMECs, correlating with increased apoptosis.
- Co-culture with ICH models induced M1 polarization and heightened inflammatory responses in microglia.
- Inhibition of BCL-3 reversed microglial polarization and inflammatory responses, improving outcomes in animal models.
Conclusions:
- BCL-3 significantly modulates the inflammatory response in the brain microvascular endothelial cell/microglia microenvironment post-ICH.
- Targeting BCL-3 presents a promising therapeutic strategy for managing intracerebral hemorrhage.
Abstract:
Intracerebral hemorrhage (ICH) is a severe disease with high mortality. Recently, the role of BCL-3 in ICH has started to gain attention, but its mechanism remains unclear. A collagenase injection method was used to establish an ICH model in rats, and the expression of BCL-3 were detected. Rat brain microvascular endothelial cells (rBMECs) were isolated and induced with Hemin to establish an in vitro ICH model. The expression of BCL-3 was assessed, followed by detection of cell apoptosis. In the cell model, the recruitment, polarization, and pro-inflammatory features of the microglia (MGs) were assessed after co-cultured with rBMECs. Finally, in the ICH animal model, after knockdown of BCL-3, comprehensive evaluations of inflammatory responses in brain tissue, polarization and recruitment of microglia, and apoptosis were conducted. Results revealed an upregulated expression of BCL-3 in brain tissue of the ICH animal model. In Hemin-treated rBMECs, an upward trend in BCL-3 expression was observed, accompanied by an increase of cell apoptosis. After co-culturing with the in vitro model, microglia exhibited enhanced M1 polarization and intensified inflammatory responses. However, when BCL-3 expression was inhibited in the in vitro model, a reversal occurred in the polarization tendency and inflammatory responses of microglia. Additionally, after knockdown of BCL-3 in the animal model, notable improvements occurred in M1 polarization, infiltration of macrophages, and inflammatory reactions in the brain tissue. Therefore, BCL-3 modulates the inflammatory response after ICH occurrence through the BMECs/MGs microenvironment. Additionally, BCL-3 might be a potential therapeutic target for ICH management.
