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Published on: July 5, 2024
Nimodipine modulates Bcl-2 and Bax mRNA expression after cerebral ischemia
Changqin Liu1, Ruixiang Zhou, Shenggang Sun
1Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Abstract:
In order to explore whether the member of Bcl-2 gene family, for example, Bcl-2 and Bax, are induced after cerebral ischemia, and whether expression of genes can be modulated by calcium-antagonist, the rat cerebral ischemic models were made by occluding left middle cerebral artery. The expression of Bcl-2 and Bax mRNA was measured by RT-PCR method. After middle cerebral artery occlusion (MCAO), the expression of both Bcl-2 and Bax mRNA were induced. Level of Bcl-2 mRNA increased steadily and level of Bax mRNA increased gradually at first, reached a peak after 24 h, then decreased slowly. After administration of nimodipine, Bcl-2 mRNA was up-regulated in the hippocampus 6 and 24 h after ischemia, while Bax mRNA was down-regulated 6 and 24 h after ischemia. Focal cerebral ischemia can induce proto-oncogenes to express, which was associated with apoptosis. Calcium-antagonist can up-regulate Bcl-2 mRNA and down-regulate Bax mRNA. The increased ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine. The study indicates that pharmacological modulation of Bcl-2 family member expression could become a new strategy to manage neuronal damage.
Insights
Cerebral ischemia induces Bcl-2 and Bax gene expression in rats. Calcium-antagonist nimodipine modulated these genes, suggesting a new strategy for managing neuronal damage.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Cerebral ischemia can lead to neuronal cell death via apoptosis.
- The Bcl-2 gene family plays a critical role in regulating apoptosis.
- Proto-oncogenes are implicated in the cellular response to ischemic injury.
Purpose of the Study:
- To investigate the induction of Bcl-2 and Bax gene family members following cerebral ischemia.
- To determine if calcium-antagonists can modulate the expression of these genes.
- To explore the potential of targeting Bcl-2 family members for neuroprotection.
Main Methods:
- Rat models of focal cerebral ischemia were established using middle cerebral artery occlusion (MCAO).
- Messenger RNA (mRNA) expression levels of Bcl-2 and Bax were quantified using reverse transcription polymerase chain reaction (RT-PCR).
- Nimodipine, a calcium-antagonist, was administered to assess its effects on gene expression.
Main Results:
- Both Bcl-2 and Bax mRNA were induced after MCAO.
- Bcl-2 mRNA levels showed a steady increase, while Bax mRNA levels peaked at 24 hours post-ischemia.
- Nimodipine treatment up-regulated Bcl-2 mRNA and down-regulated Bax mRNA in the hippocampus.
Conclusions:
- Focal cerebral ischemia induces proto-oncogene expression linked to apoptosis.
- Calcium-antagonists like nimodipine can alter Bcl-2 and Bax mRNA levels.
- Modulating Bcl-2 family gene expression represents a potential therapeutic strategy against ischemic neuronal damage.
