ArticleBioMed research international2022
Molecular Mechanism of Tetramethylpyrazine Ameliorating Neuroexcitotoxicity through Activating the PKA/CREB Signaling Pathway.
Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 5 citations in OpenAlex.
- From a traditional medicine monomer to a modern neurotherapeutic scaffold: a review of SAR-Driven tetramethylpyrazine derivatives for cerebrovascular and cognitive health.Frontiers in pharmacology · 2025Review
- Regulatory mechanisms of tetramethylpyrazine on central nervous system diseases: A review.Frontiers in pharmacology · 2022Review
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundExcitotoxicity plays a key role in nervous system disease and can trigger a critical cascade of reaction which affects cell viability and promotes neuronal death. Tetramethylpyrazine (TMP) reveals its effect in the treatment of neurovascular diseases by antiapoptosis. Recently, there were several studies that demonstrated that the PKA/CREB signaling pathway played a role in neural disease because of excitotoxicity, such as stroke, AD, and Parkinson's disease. In this study, we wanted to focus on the protective effect of tetramethylpyrazine against excitotoxicity through the PKA/CREB signaling pathway.
methodsIn order to verify whether tetramethylpyrazine can attenuate excitotoxicity through the PKA/CREB signaling pathway, we first used molecular docking technology to predict the combinational strength and mode of tetramethylpyrazine with the proteins in the PKA/CREB signaling pathway. Then, we determined the optimal concentration and time according to the model effect of glutamate (Glu) with different concentration gradients and action times in PC12 cells. After the determination of concentration and time of glutamate in the previous step as the model way, tetramethylpyrazine was added to determine its influence on the cell viability under different doses and times. The TUNEL assay and flow cytometry were used to detect apoptosis. RT-PCR was used to detect the expression of Bcl-2, Bax, PKA, and 5CREB genes, and Western blot was used to detect the expression of these factors.
resultTetramethylpyrazine had a good docking score (-5.312) with PKA and had a moderately docking score (-3.838) with CREB. The CCK-8 cell activity assay showed that the activity of PC12 cells decreased gradually with the increase in glutamate concentration and time, and PC12 cells were treated with 10 mM/L glutamate (the half of the inhibitory concentration (IC50)) for 12 hours. Then, the cell viability increased gradually following the increased concentration of tetramethylpyrazine. When PC12 cells were treated with 0.1 mM/L tetramethylpyrazine, the cell viability was increased significantly compared with the control group (
conclusionsThis study provided evidence that tetramethylpyrazine can protect against apoptosis caused by neuroexcitotoxicity and the protective mechanism is closely related to the activation of the PKA/CREB signaling pathway.
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