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Tetramethylpyrazine ameliorates isoflurane-induced cognitive dysfunction by inhibiting neuroinflammation via miR-150
Huaqing Cui1, Zhonghui Xu1, Chunshan Qu1
1Department of Anesthesia and Perioperative Medicine, Dongying Hospital of Traditional Chinese Medicine, Dongying, Shandong 257055, P.R. China.
Abstract:
Tetramethylpyrazine (TMP) has neuroprotective effects in the pathogenesis of some human diseases, such as Parkinson's disease. The present study aimed to investigate the role of TMP in isoflurane-induced cognitive dysfunction in rats, and further identify the mechanisms involved in the protective effects of TMP. The Morris water maze test was used to evaluate the cognitive function of rats exposed to isoflurane or treated with TMP. ELISA was conducted to evaluate the effects of isoflurane or TMP on neuroinflammation. The expression of microRNA-150 (miR-150) was measured using reverse transcription-quantitative PCR, and the potential target genes of miR-150 were predicted and verified. The impaired cognitive function induced by isoflurane in the rats was significantly ameliorated by treatment with TMP. In addition, TMP treatment in rats attenuated neuroinflammation caused by isoflurane. The expression of miR-150 was inhibited by isoflurane exposure, but was enhanced by TMP treatment in rats. Furthermore, the overexpression of miR-150 alleviated the isoflurane-induced cognitive dysfunction and neuroinflammation, while the neuroprotective effects of TMP were significantly abrogated by the knockdown of miR-150. AKT3 was a direct target of miR-150, and its mRNA expression was significantly decreased by the overexpression of miR-150 in isoflurane- and TMP-treated rats. These results demonstrated the protective effects of TMP against isoflurane-induced cognitive dysfunction, which were achieved by attenuating neuroinflammation via the regulation of the miR-150/AKT3 pathway. In addition, miR-150 may serve as a novel therapeutic target for the alleviation of cognitive dysfunction induced by anesthetics.
Insights
Tetramethylpyrazine (TMP) protects against anesthetic-induced cognitive decline by reducing neuroinflammation. This effect is mediated by the microRNA-150/AKT3 pathway, suggesting miR-150 as a therapeutic target.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Anesthetic agents like isoflurane can induce cognitive dysfunction.
- Tetramethylpyrazine (TMP) exhibits known neuroprotective properties.
- Understanding the mechanisms behind anesthetic-induced cognitive impairment is crucial for developing interventions.
Purpose of the Study:
- To investigate the protective role of TMP against isoflurane-induced cognitive dysfunction in rats.
- To elucidate the underlying molecular mechanisms, focusing on neuroinflammation and microRNA-150 (miR-150).
Main Methods:
- Morris water maze test for cognitive function assessment.
- ELISA for evaluating neuroinflammation markers.
- Reverse transcription-quantitative PCR to measure miR-150 expression.
- Prediction and verification of miR-150 target genes (AKT3).
Main Results:
- TMP treatment significantly ameliorated isoflurane-induced cognitive impairment and neuroinflammation.
- Isoflurane inhibited miR-150 expression, while TMP treatment enhanced it.
- Overexpression of miR-150 mimicked TMP's protective effects, and its knockdown abrogated them.
- AKT3 was identified as a direct target of miR-150, with its expression inversely correlated to miR-150 levels.
Conclusions:
- TMP exerts neuroprotective effects against isoflurane-induced cognitive dysfunction by attenuating neuroinflammation.
- The mechanism involves the regulation of the miR-150/AKT3 pathway.
- MicroRNA-150 represents a potential therapeutic target for mitigating anesthetic-induced cognitive dysfunction.
