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Updated: Dec 1, 2025
Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
Published on: September 2, 2020
MiR-124-3p alleviates the dezocine tolerance against pain by regulating TRAF6 in a rat model
Yan Huo1, Kun Zhang, Tao Zhang
1Department of Intensive Care Unit, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Abstract:
MicroRNAs (miRNAs) play important roles in drug tolerance and regulating pain. The purpose of the present study is to explore the regulatory mechanism of miR-124-3p on dezocine tolerance against pain in a rat model. The expression of miR-124-3p and TRAF6 in spinal cord of rats was detected by quantitative reverse-transcription PCR. The paw withdrawal latency (PWL) and maximal potential efficiency % of rats were detected by PWL assay. The levels of IL-1β and TNF-α in spinal cord tissues of rats were measured by ELISA assay. The interaction between TRAF6 and miR-124-3p was predicted by TargetScan software (http://www.targetscan.org) and confirmed by the dual-luciferase reporter assay. The protein level of TRAF6 was determined by western blot. MiR-124-3p expression was highly downregulated in a dezocine-resistant model. MiR-124-3p overexpression could alleviate dezocine tolerance in rats. TRAF6 expression was significantly upregulated in a dezocine-resistant model. MiR-124-3p targeted TRAF6 and TRAF6 was negatively modulated by miR-124-3p. In addition, overexpression of TRAF6 could reverse the inhibitory effects of miR-124-3p on dezocine tolerance. Overexpression of miR-124-3p alleviates dezocine tolerance against pain via regulating TRAF6 in a rat model, providing a possible solution to address dezocine tolerance in clinical.
Insights
MicroRNAs (miRNAs) regulate pain and drug tolerance. This study shows that increasing miR-124-3p levels in rats reduces tolerance to dezocine pain relief by targeting TRAF6.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- MicroRNAs (miRNAs) are critical regulators of gene expression involved in pain perception and drug tolerance.
- Dezocine is an analgesic, but its efficacy can be limited by the development of drug tolerance.
- Understanding the molecular mechanisms underlying dezocine tolerance is crucial for developing effective pain management strategies.
Purpose of the Study:
- To investigate the role of miR-124-3p in the development of dezocine tolerance in a rat pain model.
- To elucidate the regulatory mechanism of miR-124-3p in controlling dezocine tolerance against pain.
Main Methods:
- Quantitative reverse-transcription PCR (qRT-PCR) to measure miR-124-3p and TRAF6 expression in rat spinal cords.
- Paw withdrawal latency (PWL) assay to assess pain sensitivity and tolerance.
- Enzyme-linked immunosorbent assay (ELISA) for IL-1β and TNF-α levels.
- Bioinformatic prediction (TargetScan) and dual-luciferase reporter assay to confirm miR-124-3p and TRAF6 interaction.
- Western blot to determine TRAF6 protein levels.
Main Results:
- miR-124-3p expression was significantly downregulated in rats exhibiting dezocine resistance.
- Overexpression of miR-124-3p effectively alleviated dezocine tolerance, while TRAF6 expression was upregulated.
- miR-124-3p directly targets TRAF6, negatively regulating its expression. TRAF6 overexpression reversed the inhibitory effect of miR-124-3p on dezocine tolerance.
Conclusions:
- miR-124-3p plays a protective role against dezocine tolerance by targeting and downregulating TRAF6.
- Modulating miR-124-3p levels offers a potential therapeutic strategy to overcome dezocine tolerance in clinical pain management.
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