Related Experiment Video
Updated: Aug 2, 2025
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
AdipoRon Engages Microglia to Antinociception through the AdipoR1/AMPK Pathway in SNI Mice
Qian Fang1, Jie Li1, Yaping Wang2
1Department of Rehabilitation, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282 Guangdong, China.
Background:
Microglia-associated neuroinflammation plays a crucial role in the initiation and development of neuropathic pain (NeuP). AdipoRon is an analog of adiponectin that exerts an anti-inflammatory effect in various diseases through the adiponectin receptor 1 (AdipoR1) signaling mechanism. Adenosine monophosphate-activated protein kinase (AMPK) is a downstream target of AdipoR1, and the AdipoR1/AMPK pathway is involved in the regulation of inflammation. This study is aimed at investigating whether AdipoRon could alleviate NeuP by inhibiting the expression of microglia-derived tumor necrosis factor-alpha (TNF-α) through the AdipoR1/AMPK pathway.
Methods:
In vivo, the NeuP model was established in mice through the spared nerve injury. The von Frey test was used to detect the effect of AdipoRon on the mechanical paw withdrawal threshold. Western Blot was performed to detect the effects of AdipoRon on the expression of TNF-α, AdipoR1, AMPK, and p-AMPK. Immunofluorescence was performed to observe the effects of AdipoRon on spinal microglia. In vitro, lipopolysaccharide (LPS) was used to induce inflammatory responses in BV2 cells. The effect of AdipoRon on cell proliferation was detected by CCK-8. qPCR was used to examine the effects of AdipoRon on the expression of TNF-α and polarization markers. And the effect of AdipoRon on the AdipoR1/AMPK pathway was confirmed by Western Blot.
Results:
Intraperitoneal injection of AdipoRon alleviated mechanical nociception in SNI mice, and the application of AdipoRon reduced the expression of TNF-α and the number of microglia in the ipsilateral spinal cord. Additionally, AdipoRon decreased the protein level of AdipoR1 and increased the protein level of p-AMPK in the ipsilateral spinal cord. In vitro, AdipoRon inhibited BV2 cell proliferation and reversed LPS-induced TNF-α expression and polarization imbalance. Furthermore, AdipoRon reversed the LPS-induced increase in AdipoR1 expression and decrease in p-AMPK expression in BV2 cells.
Conclusions:
AdipoRon may alleviate NeuP by reducing microglia-derived TNF-α through the AdipoR1/AMPK pathway.
Insights
AdipoRon alleviates neuropathic pain (NeuP) by reducing microglia-derived tumor necrosis factor-alpha (TNF-α) via the adiponectin receptor 1 (AdipoR1)/adenosine monophosphate-activated protein kinase (AMPK) pathway. This study demonstrates AdipoRon
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia-driven neuroinflammation is central to neuropathic pain (NeuP) development.
- AdipoRon, an adiponectin analog, targets the AdipoR1/AMPK pathway for anti-inflammatory effects.
- The AdipoR1/AMPK pathway regulates inflammatory responses.
Purpose of the Study:
- To investigate AdipoRon's efficacy in alleviating NeuP.
- To determine if AdipoRon inhibits microglia-derived tumor necrosis factor-alpha (TNF-α) via the AdipoR1/AMPK pathway.
Main Methods:
- Established a NeuP mouse model using spared nerve injury (SNI).
- Assessed mechanical allodynia using the von Frey test.
- Utilized Western Blot, immunofluorescence, and qPCR to analyze molecular and cellular changes in vivo and in vitro (BV2 cells).
Main Results:
- AdipoRon treatment reduced mechanical hypersensitivity in SNI mice.
- AdipoRon decreased TNF-α expression and microglia activation in the spinal cord.
- In vitro, AdipoRon inhibited inflammatory responses and modulated the AdipoR1/AMPK pathway in BV2 cells.
Conclusions:
- AdipoRon effectively alleviates neuropathic pain.
- The mechanism involves the inhibition of microglia-derived TNF-α through the AdipoR1/AMPK pathway.
