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[The Analgesia of Oxymatrine Affecting Calcium Channel and GABA Release]
Objective:
To explore the analgesia of oxymatrine (OMT) affecting high voltage-dependent calcium channels (HVDCCs) and GABA release under neuropathic pain condition.
Methods:
Totally 66 C57BL/6 mice were randomly divided into the sham-operation group, the model group, and the OMT group, 22 in each group. Neuropathic pain models were established by partial sciatic nerve ligation (PSNL). Hind paw plantar mechanical response threshold (MWT) was measured by up-and-down method with Von-Frey filament. mRNA expression of HVDCCs in brains and spinal cords was detected with Real-time PCR and concentration of GABA was determined using ELISA kit.
Results:
Compared with day 0, the left hind paw MWTwas decreased on day 7, 10, and 14 in the model group (P < 0.05). Compared with the sham-operation group, the left hind paw MWT was significantly reduced in the model group on day 7 (P < 0.05). The MWT of PSNL ipsilateral hind paw was decreased on day 7 before OMT administration, when compared with day 0 (P < 0.05), and increased after OMT administration (P < 0.05). Compared with the sham-operation group, mRNA levels of Cav1.2, Cav1.3, Cav2.1, and Cav2.3 in brain tissues were increased and those of Cav2.2 were decreased significantly in the model group (P < 0.05). In spinal cord tissues, mRNA levels of Cav1.2 and Cav1.3 were increased, but those of Cav2.1, Cav2.2, and Cav2. 3 were decreased significantly in the model group, when compared with those of the sham-operation group (P < 0.05). Compared with the model group, mRNA levels of Cavl.2, Cavl.3, Cav2.1, and Cav2. 3 in brain tissues were decreased, and those of Cav2.2 were increased significantly in the OMT group (P < 0.05). In spinal cord tissues of the OMT group, mRNA levels of Cav1.3 decreased and those of Cav2.1, Cav2.2, and Cav2.3 increased significantly with statistical difference, when compared with those of the model group (P < 0.05). Compared with the sham-operation group, GABA levels in brain tissues decreased in the model group (P < 0.05). Compared with the model group, GABA levels in brain tissues increased in the OMT group (P < 0.05). There was no statistical difference in GABA levels of spinal cord tissues among these groups (P > 0.05).
Conclusions:
OMT had analgesic effect on neuropathic pain, which might be probably related to HVDDCs. Cav2.2 might directly affect GABA release.
Insights
Oxymatrine (OMT) demonstrates analgesic effects on neuropathic pain by modulating high voltage-dependent calcium channels (HVDCCs). This treatment also influences gamma-aminobutyric acid (GABA) release, suggesting a potential therapeutic mechanism.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Neuropathic pain is a debilitating condition often associated with altered neuronal excitability.
- High voltage-dependent calcium channels (HVDCCs) play a crucial role in neuronal signaling and pain transmission.
- GABAergic system dysfunction is implicated in the pathophysiology of neuropathic pain.
Purpose of the Study:
- To investigate the analgesic effects of oxymatrine (OMT) in a mouse model of neuropathic pain.
- To explore the impact of OMT on HVDCCs expression in the brain and spinal cord.
- To examine the influence of OMT on GABA release in the central nervous system.
Main Methods:
- Establishment of a neuropathic pain model in C57BL/6 mice using partial sciatic nerve ligation (PSNL).
- Assessment of mechanical withdrawal threshold (MWT) using the Von-Frey filament test.
- Quantification of HVDCCs mRNA expression via Real-time PCR and GABA concentration using ELISA.
Main Results:
- PSNL induced significant mechanical allodynia, which was reversed by OMT administration.
- OMT modulated the mRNA expression of various HVDCC subtypes (Cav1.2, Cav1.3, Cav2.1, Cav2.3, Cav2.2) in both brain and spinal cord tissues.
- OMT treatment increased GABA levels in brain tissues, while spinal cord GABA levels remained unchanged.
Conclusions:
- Oxymatrine exhibits significant analgesic effects in a mouse model of neuropathic pain.
- The therapeutic action of OMT is likely mediated through the modulation of HVDCCs.
- Cav2.2 may play a direct role in regulating GABA release, contributing to OMT's analgesic properties.
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