Korean J Physiol Pharmacol.
2026 May;30(3):231-239. 10.4196/kjpp.25.317.
Aloin attenuates NMDA receptor by modulating calcium response on substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice
- Affiliations
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- 1Department of Oral Physiology, School of Dentistry and Institute of Oral Bioscience, Jeonbuk National University, Jeonju 54896, Korea
- 2Faculty of Odonto- Stomatology, Hue University of Medicine and Pharmacy, Hue University, Hue 530000, Vietnam
- 3Department of Oral Medicine, School of Dentistry & Institute of Oral Bioscience, Jeonbuk National University, Jeonju 54896, Korea
- 4Research Institute of Clinical Medicine of Jeonbuk National University - Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju 54907, Korea
- KMID: 2580788
- DOI: http://doi.org/10.4196/kjpp.25.317
Abstract
- Aloe vera extracts, particularly aloin, have been widely used in traditional Chinese medicine for their anti-inflammatory and detoxifying properties. Recent studies suggest that aloin may also exert neuroprotective effects, though its specific mechanisms remain unclear. Glutamate excitotoxicity, a critical factor in neurodegenerative and pain-related disorders, is mediated primarily by N-methyl-D-aspartic acid (NMDA) receptors, which regulate calcium influx and neuronal excitability. Meanwhile, substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) plays a central role in processing orofacial pain, where glutamate is a key excitatory neurotransmitter. Using whole-cell patch-clamp electrophysiology and calcium imaging techniques in mice SG neurons of the Vc, we examined aloin’s effects on glutamate receptor-mediated responses. Aloin selectively inhibited NMDA-induced responses without affecting AMPA or kainate receptor activity. The suppression of NMDA-mediated currents by aloin was linked to changes in Ca2+ influx but occurred independently of voltage-gated sodium channels and action potential generation. Calcium imaging revealed that aloin reduced NMDA-induced intracellular calcium influx, supporting its role in mitigating NMDA-mediated excitotoxicity. Furthermore, aloin significantly suppressed the spontaneous firing activity of SG neurons, suggesting its broader regulatory effects on neuronal excitability. Our findings demonstrate that aloin attenuates NMDA receptor-induced excitatory signaling by regulating calcium response. This specificity highlights aloin’s potential as a therapeutic candidate for conditions involving glutamate excitotoxicity and orofacial pain regulation.
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