Combinatorial chemistry & high throughput screening · 2026
Acupoint Catgut Embedding Alleviates Neuropathic Pain by Regulating Sigma-1 Receptor Expression.
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Xie Heng-Tao, Feng Xiao-Bo, Du Kai-Rong
Аннотация
INTRODUCTION: Acupoint Catgut Embedding (ACE), also known as acupuncture catgut implantation, exerts analgesic effects by inhibiting Sig-1R. This study aimed to evaluate the modulatory effect of ACE on Sig-1R and its mechanism of action in alleviating nerve pain.
METHODS: We assessed behavioral changes in mechanosensitive and thermosensitive pain in rats. Spinal cord tissue damage was examined using HE staining, while apoptosis was evaluated through TUNEL staining. Sig-1R expression in spinal cord tissue was analyzed via immunohistochemistry.
RESULTS: ACE and Sig-1R antagonists significantly reduced paw withdrawal frequency (PWF), decreased the expression of Bax and cleaved caspase-3 proteins, and alleviated morphological damage in spinal cord cells. They also increased the expression of Bcl-2 and prolonged paw withdrawal latency (PWL) in rats. Additionally, ACE and Sig-1R antagonists reduced levels of TNF-α, IL-1β, and IL-6, as well as malondialdehyde (MDA), while elevating levels of Superoxide Dismutase (SOD) and Glutathione Peroxidase (GPx) in both serum and spinal cord tissues. Furthermore, they downregulated the protein expression of p-ERK1/2, p38 MAPK, and Nox2, reduced the number of Th1 and Th17 cells, and increased the number of Th2 and Treg cells.
DISCUSSION: Currently, the mechanism of action of ACE on neuropathic pain caused by peripheral nerve injury based on Sig-1R is still unclear. This study evaluated the mechanism by which ACE alleviates neuralgia by regulating the expression of Sig-1R in the spinal cord. In future work, we aim to conduct additional experiments to determine the precise localization of T cells within the spinal cord and to further investigate their direct interactions with glial cells.
CONCLUSION: ACE effectively alleviates nerve pain by modulating Sig-1R expression in the spinal cord, thereby regulating inflammatory responses, oxidative stress, and associated signaling pathways.
METHODS: We assessed behavioral changes in mechanosensitive and thermosensitive pain in rats. Spinal cord tissue damage was examined using HE staining, while apoptosis was evaluated through TUNEL staining. Sig-1R expression in spinal cord tissue was analyzed via immunohistochemistry.
RESULTS: ACE and Sig-1R antagonists significantly reduced paw withdrawal frequency (PWF), decreased the expression of Bax and cleaved caspase-3 proteins, and alleviated morphological damage in spinal cord cells. They also increased the expression of Bcl-2 and prolonged paw withdrawal latency (PWL) in rats. Additionally, ACE and Sig-1R antagonists reduced levels of TNF-α, IL-1β, and IL-6, as well as malondialdehyde (MDA), while elevating levels of Superoxide Dismutase (SOD) and Glutathione Peroxidase (GPx) in both serum and spinal cord tissues. Furthermore, they downregulated the protein expression of p-ERK1/2, p38 MAPK, and Nox2, reduced the number of Th1 and Th17 cells, and increased the number of Th2 and Treg cells.
DISCUSSION: Currently, the mechanism of action of ACE on neuropathic pain caused by peripheral nerve injury based on Sig-1R is still unclear. This study evaluated the mechanism by which ACE alleviates neuralgia by regulating the expression of Sig-1R in the spinal cord. In future work, we aim to conduct additional experiments to determine the precise localization of T cells within the spinal cord and to further investigate their direct interactions with glial cells.
CONCLUSION: ACE effectively alleviates nerve pain by modulating Sig-1R expression in the spinal cord, thereby regulating inflammatory responses, oxidative stress, and associated signaling pathways.