Acupoint Catgut Embedding Alleviates Neuropathic Pain by Regulating Sigma-1 Receptor Expression

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.

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.

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.

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.

ACE effectively alleviates nerve pain by modulating Sig-1R expression in the spinal cord, thereby regulating inflammatory responses, oxidative stress, and associated signaling pathways.