Immunity, inflammation and disease · 2025
Electroacupuncture of Guanyuan (CV4) Acupoint Improved Pelvic Inflammatory Disease Pain by Inhibiting Neuroinflammation and Sympathetic Activity.
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Qu Jinyu, Peng Yingchun, Shen Xuefang, Xiong Jin, Wang Huan, Xiao Xiang, Wang Yili
Аннотация
OBJECTIVE: To investigate the underlying mechanisms through which electroacupuncture (EA) at the Guanyuan (CV4) acupoint inhibits sympathetic activity and neurogenic inflammatory responses to relieve pain in rats with pelvic inflammatory disease (PID).
METHODS: Escherichia coli and Staphylococcus aureus were used to establish a PID rat model. EA was evaluated at frequencies of 2, 100, and 2/100 Hz, and 2/100 Hz was selected for subsequent investigation. The rats were randomly divided into the control, model, EA-guanyuan (2/100 Hz), and EA-nonsensitized groups (n = 6). Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were assessed using von Frey filaments. Hematoxylin and eosin staining was performed to evaluate the histopathology. The tyrosine hydroxylase (TH) expression was analyzed using immunofluorescence (IF) staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), transforming growth factor-β1 (TGF-β1), intercellular cell adhesion molecule-1 (ICAM-1), 5-hydroxytryptamine receptor 3 (5-HT3R), substance P (SP), hyaluronic acid (HA), and bradykinin (BK) were measured using an enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to measure the expression of 5-HT3R, calcitonin gene-related peptide (CGRP), HA, Kininogen 1 (KNG1), prostaglandin I2 (PGI2), and trefoil factor 2 (TFF2). Transmission electron microscopy (TEM) was used to observe synaptic connections.
RESULTS: EA at CV4 reduced the behavioral pain score (p < 0.05), increased MWT and TWL, and alleviated uterine tissue pathological damage in rats. EA at CV4 reduced the levels of 5-HT3R, CGRP, BK, HA, KNG1, PGI2SP, TGF-β1, ICAM-1, and TNF-α, and increased IL-2 levels (p < 0.05). Furthermore, EA at CV4 inhibited sympathetic activity by decreasing TH expression (p < 0.05). Additionally, EA at CV4 restored the synaptic connections between the pelvic nerves of the dorsal commissural neuron (DCN).
CONCLUSION: EA at CV4 alleviated the pathological damage and pain sensitization of uterine tissue in rats with PID by inhibiting sympathetic activity and neurogenic inflammatory response.
METHODS: Escherichia coli and Staphylococcus aureus were used to establish a PID rat model. EA was evaluated at frequencies of 2, 100, and 2/100 Hz, and 2/100 Hz was selected for subsequent investigation. The rats were randomly divided into the control, model, EA-guanyuan (2/100 Hz), and EA-nonsensitized groups (n = 6). Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were assessed using von Frey filaments. Hematoxylin and eosin staining was performed to evaluate the histopathology. The tyrosine hydroxylase (TH) expression was analyzed using immunofluorescence (IF) staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), transforming growth factor-β1 (TGF-β1), intercellular cell adhesion molecule-1 (ICAM-1), 5-hydroxytryptamine receptor 3 (5-HT3R), substance P (SP), hyaluronic acid (HA), and bradykinin (BK) were measured using an enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to measure the expression of 5-HT3R, calcitonin gene-related peptide (CGRP), HA, Kininogen 1 (KNG1), prostaglandin I2 (PGI2), and trefoil factor 2 (TFF2). Transmission electron microscopy (TEM) was used to observe synaptic connections.
RESULTS: EA at CV4 reduced the behavioral pain score (p < 0.05), increased MWT and TWL, and alleviated uterine tissue pathological damage in rats. EA at CV4 reduced the levels of 5-HT3R, CGRP, BK, HA, KNG1, PGI2SP, TGF-β1, ICAM-1, and TNF-α, and increased IL-2 levels (p < 0.05). Furthermore, EA at CV4 inhibited sympathetic activity by decreasing TH expression (p < 0.05). Additionally, EA at CV4 restored the synaptic connections between the pelvic nerves of the dorsal commissural neuron (DCN).
CONCLUSION: EA at CV4 alleviated the pathological damage and pain sensitization of uterine tissue in rats with PID by inhibiting sympathetic activity and neurogenic inflammatory response.