Abstract：Objective: To investigate the study of the ameliorative effect of nudging to regulate the BDNF/Trkb/p38/JNK pathway on rats with myofascial pain syndrome.Methods: 40 SPF grade rats were selected as experimental subjects and divided into 4 groups of 10 rats each by random number table method, 30 were selected to perform modeling of myofascial pain syndrome, a total of 3 failed, and the remaining 27 were grouped into 10 blank groups (normal feeding, no modeling and treatment), 9 model groups (normal feeding, modeling, no treatment), 9 nudging groups (modeling, normal feeding, and the trigger point localized by 0.5kg of force press), 9 nudging + K-252a group (normal rearing, modeling, intervention trigger point localized at 0.5kg of force press + 500nmol/L concentration of K-252a). After the final intervention in each group, 4ml of blood was collected from the abdominal aorta, and spinal cord tissue from the L4-6 lumbar enlargement segment was harvested. Serum inflammatory factors and stress markers in the abdominal aorta blood were detected using ELISA. Expression of the cell marker OX-42 in spinal cord tissue was assessed via immunohistochemistry. Western Blot analysis was performed to detect levels of BDNF, Trkb, p38, JNK proteins in the L4-6 lumbar bulging segment spinal cord tissue. Results: Compared with the blank group, the model group, massage group, and massage + K-252a group exhibited statistically significant increases in spontaneous activity frequency, IL-8, IL-6, MDA, GSH, β-endorphin levels, and OX-42, BDNF, Trkb, p38, and JNK protein expression (P<0.05). SOD, substance P, and IL-10 levels decreased, while thermal withdrawal latency shortened, with statistically significant differences (P<0.05); Compared with the model group, the massage group exhibited statistically significant reductions in P-substance, MDA, GSH, spontaneous action potential frequency, IL-8, and IL-6 levels, as well as OX-42, BDNF, Trkb, p38, and JNK protein expression levels were significantly lower in the massage group than in the model group (P<0.05). Conversely, levels of β-endorphin, SOD, heat-withdrawal latency, and IL-10 were significantly elevated in the massage group (P<0.05); Compared with the massage group, the massage plus K-252a group showed significantly lower levels of SOD, IL-10, β-endorphin, and heat-withdrawal paw latency, with statistically significant differences (P<0.05). Levels of IL-8, spontaneous action potential frequency, IL-6, MDA, GSH, substance P, OX-42 expression, BDNF, Trkb, p38, JNK protein expression levels were significantly increased, with statistically significant differences (P < 0.05).Conclusion: Massage therapy can effectively alleviate pain in rat models of myofascial pain syndrome. Its mechanism of action may be related to regulating the BDNF/Trkb/p38/JNK signaling pathway, inhibiting the expression of OX-42 in the spinal cord, reducing inflammatory responses, and improving oxidative stress conditions.
吴苏旻, 喻仁宇, 沈重庆, 林丹椿. 推拿调节BDNF/Trkb/p38/JNK通路对肌筋膜疼痛综合征大鼠的改善作用研究[J]. 河北医学, 2025, 31(12): 1976-1983.
WU Sumin, YU Renyu, SHEN Chongqing, et al. Study on the Ameliorative Effect of Massage to Regulate BDNF/Trkb/p38/JNK Pathway on Rats with Myofascial Pain Syndrome. HeBei Med, 2025, 31(12): 1976-1983.
2025, Vol. 31 
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