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Exploring Potential Mechanistic Aspects of "Biaoben acupoint " acupuncture for Lumbar Disc Herniation using 4D Proteomics

ABSTRACT: Objective To investigate the mechanism of action of "Biaoben acupoint " acupuncture in treating Lumbar Disc Herniation (LDH) by identifying differentially expressed plasma proteins (DEPs) using timsTOF Pro-based 4D Data-Independent Acquisition (DIA) proteomics and correlating them with clinical indicators. Methods This study enrolled 10 healthy subjects (healthy group) and 10 patients with LDH (experimental group). The experimental group received "Biaoben acupoint" acupuncture treatment for 3 weeks. Clinical outcomes, including Visual Analogue Scale (VAS) for pain, Oswestry Disability Index (ODI) for lumbar function, and Japanese Orthopaedic Association (JOA) score for neurological status, were assessed before and after treatment. Plasma samples were collected for proteomic analysis. Results Acupuncture treatment significantly improved VAS, ODI, and JOA scores in the experimental group compared to baseline (p<0.001). Proteomic analysis quantified 3685 proteins, identifying 376 DEPs across the healthy group and the experimental group (before and after treatment). Bioinformatics analysis revealed that these DEPs were primarily enriched in pathways related to cell structure and adhesion (e.g., cytoskeleton remodeling, focal adhesion), inflammation and immune signaling (e.g., chemokine and cytokine signaling), and cell signal transduction (e.g., calcium signaling, Rap1 pathway). Core DEPs included ACTB, CXCR4, ACTN1, CXCL12, SELP, and CCN2. Correlation analysis demonstrated that the expression levels of CXCL12, ACTN1, CXCR4, and CCN2 were significantly correlated with VAS, ODI, and JOA scores. Conclusion "Biaoben acupoint" acupuncture likely exerts its therapeutic effects by modulating multiple biological pathways related to inflammatory/immune responses, cytoskeleton organization, cell structure/adhesion, and tissue repair, thereby improving pain, lumbar function, and neurological deficits in LDH patients. Proteins such as CXCL12, ACTN1, CXCR4, and CCN2 are potential key mediators of these therapeutic effects.

ORGANISM(S): Homo Sapiens

SUBMITTER: Shimin Zhang

PROVIDER: PXD067489 | iProX | Tue Aug 19 00:00:00 BST 2025

REPOSITORIES: iProX

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Project description:Background and aims: Preclinical data suggest that the chemokine receptor 2 (CCR2) is involved in the pathophysiology of neuropathic pain through modulation of neuronal excitability, synaptic transmission and activation of spinal cord microglia. CCR2-antagonists have shown to be effective in preclinical models of neuropathic pain. The aim of this study was to evaluate the analgesic efﬁcacy, safety and tolerability of a novel CCR2-antagonist, AZD2423, in patients with painful diabetic neuropathy (PDN). Methods: This was a double-blind, randomized, parallel-group, multi-center study in patients with sym- metric distal sensory polyneuropathy due to type 1 or 2 diabetes and duration of neuropathic pain between 3 months and 5 years. Concomitant treatment with neuropathic pain medications (e.g. anticon- vulsants, tricyclic antidepressants, serotonin-noradrenaline uptake inhibitors, opioids, topical lidocaine or capsaicin) was not allowed. 134 patients with PDN were equally randomized to 28 days oral admin- istration of 20 mg AZD2423, 150 mg AZD2423, or placebo. The primary efﬁcacy variable was the change of average pain score from 5-days baseline to the last 5 days of treatment, measured with numerical rating scale (NRS, 0–10). The secondary efﬁcacy measures included NRS worst pain scores, patient global impression of change, pain interference on sleep and activity, and neuropathic pain symptom inventory (NPSI). Results: The change of NRS average pain score was not signiﬁcantly different between treatment groups (AZD2423 20 mg: −1.50; AZD2423 150 mg: −1.35; placebo: −1.61). The NPSI total score and three out of ﬁve subscores (evoked pain, pressing/deep pain and paresthesia/dysesthesia) tended to be reduced more by AZD2423 150 mg than by placebo. No other secondary efﬁcacy variables differed between treatment groups. The frequency and type of adverse events for AZD2423 were similar to placebo. The achieved plasma levels of AZD2423 in the two dose groups were in line with predictions from pharmacokinetic data previously obtained in healthy volunteers. Dose-dependent increase of plasma levels of the ligand of CCR2 (CCL2; chemokine ligand 2) and decrease of the mean levels of monocytes (−27% by AZD2423 150 mg) suggested that the administrated doses of AZD2423 interacted with the CCR2 target. Conclusion: The CCR2-antagonist AZD2423 showed no analgesic efﬁcacy in PDN based on NRS average pain scores and global and functional pain outcome measures. The NPSI data suggested possible effects on certain sensory components of pain. There were no major safety or tolerability concerns.

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Exploring Potential Mechanistic Aspects of "Biaoben acupoint " acupuncture for Lumbar Disc Herniation using 4D Proteomics

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