Hai-Li Li,1– 3 Xing-Ping Tan,1,3 Xiao-Die Wang,1,3 Ren-Tian Guo,1,3 Jiang-Lin Wang1,3,4 

1Department of Pain Management, The Affiliated Hospital, Southwest Medical University, Luzhou, People’s Republic of China; 2Department of Anesthesiology, The Affiliated Tianfu Hospital, Southwest Medical University, Meishan, People’s Republic of China; 3Anesthesiology and Critical Care Medicine Key Laboratory of Luzhou, Southwest Medical University, Luzhou, Sichuan, People’s Republic of China; 4Department of Pain Management, The Affiliated Tianfu Hospital, Southwest Medical University, Meishan, People’s Republic of China

Correspondence: Jiang-Lin Wang, Pain Department, The Affiliated Hospital, Southwest Medical University, No. 25 Pacific Street, Luzhou, 646000, People’s Republic of China, Tel +8618090880626, Fax +0830-3165469, Email jianglin523@swmu.edu.cn

Background and Purpose: Central post-stroke pain (CPSP) is directly caused by cerebrovascular diseases that affect the central somatosensory system. It is a serious, chronic central neuropathic pain that responds poorly to first-line drugs. Oxymatrine (OMT), a monomer derived from the traditional Chinese medicine Sophora flavescens Ait. exhibits anti-inflammatory, analgesic, and organ- and tissue-protective properties. This study aimed to investigate the therapeutic effects of OMT in a rat model of CPSP.
Methods: Gene Ontology (GO) enrichment analysis was initially employed to elucidate the role of OMT on CPSP target proteins in terms of gene function. Then the CPSP model was induced through focal hemorrhage in the ventral posterolateral nucleus (VPL). Rats were randomly assigned to five groups (n = 10): sham + NaCl, CPSP + NaCl, and CPSP + OMT (100 mg/kg, 200 mg/kg, 400 mg/kg). Daily intraperitoneal injections of NaCl or varying doses of OMT were administered from days 7 to 14 after model establishment, and paw withdrawal mechanical thresholds (PWMT) were assessed. The optimal OMT dose (200 mg/kg) was determined based on PWMT measurements. On day 14, inflammatory markers (IL-1β, IL-6, TNF-α) and alterations in microglia and astrocyte activity at the thalamic lesion site were analyzed.
Results: Elevated levels of IL-1β, IL-6, and TNF-α (P < 0.05) and activation of microglia and astrocytes were observed around the peri-thalamic lesion in CPSP rats. OMT administration significantly reduced mechanical allodynia (P < 0.05), decreased inflammatory cytokine expression (P < 0.05), and inhibited microglial and astrocytic activation.
Conclusion: OMT mitigates central post-stroke pain in rats by attenuating the inflammatory response at the thalamic lesion site.

Keywords: central post-stroke pain, oxymatrine, inflammation, thalamic lesions, mechanical allodynia