Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Brazilian Mimosa targets CXCR3 to promote M2 polarization for treating limb numbness in cervical spondylosis.
СтатьяНазвание и аннотация: Перевод в очереди
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Yuan Jiaguo, Su Yanghao, Liu Xiangyu, Liu Shicheng, Ma Yingxin, Yao Yufan, Huang Jiahong, Huang Enxi, Cui Yingdan, Yang Zihao, Li Weijie, Liu Shanshan, Li Wenjuan, Cui Zhizhong
Аннотация
BACKGROUND: Cervical spondylotic radiculopathy (CSR) is a prevalent neurological disorder caused by chronic nerve root compression. Currently, there are no disease-modifying therapies available for CSR.
PURPOSE: This study aimed to investigate the therapeutic potential of the aqueous extract of Brazilian Mimosa (BM) in alleviating CSR-induced sensory dysfunction through immunomodulatory and neuroprotective mechanisms.
STUDY DESIGN: A preclinical study utilizing a rat model of unilateral C7 nerve root compression to simulate CSR pathology.
METHODS: Rats exhibiting CSR-like symptoms were treated with an aqueous extract of BM. Behavioral tests (Von Frey filaments, BBB scale) assessed pain thresholds and motor function. Electrophysiological (SEP) measurements evaluated nerve conduction. Molecular analyses (flow cytometry, Western blot, ELISA, qPCR) examined microglial polarization, cytokine expression, and CXCR3-STAT3 pathway involvement. Toxicity was evaluated via histopathology and alopecia assessment.
RESULTS: BM treatment significantly restored mechanical pain thresholds (from 3.3 ± 0.76 g to 8.98 ± 0.73 g, *p* < 0.01) and improved nerve conduction velocity. BM promoted microglial M2 polarization via the CXCR3-STAT3 pathway, increasing the production of anti-inflammatory cytokines IL-10 and TGF-β while suppressing M1 macrophage activity. STAT3 inhibition abolished these effects (*p* < 0.001), confirming pathway dependency. Although BM exhibited no hepatorenal or pulmonary toxicity, it induced dose-dependent alopecia (42.3 % hair loss, *p* < 0.001).
CONCLUSION: BM alleviates CSR-induced sensory deficits by driving microglial M2 polarization through CXCR3-STAT3 signaling. These findings validate the traditional use of BM and propose a novel immunometabolic axis for treating neuroinflammatory conditions, highlighting its potential as a therapeutic agent for compressive neuropathies.
PURPOSE: This study aimed to investigate the therapeutic potential of the aqueous extract of Brazilian Mimosa (BM) in alleviating CSR-induced sensory dysfunction through immunomodulatory and neuroprotective mechanisms.
STUDY DESIGN: A preclinical study utilizing a rat model of unilateral C7 nerve root compression to simulate CSR pathology.
METHODS: Rats exhibiting CSR-like symptoms were treated with an aqueous extract of BM. Behavioral tests (Von Frey filaments, BBB scale) assessed pain thresholds and motor function. Electrophysiological (SEP) measurements evaluated nerve conduction. Molecular analyses (flow cytometry, Western blot, ELISA, qPCR) examined microglial polarization, cytokine expression, and CXCR3-STAT3 pathway involvement. Toxicity was evaluated via histopathology and alopecia assessment.
RESULTS: BM treatment significantly restored mechanical pain thresholds (from 3.3 ± 0.76 g to 8.98 ± 0.73 g, *p* < 0.01) and improved nerve conduction velocity. BM promoted microglial M2 polarization via the CXCR3-STAT3 pathway, increasing the production of anti-inflammatory cytokines IL-10 and TGF-β while suppressing M1 macrophage activity. STAT3 inhibition abolished these effects (*p* < 0.001), confirming pathway dependency. Although BM exhibited no hepatorenal or pulmonary toxicity, it induced dose-dependent alopecia (42.3 % hair loss, *p* < 0.001).
CONCLUSION: BM alleviates CSR-induced sensory deficits by driving microglial M2 polarization through CXCR3-STAT3 signaling. These findings validate the traditional use of BM and propose a novel immunometabolic axis for treating neuroinflammatory conditions, highlighting its potential as a therapeutic agent for compressive neuropathies.