The mechanism of neuropathic pain is considered to be multifactorial.In recent years,a large number of studies have found that the rodent model are promising models for preclinical neuropathic pain,and massage acts on the development of NP through a variety of molecular mechanism.Based on two rodent models of chronic compressive injury and spinal nerve ligation,this paper regulated astrocytes and M1 microglia from massage to reduce neuroinflammation,inhibit the activation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase,and reduced the expression of Ca2+ion channels,thereby reducing the hyperexcitability of injury-sensitive neurons and inhibiting the secretion of pro-inflammatory factors interleukin-1β/18/6 and inflammatory mediators vesicle glutamate transporter 2,NOD-like receptor protein 3 inflammasome,long-chain non-coding RNA BANCR.Then,the expression of the nociceptor adenosine triphosphate receptor P2X3 and the piezoelectric mechanically sensitive ion channel component 2 were reduced,and the transmission of γ-aminobutyric acid in the pain circuit were regulated.This paper summarized the molecular mechanism of tui na in alleviating neuroinflammation,inhibiting neuronal apoptosis and promoting synaptic remodeling in neuropathic pain,in order to provide theoretical references for further clinical application and research.
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