licochalcone-a and Neuralgia

licochalcone-a has been researched along with Neuralgia* in 2 studies

Other Studies

2 other study(ies) available for licochalcone-a and Neuralgia

ArticleYear
Licochalcone Mediates the Pain Relief by Targeting the Voltage-Gated Sodium Channel.
    Molecular pharmacology, 2023, Volume: 104, Issue:4

    Licorice is a traditional Chinese medicine and recorded to have pain relief effects in national pharmacopoeia, but the mechanisms behind these effects have not been fully explored. Among the hundreds of compounds in licorice, licochalcone A (LCA) and licochalcone B (LCB) are two important components belonging to the chalcone family. In this study, we compared the analgesic effects of these two licochalcones and the molecular mechanisms. LCA and LCB were applied in cultured dorsal root ganglion (DRG) neurons, and the voltage-gated sodium (Na

    Topics: Animals; Ganglia, Spinal; HEK293 Cells; Humans; NAV1.7 Voltage-Gated Sodium Channel; Neuralgia; Sodium; Sodium Channel Blockers; Voltage-Gated Sodium Channels

2023
Licochalcone A Attenuates Chronic Neuropathic Pain in Rats by Inhibiting Microglia Activation and Inflammation.
    Neurochemical research, 2021, Volume: 46, Issue:5

    Immune response plays a vital role in the pathogenesis of neuropathic pain. Immune response-targeted therapy becomes an effective strategy for treating neuropathic pain. Licochalcone A (Lic-A) possesses anti-inflammatory and neuroprotective effects. However, the potential of Lic-A to attenuate neuropathic pain has not been well explored. To investigate the protective effect and evaluate the underlying mechanism of Lic-A against neuropathic pain in a rat model. Chronic constriction injury (CCI) surgery was employed in rats to establish neuropathic pain model. Rats were intraperitoneally administrated with Lic-A (1.25, 2.50 and 5.00 mg/kg) twice daily. Mechanical withdrawal threshold and thermal withdrawal latency were used to evaluate neuropathic pain. After administration, the lumbar spinal cord enlargement of rats was collected for ELISA, Western blot and immunofluorescence analysis. Mechanical withdrawal threshold and thermal withdrawal latency results showed that Lic-A significantly attenuated CCI-evoked neuropathic pain in dose-dependent manner. Lic-A administration also effectively blocked microglia activation. Moreover, Lic-A suppressed p38 phosphorylation and the release of inflammatory factors such as tumor necrosis factor-α, interleukin-1 and interleukin-6. Our findings provide evidence that Lic-A may have the potential to attenuate CCI-evoked neuropathic pain in rats by inhibiting microglia activation and inflammatory response.

    Topics: Animals; Calcium-Binding Proteins; Chalcones; Chronic Disease; Constriction, Pathologic; Inflammation; Interleukin-1beta; Interleukin-6; Male; Microfilament Proteins; Microglia; Neuralgia; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Rats, Sprague-Dawley; Sciatic Nerve; Spinal Cord Dorsal Horn; Tumor Necrosis Factor-alpha

2021