Effect and mechanism of ginsenoside Rg1 in alleviating neuropathic pain in rats
10.13406/j.cnki.cyxb.003839
- VernacularTitle:人参皂苷Rg1对大鼠神经病理性疼痛的缓解作用和机制研究
- Author:
Qiang GUO
1
;
Kun WANG
;
Caiyan DANG
;
Xiaomeng GAO
Author Information
1. 西安市中心医院疼痛科,西安 710004
- Keywords:
ginsenoside Rg1;
neuropathic pain;
neuroglial cell;
inflammatory factor;
Toll-like receptor 4
- From:
Journal of Chongqing Medical University
2025;50(10):1418-1425
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role and analgesic mechanism of ginsenoside Rg1(GRg1)in neuropathic pain in rats.Methods:A total of 30 adult male Sprague-Dawley rats were randomly divided into sham-operation group,spared nerve injury(SNI)group,GRg1 group,GRg1+empty vector group(GRg1+vector group),and GRg1+TLR4 overexpression plasmid group(GRg1+TLR4 group),with 6 rats in each group.The SNI method was used to establish a rat model of neuropathic pain in the latter four groups,and after successful modeling,GRg1 was given by gavage for 14 days,while the plasmid was injected via the caudal vein.The sciatic nerve was exposed for the sham-operation group without any injury manipulation.A mechanical pain threshold detector and a radiation thermal pain threshold detector were used to measure mechanical withdrawal threshold and thermal withdrawal latency on day 1 before surgery and on days 1,3,7,and 14 after surgery.L4-L6 spinal cord tissue samples were collected,and quantitative real-time PCR,Western blot,and indirect immunofluorescence assay were used to measure the mRNA and protein expression levels of GFAP,a marker for astrocyte activation,and Iba-1,a marker for microglial cells;ELISA was used to measure the content of IL-1β,TNF-α,and CXCL1 in spinal cord tissue,and colorimetry was used to mea-sure the content of NO in spinal cord tissue;molecular docking was used to investigate the binding ability and interaction mode between GRg1 and TLR4.Results:GRg1 restored mechanical withdrawal threshold(F=24.67,P=0.000)and thermal withdrawal latency in SNI rats(F=8.058,P=0.034)and downregulated the expression lev-els of GFAP(mRNA:F=37.74,P=0.000;protein:F=98.71,P=0.001)and Iba-1(mRNA:F=62.11,P=0.000;protein:F=187.0,P=0.000)in spinal cord tissues of SNI rats,and it also reduced the levels of IL-1β(F=56.96,P=0.000),TNF-α(F=55.25,P=0.000),CXCL1(F=93.54,P=0.000)and NO(F=30.57,P=0.000)in the spinal cord tissues of SNI rats.The study on mechanisms showed highly stable binding between GRg1 and TLR4,and GRg1 downregulated the expression level of TLR4(mRNA:F=62.66,P=0.000;protein:F=53.52,P=0.000)and the phosphorylation levels of p38(F=300.3,P=0.000)and p65(F=121.6,P=0.000)in spinal cord tis-sues of SNI rats,whereas the overexpression of TLR4 reversed the effect of GRg1(Mechanical Paw Withdrawal Threshold:F=24.67,P=0.000;Thermal Paw Withdrawal Latency:F=8.058,P=0.034;GFAP,mRNA:F=37.74,P=0.009;Protein:F=98.71,P=0.000;Iba-1,mRNA:F=62.11,P=0.006;Protein:F=187.0,P=0.000;IL-1β:F=56.96,P=0.006;TNF-α:F=55.25,P=0.000;CXCL1:F=93.54,P=0.000;NO:F=30.57,P=0.042;TLR4,mRNA:F=62.66,P=0.000;Protein:F=53.52,P=0.000;p38 Phosphorylation Level:F=300.3,P=0.000;p65 Phosphorylation Level:F=121.6,P=0.000).Conclusion:GRg1 may exert an analgesic effect on SNI rats by regulating the TLR4-p38/MAPK-NF-κB signaling pathway and activating the activation of astrocytes and microglial cells in spinal cord tissue.
