Related Experiment Video
Updated: Jul 17, 2026
Three-dimensional Imaging of Nociceptive Intraepidermal Nerve Fibers in Human Skin Biopsies
Published on: April 29, 2013
[Helminth derived Immunomodulatory Glycan LNFP3 Impairs Pathogenesis of Peripheral Neuropathic Pain and Spinal Glial
You-Quan Ding1, Hhong-Yi Ren1, Xia Xiao1
1Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University,Chengdu 610041,China.
Objectives:
To investigate the effect of helminth-derived immunomodulatory glycan lacto-N-fucopentaose3(LNFP3) on the pathogenesis of neuropathic pain and spinal glial activation in the corresponding time windows after adult rat tibial nerve permanent transection (modified spared nerve injury, mSNI).
Methods:
Ten weeks old male adult Sprague-Dawley (SD) rats weighing 250-300 g were randomly grouped into four groups: sham-operated group (n =6), mSNI group (n =6), mSNI plus bovine serum albumin (BSA) group (n =12) and mSNI plus LNFP3 group (n=12). Rats were subjected to surgical operation or sham operation on the right tibial nerves and were intraperitoneal injected BSA or LNEP3-BSA conjugates by the group design. Animals from each group (n=6 per group) were subjected to the plantar test,von Frey hairs test, pinprick test and acetone test for critical evaluation of region-specific pain responses on the plantar sural and saphenous skin territories of ipsilateral and contralateral hindpaws after injuries. Transverse frozen sections of L3-4 spinal cords from the remaining animals of mSNI plus BSA group and mSNI plus LNFP3 group 7 and 14 d after injury (n=3 for each time point per group)were prepared and subjected to immunofluorescent staining of microglia/macrophage marker [cluster of differentiation molecule 11b (CD11b)] and astrocyte marker [glial fibrillary acidic protein (GFAP)], for analysis of spinal glial activation.
Results:
After adult rat mSNI, early systematic administration of LNFP3 significantly but not completely attenuated region-specific pathological pain evoked by mechanical and thermal stimuli on the sural and saphenous skin territories of rat hindpaw plantar surfaces in acute (4/5 d after injuries) and subacute (7/8 d and 14/15 d after injuries) phases. Meanwhile, in the ipsilateral spinal cord dorsal horns, this early systematic treatment inhibited microglia/macrophage activation 7 d after injury and astrocyte activation 7 and 14 d after injury.
Conclusions:
Early systematic administration of LNFP3 impairs the pathogenesis (acute induction and chronic transition) of neuropathic pain and spinal glial activation in the corresponding time windows after adult rat mSNI.
