Triptolide is a potent immunosuppressive drug capable of inhibiting T cell 
activation and proliferation. Recent studies show that T cells play an important 
role in neuropathic pain following nerve injury in rats. In this study, we 
investigated the effect of triptolide on T cell activation and development of 
neuropathic pain. Neuropathic pain by chronic constriction injury (CCI) was 
induced by loose ligation of the sciatic nerve in Sprague-Dawley rats. 
Triptolide (5 or 10 μg/kg) or vehicle (DMSO) was administered intrathecally 
after surgery for 7 days (n=8 per group). The right hind paw withdrawal 
threshold to von Frey filament stimuli and withdrawal latency to radiant heat 
were determined before and after the surgery (days 0 to 7). NF-κB activation and 
pro-inflammatory cytokine (TNF-α and IL-2) expression were determined by ELISA, 
Western blot, and real time-PCR. CCI of the sciatic nerve induced mechanical 
allodynia and thermal hyperalgesia in these rats. Intrathecal triptolide (5 and 
10 μg/kg) suppressed the development of allodynia and thermal hyperalgesia. It 
also inhibited CCI-induced inflammation and T cell activation, by decreasing 
spinal cord TNF-α, IL-2 and NF-κB p65 levels. Motor dysfunction was not observed 
after triptolide treatment. In the present study, we demonstrated the 
suppressive effect of triptolide on the development of neuropathic pain. 
Therefore, triptolide could be a promising immunosuppressive agent in the 
treatment of neuropathic pain. Further studies are required to examine the 
safety of intrathecal triptolide for clinical application.