Tranilast attenuates neuropathic pain during type-2 diabetes by inhibiting hypoxia-induced pro-inflammatory cytokines in Zucker diabetic fatty rat model

Background The modulatory effect of tranilast on neuropathic pain in type-2 diabetes (T2DM) remains unclear. Methods We monitored interleukin (IL)-1 beta, nuclear factor-kappa B (NF-kappa B) and tumour necrosis factor-alpha (TNF-alpha) levels during the progression of T2DM induced neuropathic pain in rats, and assessed the impact of tranilast treatment of increasing concentrations (0, 200 and 400 mg/kg/day via oral gavage in 1% NaHCO3 delivered as 100 mg/kg twice a day) on the levels of cytokine production, as well as on the thermal hyperalgesia and mechanical allodynia. Results The rats developed hyperglycaemia accompanied with elevated levels of NF-kappa B, IL-1 beta and TNF-alpha in the rostral ventromedial medulla at the age of 16 weeks. Tranilast administration dose dependently alleviated thermal hyperalgesia as well as mechanical allodynia, which was associated with its ability in inhibiting hypoxia-induced levels of NF-kappa B, IL-1 beta and TNF-alpha. Conclusion Tranilast plays crucial roles in modulating T2DM-related neuropathic pain, likely through inhibiting hypoxia.

Automated summary

Tranilast plays a crucial role in modulating T2DM-related neuropathic pain, likely through inhibiting hypoxia.