Minocycline attenuates the development of diabetic neuropathy by modulating DREAM and BDNF protein expression in rat spinal cord.

Abstract

This study investigates the effects of minocycline (an inhibitor of microglial activation) administration on the expression level of spinal BDNF and DREAM proteins in diabetic neuropathic pain (DNP) rats. The rats were divided into four groups (n= 16): non-diabetic control, diabetic control and diabetic rats receiving minocycline (80μg/day or 160μg/day). The diabetic rat model was induced by intraperitoneal injection of streptozotocin (60mg/kg STZ). Tactile allodynia was assessed on day-0 (baseline), day-14 (pre-intervention) and day-22 (post-intervention). Minocycline at doses of 80μg and 160μg were given intrathecally from day-15 until day-21. On day-23, formalin test was conducted to assess nociceptive behaviour response. The spinal expression of OX-42 and level of BDNF and DREAM proteins were detected by immunohistochemistry and western blot analyses. Diabetes rats showed significant tactile allodynia and nociceptive behaviour. Thesewere accompanied by augmented expression of spinal OX-42, BDNF and DREAM protein levels. Both doses of minocycline attenuated tactile allodynia and nociceptive behaviour and also suppressed the diabetic-induced increase in spinal expressions of OX-42, BDNF and DREAM proteins. This study revealed that minocycline could attenuate DNP by modulating spinal BDNF and DREAM protein expressions.