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

AIM

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.

METHODS

The rats were divided into four groups ( = 16): non-diabetic control, diabetic control and diabetic rats receiving minocycline (80 μg/day or 160 μg/day). The diabetic rat model was induced by intraperitoneal injection of streptozotocin (60 mg/kg STZ). Tactile allodynia was assessed on day-0 (baseline), day-14 (pre-intervention) and day-22 (post-intervention). Minocycline at doses of 80 μg and 160 μg 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.

RESULTS

Diabetes rats showed significant tactile allodynia and nociceptive behaviour. These were 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.

CONCLUSION

This study revealed that minocycline could attenuate DNP by modulating spinal BDNF and DREAM protein expressions.