Methods: Thirty Sprague-Dawley rats were randomly assigned to control (non-diabetic), PDN and non-PDN groups (n = 10). The rats were induced with diabetes by streptozotocin injection (60 mg/kg). Tactile allodynia and thermal hyperalgesia were assessed on day 0, 14 (week 2) and 21 (week 3) in the rats. The rats were sacrificed and the spinal cord tissue was collected for the measurement of oxidative stress (malondialdehyde (MDA), superoxide dismutase (SOD) and catalase) and pro-inflammatory markers (interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α)).
Results: PDN rats demonstrated a marked tactile allodynia with no thermal hyperalgesia whilst non-PDN rats exhibited a prominent hypo-responsiveness towards non-noxious stimuli and hypoalgesia towards thermal input. The MDA level and pro-inflammatory TNF-α was significantly increased in PDN rats whilst catalase was reduced in these rats. Meanwhile, non-PDN rats demonstrated reduced SOD enzyme activity and TNF-α level and increased MDA and catalase activity.
Conclusion: The changes in oxidative stress parameters and pro-inflammatory factors may contribute to the changes in behavioural responses in both PDN and non-PDN rats.
Methods: The rats were divided into four groups (n = 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.