Prophylactic and Antinociceptive Effects of Coenzyme Q10 on Diabetic Neuropathic Pain in a Mouse Model of Type 1 Diabetes

• Published in: Anesthesiology (Philadelphia) 2013-04, Vol.118 (4), p.945-954
• Main Authors: YAN PING ZHANG, EBER, Ariel, YUE YUAN, ZHE YANG, RODRIGUEZ, Yiliam, LEVITT, Roy C, TAKACS, Peter, CANDIOTTI, Keith A
• Format: Article
• Language: English
• Subjects: Analgesics - pharmacology; Animals; Biological and medical sciences; Body Weight - drug effects; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Type 1 - complications; Diabetes. Impaired glucose tolerance; Diabetic Neuropathies - complications; Diabetic Neuropathies - drug therapy; Disease Models, Animal; Dose-Response Relationship, Drug; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Lipid Peroxidation; Male; Medical sciences; Mice; Mice, Inbred C57BL; Nervous system (semeiology, syndromes); Neurology; Oxidative Stress; Reverse Transcriptase Polymerase Chain Reaction - methods; Ubiquinone - analogs & derivatives; Ubiquinone - pharmacology; Vitamins - pharmacology; Weight Loss - drug effects
• ISSN: 0003-3022; 1528-1175
• DOI: 10.1097/aln.0b013e3182829b7b

Oxidative stress is a key factor implicated in the development of diabetic neuropathy. This study evaluates the prophylactic and antinociceptive effects of the antioxidant coenzyme Q10 (CoQ10) on diabetes-induced neuropathic pain in a diabetic mouse model. Total 56 mice with type 1 diabetes induced by streptozotocin were used, 20 normal mice were used as control. Mechanical and thermal nociceptive behavioral assays were applied to evaluate diabetic neuropathic pain. Tissue lipid peroxidation, immunohistochemistry, reverse transcription, and polymerase chain reaction were used to evaluate the molecular mechanisms of CoQ10. Data are presented as mean ± SEM. CoQ10 administration was associated with reduced loss of body weight compared with nontreated diabetic mice, without affecting blood glucose levels. Low dose and long-term administration of CoQ10 prevented the development of neuropathic pain. Treatment with CoQ10 produced a significant dose-dependent inhibition of mechanical allodynia and thermal hyperalgesia in diabetic mice. Dorsal root ganglia, sciatic nerve, and spinal cord tissues from diabetic mice demonstrated increased lipid peroxidation that was reduced by CoQ10 treatment. CoQ10 administration was also noted to reduce the proinflammatory factors in the peripheral and central nervous system. The results of this study support the hypothesis that hyperglycemia induced neuronal oxidative damage and reactive inflammation may be pathogenic in diabetic neuropathic pain. CoQ10 may be protective by inhibiting oxidative stress and reducing inflammation by down-regulating proinflammatory factors. These results suggest that CoQ10 administration may represent a low-risk, high-reward strategy for preventing or treating diabetic neuropathy.