Français
Authors
Y. Jiao, Y. Yu, B. Li, Y. H. Yu
Lab
Tianjin Medical University General Hospital, Tianjin, China
Journal
Chinese Journal of Contemporary Neurology and Neurosurgery
Abstract
Objective
To investigate the effect of hydrogen on streptozotocin (STZ)-induced diabetic rat models with peripheral neuropathy and explore the possible mechanism.
Methods
Eighteen male Sprague⁃Dawley (SD) rats were randomly divided into model group (N = 6), hydrogen-treated group (N = 6) and normal control group (N = 6). After fasting for 12 h, experimental diabetic rat models were established by intraperitoneal injection of STZ (65 mg/kg of single dose), while normal control group only received a same dose of citrate buffer. Diabetes was confirmed with a fasting plasma glucose more than 16.67 mmol/L 48 h after STZ injection. After diabetic models were established successively, hydrogen-rich saline (5 ml/kg) was administered by intraperitoneal injection in hydrogen-treated group daily in 7th and 8th week after diabetes induction. Corresponding model and normal control groups received a same dose of normal saline. Changes of sciatic function and pain behavior in rats of different groups were measured to investigate the effect of hydrogen-rich saline. Proinflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and nuclear factor-kappaB (NF-κB) p65 expression were then determined to clarify the possible mechanism of hydrogen-mediated protection.
Results
1) Compared with normal control group, body weight in model group decreased significantly, while plasma glucose levels increased significantly (P = 0.000, for all) 8 weeks after STZ induction. Hydrogen did not show any effects on body weight and plasma glucose levels of treated rat models in comparison with model group (P = 0.256, 0.821). 2) Compared with normal control group, motor nerve conduction velocity (MNCV), heat pain threshold (HPT) and mechanical withdrawal threshold (MWT) decreased significantly in model group (P = 0.000, for all), but increased significantly in hydrogen-treated group when compared with model group in the 8th week (P = 0.000, for all). 3) Hydrogen also reduced the positively expressed cells of NF-κB p65 (P = 0.000) as well as levels of TNF-α and IL-6 (P = 0.000, for all).
Conclusion
Inflammation may participate and exaggerate painful diabetic neuropathy. Besides, hydrogen has the protective potential of ameliorating neuroinflammation and peripheral nerve injury by suppressing NF-κB pathway and its downstream inflammatory cytokines.
BIOSEB Instruments Used:
Electronic Von Frey 4 (BIO-EVF4),Electronic Von Frey 5 with embedded camera (BIO-EVF5)
