| dc.description.abstract | AIM: Ozone, which hastherapeutic effect in many pathologies, partially prevented diabetic neuropathy in ratsin our previousstudy. In
the present study, it was investigated that the mechanisms mediating the neuroprotective effects of ozone in diabetic neuropathy.mly
divided into 6 groups (n=7): control (C), ozone (O), diabetic (D),
ozone-treated diabetic (DO), insulin-treated diabetic (DI), and
ozone- and insulin-treated diabetic (DOI). Diabetes was induced by
a single injection of streptozotocin (60mg/kg, i.p.), after which insulin was administered (3 IU, i.p., once a day) to the DI and DOI groups for 6 weeks, and 1.1mg/kg (50µg/ml, i.p., once a day) ozone
was given to the O, DO, and DOI groups for 6 weeks. 6 weeks after
the induction of diabetes, the electrophysiological, biochemical and
histopathological tests were made. Data were analysed using the
one way ANOVA and post hoc Tukey tests. p<0.05 was considered
statistically significant.
RESULTS: While the blood glucose, HbA1c, plasma total oxidantstatus, oxidative stressindex and apoptotic cell number of the D group
were significantly higher than the C and O groups, the same values
of DO, DI and DOI groups were significantly lower than the D group.
While the nerve conduction velocity, amplitude of compound action potential, axon number and endoneural capillary number of
the D group were significantly lower than the C and O groups, the
same values of DO, DI and DOI groups were significantly higher than
the D group.
CONCLUSIONS: Consistent with previous studies, ozone reduced
the blood glucose and HbA1c levels, and partially prevented diabetic neuropathy in this study. These findings indicate that the neuroprotective effect of ozone in diabetic neuropathy are mediated
through oxidative stress, vascular and apoptotic mechanisms. We
believe that ozone, as a potential therapeutic agent for diabetic
neuropathy, a focus on ozone and a molecule to be investigated in
detail | en_US |
