Background: Diabetic peripheral neuropathy (DPN) is a common complication of
diabetes with a complex pathogenesis. Study has reported that oxidative stress and nitrative
stress are all involved in the DPN. However, the mechanism between them is still unclear. In the
present study, we investigated whether miR-106a regulated 12/15-Lipoxygenase (12/15-LOX) of
oxidative/nitrative stress (OS/NS) in DPN.
Methods: Dorsal root ganglion (DRG) was isolated from 10 healthy mice and 10 DPN mice. DPN
mouse model was established by the injection of streptozotocin (STZ), and high glucose was used
for inducing the in vitro model of DPN.
Results: In DPN mice, the levels of fasting blood-glucose (FBG) level, Methane Dicarboxylic
Aldehyde (MDA) and the Inducible Nitric Oxide Synthase (iNOS) were increased, while the levels
of motor nerve conduction velocity (MNCV), sensory nerve conduction velocity (SNCV) and
superoxide dismutase (SOD) were decreased. MiR-106a level in DRG cells of DPN was decreased.
The 12/15-LOX expression and cell apoptosis were increased. DRG cells subjected to high
glucose resulted in the same effects as above. MiR-106a was observed to target 12/15-LOX and
regulated its expression. MiR-106a overexpression reversed the effect that was induced by high
glucose, however, overexpression of 12/15-LOX reversed the effect that was induced by miR-106a
Conclusion: MiR-106 may be associated with 12/15-LOX mediated OS/NS in DPN and may be
considered as a potential therapeutic target.