Objective:To examine the mechanism underlying the beneficial role of cinnamaldehyde on oxidative damage and apoptosis in high glucose(HG)-induced dorsal root ganglion(DRG) neurons in vitro.Methods:HG-treated DRG neurons were developed as an in vitro model of diabetic neuropathy.The neurons were randomly divided into five groups:the control group,the HG group and the HG groups treated with 25,50 and 100 nmol/L cinnamaldehyde,respectively.Cell viability was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay and apoptosis rate was evaluated by the in situ TdT-mediated dUTP nick end labeling(TUNEL) assay.The intracellular level of reactive oxygen species(ROS) was measured with flow cytometry.Expression of nuclear factor-kappa B(NF- κ B),inhibitor of k B(I κ B),phosphorylated I κ B(p-l κ B),tumor necrosis factor(TNF)-α,interleukin-6(IL-6) and caspase-3 were determined by western blotting and real-time quantitative reverse transcription polymerase chain reaction(RT-PCR).Expression of nuclear factor erythroid 2-related factor 2(Nrf2) and hemeoxygenase-1(HO-1) were also measured by western blotting.Results:Cinnamaldehyde reduced HG-induced loss of viability,apoptosis and intracellular generation of ROS in the DRG neurons via inhibiting NF- κ B activity.The western blot assay results showed that the HG-induced elevated expressions of NF- κ B,I κ B and p-l κ B were remarkably reduced by cinnamaldehyde treatment in a dose-dependent manner(P<0.01).The HG-induced over-expression of NF-k B p65 mRNA was remarkably attenuated after cinnamaldehyde treatment in a dose-dependent manner(P<0.01).However,the expressions of Nrf2 and HO-1 were not upregulated.Treatment with cinnamaldehyde not only attenuated caspase-3 activation and the caspase cleavage cascade in DRG neurons,but also lowered the elevated IL-6,TNF- α,cyclo-oxygenase and inducible nitric oxide synthase levels,indicating a reduction in inflammatory damage.Conclusions:Cinnamaldehyde protected DRG neurons from the deleterious effects of HG through inactivation of NF- k B pathway but not through activation of Nrf2/HO-1.And thus cinnamaldehyde may have potential application as a treatment for DPN. Objective: To examine the mechanism underlying the beneficial role of cinnamaldehyde on oxidative damage and apoptosis in high glucose (HG) -induced dorsal root ganglion (DRG) neurons in vitro. Methods: HG-treated DRG neurons were developed as an in vitro model of diabetic neuropathy.The neurons were randomly divided into five groups: the control group, the HG group and the HG groups treated with 25, 50 and 100 nmol / L cinnamaldehyde, respectively. Cell viability was examined by 3- (4,5-dimethylthiazol -2-yl) -2,5-diphenyltetrazolium bromide (MTT) assay and apoptosis rate was evaluated by the in situ TdT-mediated dUTP nick end labeling (TUNEL) assay.The intracellular level of reactive oxygen species (ROS) was measured with flow cytometry.Expression of nuclear factor-kappa B (NF- κ B), inhibitor of k B (I κ B), phosphorylated I κ B (pl κ B), tumor necrosis factor (TNF) -α, interleukin- IL-6) and caspase-3 were determined by western blotting and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). Expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase- 1 (HO- 1) also also measured by western blotting. Results: Cinnamaldehyde reduced HG- induced loss of viability, apoptosis and intracellular generation of ROS in the DRG neurons via inhibiting NF-κB activity. The western blot assay showed showed the the HG-induced elevated expressions of NF- κ B, I κ B and pl κ B. were remarkably reduced by cinnamaldehyde treatment in a dose -dependent manner (P <0.01). The HG-induced over-expression of NF-κB p65 mRNA was remarkably attenuated after cinnamaldehyde treatment in a dose-dependent manner (P <0.01) .However, the expressions of Nrf2 and HO- 1 were not upregulated. Treatment with cinnamaldehyde not only attenuated caspase-3 activation and the caspase cleavage cascade in DRG neurons, but also lowered the elevated IL-6, TNF- alpha, cyclo-oxygenase and inducible nitric oxide synthase levels, indicating a reduction in inflammatory damage. Conclusions: Cinnamaldehyde protectedDRG neurons from the deleterious effects of HG through inactivation of NF-κB pathway but not through activation of Nrf2 / HO-1.And therefore cinnamaldehyde may have potential application as a treatment for DPN.