Anti-oxidative and anti-inflammatory effects of cinnamaldehyde on protecting high glucose-induced damage in cultured dorsal root ganglion neurons of rats

Chin J Integr Med. 2016 Jan;22(1):19-27. doi: 10.1007/s11655-015-2103-8. Epub 2015 Nov 17.

Abstract

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-κB), inhibitor of κB (IκB), phosphorylated IκB (p-IκB), 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-κB activity. The western blot assay results showed that the HG-induced elevated expressions of NF-κB, IκB and p-IκB 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-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-κB pathway but not through activation of Nrf2/HO-1. And thus cinnamaldehyde may have potential application as a treatment for DPN.

Keywords: cinnamaldehyde; dorsal root ganglion; high glucose; nuclear factor erythroid 2-related factor 2; nuclear factor-kappa B.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acrolein / administration & dosage
  • Acrolein / analogs & derivatives*
  • Acrolein / pharmacology
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Apoptosis / drug effects
  • Blotting, Western
  • Caspase 3 / metabolism
  • Cell Survival / drug effects
  • Cells, Cultured
  • Ganglia, Spinal / drug effects
  • Ganglia, Spinal / metabolism
  • Ganglia, Spinal / pathology*
  • Glucose / toxicity*
  • Heme Oxygenase (Decyclizing) / metabolism
  • I-kappa B Proteins / metabolism
  • Interleukin-6 / metabolism
  • NF-E2-Related Factor 2 / metabolism
  • NF-kappa B / metabolism
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology*
  • Neuroprotective Agents / pharmacology*
  • Oxidation-Reduction / drug effects
  • Phosphorylation / drug effects
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • I-kappa B Proteins
  • Interleukin-6
  • NF-E2-Related Factor 2
  • NF-kappa B
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Acrolein
  • Heme Oxygenase (Decyclizing)
  • Caspase 3
  • Glucose
  • cinnamaldehyde