[Effects of N-acetylcysteine upon methylglyoxal-induced damage in hippocampal neuronal cells].

OBJECTIVE

To explore the effects of N-acetylcysteine (NAC) upon the methylglyoxal (MG)-induced injury of hippocampal neuronal cells.

METHODS

Primary cultures of 1-day-old SD rat hippocampal neuron were exposed to MG and/or NAC for 24 h respectively. Apoptosis was quantified by flow cytometer using annexin V-FITC and propidium iodide (PI) staining. The level of intracellular reactive oxygen species (ROS) was measured by an oxidant-sensitive dye 2,7-dichlorofluorescin diacetate (DCFH). The protein and mRNA levels of BDNF and TrkB were assayed with Western blot and real-time reverse-transcription polymerase chain reaction (RT-PCR) respectively.

RESULTS

After a 24 h cell incubation with 100 micromol/L MG, the ratio of apoptotic cells in MG group (8.80 +/- 0.31)% significantly increased versus the control group (1.60 +/- 0.15)% and MG+NAC group (4.83 +/- 0.31)% respectively. The level of intracellular oxidation of MG group (10 229 +/- 946) also significantly increased versus the NAC group (2118 +/- 320), control group (4265 +/- 82), MG + NAC group (3886 +/- 415) and pretreated NAC + MG group (2997 +/- 606). MG increased the cellular levels of BDNF but decreased the TrkB mRNA and protein expression significantly. However, NAC significantly decreased the BDNF and increased the TrkB mRNA and protein expression in rat hippocampal neuron after MG induction. All these differences were considered statistically significant.

CONCLUSION

MG-induced neurotoxicity in hippocampal neurons is mediated by oxidative stress and it can impair the BDNF/TrkB signal pathway. Antioxidant NAC has protective effect upon MG-induced neurotoxicity through its antiapoptotic action and its antioxidant effect on ROS level. And it works partly by activating the BDNF/TrkB signal pathway.