Endoplasmic reticulum stress is a results of damage endoplasmic reticulum and resultant endoplasmic reticulum stress lead to abnormal ion channel function, gene expression, transcriptional regulation, metabolism and protein folding. Endoplasmic reticulum condition produced by variety of adverse stimulation such as predominantly hyperglycemia, production and accumulation of ROS and many type of inflammatory factors. Recent research also show that ER stress regulated by using chemical molecular chaperons, such as 4-Phenylbutyric acid (4-PBA) which is attenuate cell damage and produce cytoprotection, although the precise mechanism involved in this process is unclear and may be related to indirect inhibition of oxidative stress. In this work, we verified the hypothesis that 4-PBA could attenuate voltage gated sodium channels in dorsal root ganglion with hyperglycemia (diabetic neuropathy). In addition, we explored the underlying molecular mechanisms involved by investigating whether oxidative stress is inhibited through down-regulation of ER stress and whether inflammation is suppressed through the attenuation of ER stress and oxidative stress by
Endoplasmic reticulum stress is a results of damage endoplasmic reticulum and resultant endoplasmic reticulum stress lead to abnormal ion channel function, gene expression, transcriptional regulation, metabolism and protein folding. Endoplasmic reticulum condition produced by variety of adverse stimulation such as predominantly hyperglycemia, production and accumulation of ROS and many type of inflammatory factors. Recent research also show that ER stress regulated by using chemical molecular chaperons, such as 4-Phenylbutyric acid (4-PBA) which is attenuate cell damage and produce cytoprotection, although the precise mechanism involved in this process is unclear and may be related to indirect inhibition of oxidative stress. In this work, we verified the hypothesis that 4-PBA could attenuate voltage gated sodium channels in dorsal root ganglion with hyperglycemia (diabetic neuropathy). In addition, we explored the underlying molecular mechanisms involved by investigating whether oxidative stress is inhibited through down-regulation of ER stress and whether inflammation is suppressed through the attenuation of ER stress and oxidative stress by