Effects of alpha lipoic acid on TRPV1 cation channel in dorsal root ganglion of diabetes-induced rats

Authors : Yener YAZĞAN

Pages : 796-796

Doi:10.37212/jcnos.610159

View : 21 | Download : 10

Publication Date : 2018-08-18

Article Type : Conference Paper

Abstract :Diabetes is a common chronic metabolic disease  worldwide. It causes diabetes, tissue degenerations, cell  death and associated functional disability. Diabetes also  causes the development of common diseases such as  cardiovascular and nervous diseases. The most  important pathophysiological mechanisms that are  accepted in describing diabetic degenerative processes  are oxidative stress damage insert ignore into journalissuearticles values(El-Refaei et al. 2014);.  Neuropathic pain is induced by several factors including  inflammation, excessive Ca2+ influx, oxidative stress  and tissue degeneration. Inflammatory reactions in  destroying neurons lead to the activation of the pain  molecular pathway. In addition, destruction cell  membranes induce excessive Ca2+ entry in the neurons,  because the Ca2+ concentration is about 10.000 times  higher in out of the neurons than in the inside of the  neuron. Overload Ca2+ influx into cytosol and it leads to  excessive production of ROS in the neurons. Alpha  lipoic acid insert ignore into journalissuearticles values(ALA); is an important member of the thiol  cycle because it is containing the sulfur groups. It is  powerful antioxidant substance and it can prevent the  complications of diabetes insert ignore into journalissuearticles values(Ghibu et al. 2009);. Transient  receptor potential insert ignore into journalissuearticles values(TRP); channels have six subfamilies  and 28 members in human. Most of these channels are  responsible in dorsal root ganglia insert ignore into journalissuearticles values(DRG); neurons for the  Ca2+ permeation especially in neuronal cells. Expression  level of the TRPV1 channels is high in the DRG  neurons and they show oxidative stress dependent  activation. The TRPV1 channel expression levels in the  DRG increased in different types of pain.  Forty female rats were divided into four groups:  First group was used as control. Second group used as  diabetic. Third and fourth groups received ALA and  STZ+ALA, respectively. Diabetes was induced using a  single dose of intraperitoneal STZ. On 14th day of DRG  samples were freshly taken from all animals. In plate  reader analyses, we observed modulator role of ALA on  apoptosis, caspase 3, caspase 9, mitochondrial  depolarization and cytosolic ROS production values on  TRPV1 channel in the DRG neurons. In addition, we  observed modulator role of ALA on intracellular Ca2+  concentration through inhibition of TRPV1 in  neuropathic pain-induced rats.  In conclusion, in our diabetes experimental model,  oxidative stress are involved in the Ca2+ entry-induced  neuronal death, and modulation of this channel activity  by ALA pretreatment may account for their  neuroprotective activity against apoptosis.
Keywords : Apoptosis, Oxidative stress, Alpha lipoic acid, Diabetes