Alpha lipoic acid attenuates apoptosis and oxidative stress in the dorsal root ganglion of diabetes-induced rats.

YAZĞAN, Betül; YAZĞAN, Yener; NAZIROĞLU, Mustafa

Neuropathic pain can arise from a wide variety injury to peripheral, including diabetes, and is characterized by spontaneous pain, hyperalgesia and allodynia which can persist long after the initial injury is resolved. Oxidative stress has been linked to cell death and neuropathic pain (Kahya et al. 2017). Alpha lipoic acid (ALA) has been considered a potent antioxidant that detoxifies a variety of reactive oxygen species in diabetes. As a sulfur containing substance, ALA is containing sulfur groups and it is a member of thiol cycles. A results of recent study indicated involvement of oxidized-thiol groups on activation of several channels such as TRPA1 and TRPV1 in neurons (Ogawa et al. 2016). In order to better characterize the actions of ALA in the peripheral pain, we tested the effects of ALA on apoptosis and oxidative stress and in the DRG neuron of streptozotocin (STZ)-induced Wistar Albino rats were randomly 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 confocal microscope analyses, we observed modulator role of ALA on apoptosis (Annexin V and propidium iodide), caspase 3, caspase 9, mitochondrial depolarization and cytosolic ROS production values in the DRG neurons. 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.

OXIDATIVE stress; APOPTOSIS; DIABETES; OXIDATION-reduction reaction; REACTIVE oxygen species

Journal of Cellular Neuroscience & Oxidative Stress, 2018, Vol 10, Issue 2, p724

2149-7222

Academic Journal