Boric Acid Diminishes Sciatic Nerve Injury-Induced Apoptosis, Oxidative Stress, and Pain via The Block of TRPV1 Channel in Mice.

The main actors of sciatic nerve injury (SNI) are pain, apoptosis, excessive reactive oxygen species (ROS), and Ca2+ entry. However, the role of antioxidant and antiapoptotic boric acid (BoA) through TRPV1 inhibition on the actors in SNI-induced mice has not yet been elucidated. We investigated whether BoA protected the SNI actors in mice undergoing SNI. The thirty-two mice were divided into four groups: Control, BoA, SNI, and SNI + BoA. For four weeks following SNI induction, the BoA and SNI + BoA received 100 mg/kg BoA intraperitoneally. The SNI group, but not the BoA or BoA + SNI groups, indicated increases in TRPV1 current density and Ca2+ concentration induced by the TRPV1 agonist (capsaicin). The SNI + BoA group had a reduction in the increases of pain intensity (threshold of paw withdrawal and delay of thermal paw withdrawal) induced by SNI. In the brain, blood, and sciatic nerve of the SNI group, BoA and TRPV1 antagonist (capsazepine) treatments reduced the increases of mitochondrial membrane dysfunction, apoptosis, caspases (-3, -8, and -9), lipid peroxidation, mitochondrial, and intracellular ROS caused by SNI through upregulation of cell viability and antioxidants (vitamin A, vitamin E, β-carotene, glutathione, and glutathione peroxidase). In conclusion, BoA therapy reduced the rise in mitochondrial ROS, apoptosis, and Ca2+ entry in the sciatic nerve via inhibiting TRPV1. Therefore, the BoA may be a useful novel treatment through modulation of TRPV1 for oxidative stress, apoptosis, and pain produced by SNI.