Pre- and post-traumatic boric acid therapy prevents oxidative stress-mediated neuronal apoptosis in spinal cord injury

Spinal cord injury (SCI) is a serious neurological problem that affects society physically, psychosocially, and economically. After SCI, increased ROS formation and also this imbalance between free radicals and antioxidants leads to the formation of oxidative stress, especially in lipids, proteins, and nucleic acids. Boric acid (BA) shows Lewis acid properties, forms complexes with glycoproteins and glycolipids containing hydroxyl groups, and has Ca+ chelator properties. It also has antioxidant, antiapoptotic, and anticancer properties as well as oxidative stress-reducing properties

• 1
  After SCI, oxidative stress markers, such as MDA, TOS, and OSI, and apoptosis markers Cytc and Casp3 showed an increase in levels compared to Group C.
• 2
  The oxidative stress markers that increased after SCI decreased with BA+SCI application, while Cytc level, one of the apoptosis markers that increased after SCI, decreased in both groups with BA application.
• 3
  Cell, myelin, ependymal damage, and hemorrhage levels increased after SCI compared to Group C. These histological markers increased after SCI and decreased after BA+SCI.