Figure 4.

Effects on curcumin or its formulations at the behavior, electrophysiology/histopathology, and molecular levels in peripheral neuropathic and postoperative pain. I. Behavior: Curcumin or its formulations inhibit or reduce DPN (1), CIPN (2), alcoholic neuropathy (3), different peripheral injuries, such as CCI, SNC, SNI, SNL, etc., and/or postoperative pain-induced behaviors in rodent models. Curcumin and its formulations mainly inhibit or reduce mechanical (6A), cold (6B), heat (6C), and chemical-induced (6D) pain behaviors, as well as motor deficits (6E). II. Electrophysiology/Histopathology: Curcumin or its formulations protect injured DRG, decrease neuronal excitability in DRG (1), resulting in attenuation of painful neuropathic behavior. Curcumin or its formulations increase SNCV, decrease loss of DRG neurons, and increase diameter of nerve fibers (2). Furthermore, curcumin and its formulations increase MNCV, decrease neurogenic lesions (3), and atrophy of gastrocnemius muscle (4). The treatments also effectively increase myelin sheath thickness (5A) and prevent demyelination (5B). III. Molecular: Curcumin or its formulations decrease expression of NF-κB, leading to decrease in inflammatory proteins. Furthermore, the treatments increase expressions of Nrf2, leading to increase in levels of antioxidative enzymes that scavenge free radicals and ultimately reduce ROS levels. Moreover, the treatments decrease expressions of Bcl-2 and caspase-3 that lead to reduction in apoptosis and ultimately improve nerve injuries (created with BioRender).