Figure 5: Possible effects of VPA on the kidney inflammation that is induced by ischemia-reperfusion injury. Acute kidney injury (AKI) following ischemia-reperfusion injury (IRI) leads to tubular epithelial cell (TEC) dysfunction, necrosis, and endothelial activation, which in turn induces the production of proinflammatory cytokines and infiltration of inflammatory cells into the kidney, in addition to an increase in the expression of cytokines and chemokines. This autoamplification loop of inflammation and tubular damage leads to an extension of kidney damage, despite the interruption of ischemia. In the IRI model, valproic acid (VPA) attenuated kidney dysfunction and acute tubular necrosis. These findings were associated with a marked decrease of macrophage and T-cell infiltration and proliferative activity and an inhibition of proinflammatory cytokines and chemokines (TNF-α and MCP-1).