Fig. 7. Schematic representation of the mechanisms by which OPC mitigates LPS-induced renal tubular injury.
LPS shows significant toxicity in renal tubules, which is attenuated by OPC. LPS inhibits the phosphorylation of PI3K/AKT, which causes the activation of downstream apoptosis-related signaling molecules and accelerates cell death. It also stimulates the NFκB signaling pathway, increases the production of inflammatory cytokines, and aggravates the inflammatory response. OPC reverses these alterations. Additionally, OPC mitigates LPS-induced oxidative stress injury by recovering SOD activity, CTA activity, GSH content, and inhibiting the overproduction of MDA. OPC, oligomeric proanthocyanidin; LPS, lipopolysaccharide; NFκB, nuclear factor κB; GSH, glutathione; SOD, superoxide dismutase; CTA, catalase; MDA, malondialdehyde; TNF-α, tumor necrosis factor-alpha; IL-1β, interleukin-1 beta; IL-6, interleukin-6; IL-10, interleukin-10; ROS, reactive oxygen species.
© Korean J Physiol Pharmacol
