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. 2023 May 9;25(6):300. doi: 10.3892/etm.2023.11999

Figure 3.

Figure 3

Potential mechanisms of proanthocyanidins in treatment of HSP. Proanthocyanidins inhibit TLR4/MyD88/NF-κB signaling to arrest OS by eliminating oxidants such as ROS, MDA and NO, accompanied by an increase of antioxidants, such as HO-1, SOD and GSH. By inhibiting the TLR4/MyD88/NF-κB pathway, proanthocyanidins cause a decrease in Th2/Th17 cells and an increase in the Treg cells, which inhibits release of inflammatory factors (IL-1, IL-6, IL-4, IL-6, IL-17, IL-21, LTB4 and TNF-α), activation of B cells and antibody production, facilitating immune homeostasis. The aforementioned alterations improve the vascular endothelial function and vessel integrity, thereby potentially contributing to control of HSP. HSP, Henoch-Schonlein purpura; TLR4, toll-like receptor 4; MyD88, myeloid differentiation factor 88; NF-κB, nuclear factor κ-B; OS, oxidative stress; ROS, reactive oxygen species; MDA, malondialdehyde; NO, nitric oxide; HO-1, heme oxygenase-1; SOD, superoxide dismutase; GSH, glutathione; Th, T helper; Treg, regulatory T cell; IL, interleukin; TNF-α, tumor necrosis factor-α; Ig, immunoglobulin; Ɵ, suppression; ⊕, improvement; ↑↑, upregulation; ↓↓, downregulation.