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. 2022 Oct 5;13:988836. doi: 10.3389/fphar.2022.988836

FIGURE 8.

FIGURE 8

Potential molecular mechanisms underlying the neuroprotective action of resveratrol against cerebral I/R injury. AMPK, AMP-activated protein kinase; Arc, Activity-regulated cytoskeleton-associated; ARE, antioxidant response element; Bax, bcl-2-associated x; Bcl-2, b-cell lymphoma-2; BDNF, brain derived-nerve neurotrophic factor; CD31, platelet and endothelial cell adhesion molecule 1; CREB, cyclic-AMP response element binding protein; ERK, extracellular signal-regulated kinases; G6-PD, glucose 6-phosphate dehydrogenase; GSH, glutathione; HO-1, heme oxygenase 1; Hsp70, heatshockprotein70; IL-1β, interleukin-1beta; IL-6, serum interleukin-6; JAK, janus kinases; Keap l, Kelch-like ECH-associated protein 1; LC3, light chain 3; LDH, lactate dehydrogenase; LPO, lipid peroxidation; MDA, malondialdehyde; MT, metallothionein; mTOR, mammalian target of rapamycin; NF-κB, nuclear factor-κB; NLRP3, NOD-like receptor thermal protein domain associated protein 3; Nrf2, nuclear factor erythroid 2-related factor 2; p62, sequestosome-1; PI3K, phosphoinositide 3-kinase; PSA-NCAM, Polysialylated-Neural Cell Adhesion Molecule; RES, resveratrol; ROS, reactive oxygen species; Sirt1, silent mating type information regulation 2 homolog 1; STAT3, signal transducers and activators of transcription 3; SOD, superoxide dismutase; TrkB, tyrosine kinase receptor B; TLR4, Toll-like receptor 4; TNF-α, tumor necrosis factor-α; UCP2, uncoupling protein 2.