Table 2. Summary of the mechanism of hesperetin in the treatment of cerebral ischemia.
| Effect | Mechanism | References |
|---|---|---|
| Anti-oxidative stress and apoptosis | Inhibit ROS, LPO, and JNK/Bax, caspase-3 | (46-50) |
| Promote Nrf2, HO-1, and Bcl-2 | ||
| Anti-atherosclerosis | Inhibit TNF-α, MCP-1, and the G0/G1 phase | (56) |
| Promote adenosine triphosphate binding transporter A1 | ||
| Anti-inflammatory reaction | Inhibit P-NF-κB, ERK1/2, and p38 MAPK | (58-60) |
| Anti-thrombosis | Inhibit PCL-2, phosphorylation, and cyclooxygenase-1 | (24) |
| Anti-hyperlipidemia | Inhibit HMG-CoA reductase and ACAT enzymes | (65) |
| Assembled lipid for carrier protein binding | ||
| Transcription of ACAT-2 mRNA | ||
| Anti-nitric oxide damage | Inhibit iNOS | (66,68) |
ROS, reactive oxygen species; LPO, lipid peroxidation; JNK, c-Jun N-terminal kinase; BAX, Bcl-2 associated X protein; Nrf-2, nuclear factor erythroid 2-related factor 2; HO-1, heme oxygenase-1; Bcl-2, B cell lymphoma-2; TNF-α, tumor necrosis factor-α; MCP-1, monocyte chemoattractant protein-1; p-NF-κB, phosphorylated -nuclear factor-kappaB; ERK1/2, extracellular signal-regulated kinase 1/2; p38 MAPK, p38 mitogen-activated protein kinase; PLC-2, phospholipase C-2; HMG CoA, 3-hydroxy-3-methylglutaryl-coenzyme A; ACAT, acyl coenzyme cholesterol acyltransferase; iNOS, inducible nitric oxide synthase.