Table 4.
Anti-apoptotic effects of Tyr.
| Cell Culture/animal | Model | Concentration/dosage | Effect/Result | Refs. |
|---|---|---|---|---|
| Primary cultures of mouse cortical neurons | CysDA (100 µM, 24 h) | 0.1–1 µM | ↑ Cortical neuron viability | [30] |
| CATH.a neuron cell | MPP+-induced cytotoxicity (100 µM – 2 mM) | 100, 200 µM | ↓Bax, caspase-3 and -9, cytochrome C in cytosol ↑ Bcl-2, Bcl-xl, and Akt-P |
[48] |
| L6 muscle cells | H2O2-induced oxidative damage | 30–100 µM | ↓ Caspase-3 level ↓ ERK1/2, JNK and p38 phosphorylation ↑ ATP, HO-1 |
[90] |
| Caco-2 cells | Oxidized LDL (0.2 g/L) treatment | 0.25–1 mM | ↓ Pro-apoptotic processes: membrane damage, modifications of cytoskeleton network, microtubular disorganization, loss of cell-cell and cell-substrate contacts, cell detachment, and cell death ↓ Overproduction and activation of p66Shc |
[91, 92] |
| HaCaT cells | UVB (250 mJ/cm2, 10 min) | 5 mM | ↓ Caspase-3, -8, -9 activity ↓ Quantity of apoptotic and necrotic cells |
[98] |
| RAW264.7 cells | LPS-stimulation (100 ng/mL) | 1.2 mM | ↓ Phosphorylation of ERK, JNK, and p38 | [114] |
| H9c2 cells | Hypoxia (95% nitrogen and 5% CO2, 1 h) / reoxygenation | 250 ìM | ↓ Cytochrome C, caspase-3 activity, and JNK activation | [126] |
MPP+, 1-methyl-4-phenylpyridinium; CysDA, 5-S-cysteinyl-dopamine.