Animal models | EGCG dose and route | Effects | Ref |
---|---|---|---|
Tg2576 APP mice | 20 mg/kg daily for 4 months (oral gavage) | EGCG impaired Aβ formation by inhibiting APP proteolysis and by inhibiting cAbl/FE65 complex nuclear translocation and GSK3 activation. | [20] |
Swedish mutant APP-overexpressing mice (Tg APPsw line 2576) | 20 mg/kg (intraperitoneally) | EGCG induced APP processing with reduction of cerebral amyloidosis. | [24] |
APP transgenic mice | 20 mg/kg/day, for 3 months (oral gavage) | Aβ deposits were reduced by 60% in the frontal cortex and 52% in the hippocampus. | [31] |
AD mouse model | Nanolipidic particles loaded with EGCG | Improved the bioavailability and α-secretase activity induced by EGCG. | [32] |
Tg2576 mice | Fish oil (8 mg/kg/day) and EGCG (oral gavage, 62.5 mg/kg/day or 12.5 mg/kg/day) | Fish oil enhanced bioavailability of EGCG versus EGCG treatment alone. Synergetic effect of Fish oil and EGCG on the inhibition of cerebral A β deposits. | [33] |
Wistar rat model of dementia | 10 mg/kg/day for 4 weeks, oral gavage. ICV infusion of STZ (3 mg/kg) | EGCG completely abrogated the cognitive deficit, S100B content in the hippocampus, AChE activity, glutathione peroxidase activity, NO metabolites, and ROS content | [34] |
ICR mice model of systemic inflammation | 1.5 and 3 mg/kg for 3 weeks (Oral gavage). LPS (250 μg/kg) intraperitoneal | EGCG prevented LPS-induced memory impairment, apoptotic neuronal cell death, and microglia activation | [19] |
AD mouse model induced by D-gal | 2 mg/(kg/ day) or 6 mg/(kg/day) for 4 weeks, oral gavage | EGCG decreased the expression of APP and beta-Amyloid in the hippocampus of mice. | [35] |
APP/PS1 mice | 2 mg/(kg/day) or 6 mg/(kg/day) for 4 weeks, oral gave | EGCG treatment inhibited TNF-α/JNK signaling, increased the phosphorylation of Akt and glycogen synthase kinase-3β. | [37] |
SAMP8 mice | 5 and 15 mg/kg, for 60 days, intragastric | EGCG induced reduction in Aβ accumulation and increased NEP expression | [28] |