Table 1.
Summary of in vivo studies on the neuroprotective effects of caffeic acid.
| Animals | Model | Treatment | Main Outcomes | Ref. |
|---|---|---|---|---|
| Male Wistar rats | Aluminum-mediated neurotoxicity | 100 mg/kg (p.o.)—11 days | (1) Improved memory; (2) decreased AChE, CAT, and GST action; (3) decreased GSH and nitrite levels | (206) |
| Wistar rats | 10–100 mg/kg (p.o.)—30 days | (1) Recovered learning and memory; (2) reduced AChE action in cerebral cortex and striatum; and (3) enhanced AChE action in the cerebellum, hippocampus, and hypothalamus | (205) | |
| Wistar rats | Streptozotocin-mediated dementia | 10–40 mg/kg (p.o.)—21 days | (1) Attenuation of the streptozotocin-mediated learning and memory destructions; (2) enhancement in AChE action; (3) enhancement in MDA, nitrite, and protein carbonyl levels; and (4) reduction in the GSH level | (207) |
| Wistar rats | Pilocarpine-mediated seizures | 4 mg/kg (i.p.) 30 min before pilocarpine injection | (1) Anticonvulsant-like effect, (2) reduced LPO level and nitrite content, (3) enhanced SOD and CAT action | (197) |
| Fisher rats | Kainic acid-mediated neurotoxicity | 50 mg/kg (i.p.) 4 injections | (1) Extended latency to seizures, (2) decreased neuronal loss in CA3 hippocampal field | (208) |
| Male Wistar rats | Quinolinic acid-mediated neurotoxicity | 5 and 10 mg/kg (p.o.)—21 days | (1) Enhancement of locomotor action and motor coordination, (2) repaired redox status in the striatum | (209) |
| CF1 mice | Pilocarpine- and pentylenetetrazole-mediated seizures |
4 and 8 mg/kg (i.p.) 30 min before seizure induction | (1) No anticonvulsant-like effect, (2) defense against pilocarpine-mediated genotoxic injury in the hippocampus | (210) |
| Sprague–Dawley rats | Focal cerebral ischemia/reperfusion injury | 50 mg/kg (i.p.) 30 min before ischemia induction and 0, 1, 2 h | (1) Decline of neurological deficits, (2) reduced neuron loss, infarct volume, brain atrophy, and astrocyte proliferation, (3) blockage of leukotriene making | (124) |
| Sprague–Dawley rats | Cerebral ischemia/reperfusion injury | 50 mg/kg (i.p.) instantly after ischemia induction and then frequently for 12 h | (1) Enhanced neurological deficit scores, (2) decreased infraction volume, (3) reduced 5-LOX | (211) |
| C57BL/6J mice | Rotenone-mediated neurotoxicity | 50 mg/kg (p.o.) for 1 week before rotenone exposure, and then 5 days |
(1) Inhibited degeneration of dopaminergic neurons in substantia nigra, (2) more regulated metallothionein-1 and 2 in striatal astrocytes | (212) |
| C57BL/6 mice | MPTP-mediated neurotoxicity | 0.5–2% in the diet—4 weeks | (1) Reduced inflammatory cytokines levels; (2) repressed NO, prostaglandin E2, and GFAP making; (3) preserved BDNF, GDNF, and tyrosine hydroxylase levels; (4) better synthesis of dopamine | (200) |
| Sprague–Dawley rats | LPS-mediated neurotoxicity | 50 mg/kg (p.o.) 10.5, 5.5, and 0.5 h before LPS injection | Attenuation of LPS-mediated failure of dopaminergic neurons and microglial activation in the substantia nigra | (213) |