Skip to main content
. 2022 Oct 28;23(21):13074. doi: 10.3390/ijms232113074

Table 1.

The proposed neuroprotective mechanisms of caffeine after in-vivo animal exposure to neurotoxic compounds.

Neurotoxic Compound Animal Species Caffeine Dose (mg/kgbw) Proposed Mechanisms Consequences References
d-galactose Rats 3 ↓ COX-2, NOS-2, TNF-α, and IL-1β Reduction of OS-mediated neuroinflammation and cognitive dysfunction. [52]
AlCl3 Rats 1.5 ↑ BDNF
↑ Nrf2
Reduction of OS-mediated neuroinflammation and apoptotic neuronal cell loss. [56]
LPS Mice 3 ↑ Nrf2/HO-1
↑ TRL4
Reduction of OS-mediated neuroinflammation and synaptic dysregulation. [54]
LPS Mice 40 Modulation of glutamatergic neurotrasmition Reduction of activated microglia and OS-mediated neuroinflammation. [57]
Cd Mice 30 ↑ Nrf2/HO-1 Reduction of OS-mediated neuroinflammation and cognitive dysfunction. [53]
MPTP Mice 10 Modulation of glutamatergic neurotrasmition Neuroprotection. [58]
6-HODA Rats 10 or 20 ↓ TNF-α/IL-1β Neuroprotection. [59]

COX-2 (cyclo-oxygenase-2), NOS-2 (nitric oxide synthase-2), OS (oxidative stress), TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β), BDNF (brain-derived neurotrophic factor), Nrf2 (nuclear erythroid 2-related factor), HO-1 (heme oxygenase-1), LPS (lipopolysaccharides), TLR 4 (Toll-like receptor 4), MPTP (1-methyl-4-phenyl-1,2,3,6 tetra-hydropyridine), 6HODA (6 hydroxydopamine).