Resveratrol as a Therapeutic Agent for Alzheimer’s Disease

Table 2

Neuroprotective effects of resveratrol in vitro.

Cell	Exposure	Effects of resveratrol	Reference
Hippocampal slices	Glutamate treated	Downregulated ERK activation, decreased IL-1 expression, and downregulated MCP-1 in the hippocampus.	[41]
Rat cortical primary neurons	Treatment with ionomycin and H2O2	Increased SIRT1 activity and prevented cognitive decline.	[40]
Primary cortical neurons	Exposure to NMDA	Inhibited the elevation of intracellular calcium and production of ROS.	[42]
Primary hippocampal cells	A induced	Reduced A-induced cell death and decreased the phosphorylation of PKC-.	[43]
Mixed (glial/neuronal) hippocampal cells	Treated with SNP or SIN-1	Rescued hippocampal cells against NO-induced toxicity and inhibited NO generation and suppressed iNOS in LPS-activated macrophages.	[44]
Primary microglial cells	LPS-induced	Inhibit PGE2 and free radical formation and reduce LPS-mediated expression of mPGES-1 and COX-1.	[45]
Rat astroglioma C6 cells	Treated with A	Reduced NO production and iNOS expression, inhibited accumulation of PGE2, downregulated COX-2 expression, and prevented the translocation of NF-B.	[46]
RAW 264.7, BV-2, and Ba/F3 cells	Stimulated with LPS	Reduced multiple cytokines, decreased the levels of phosphorylated IKK, IB, and NF-B, inhibited STAT1 and STAT3 activation, and reduced the expression of iNOS and COX-2.	[17]
PC12 cells	A or A induced	Restored the decrease of Bcl-XL expression, inhibited the expression of Bax, blocked the activation of JNK, and suppressed the increase of NF-B DNA binding.	[47]
PC12 cells	Treated with A	Remodels A soluble oligomers and fibrillar conformers into large nontoxic aggregates.	[48]
Murine HT22 hippocampal cells and primary hippocampal neuron cells	Treated with A, MEL, and resveratrol	MEL and resveratrol inhibited the activation of ERK, reduced ROS production, rescued GSH levels, and attenuated neuronal cell death. Cotreatment exerted a synergistic effect.	[49]
APP695-HEK293 cell	Treated with A	Did not influence the APP metabolism and A production but promoted a proteasome-dependent intracellular clearance of A.	[50]
HUVEC-derived EA.hy926 cells	DMNQ-induced	Decreased the expression of Nox4 but increased the expression of SOD1 and GPx1.	[51]
SH-SY5Y neuroblastoma cells	A induced	Suppressed the extension of amyloidogenic A peptides and disaggregated A42 fibrils.	[52]
SH-SY5Y neuroblastoma cells	Treated with A complexes	Reduced the generations of A-Fe, A-Cu, and A-Zn and thus reduced their toxicity.	[2]
SK-N-SH cells	IL-1 stimulated	Reduced PGE2 and PGD2 production via the reduction of COX-2 activity.	[53]
SK-N-BE cells	TAT--syn (A30P) and A42 treatment	Inhibited the toxicity induced by TAT--syn (A30P) and A42 and SIRT1-independently reduced A42 toxicity.	[54]
APP-HEK293 and APP-N2a cell	Treated with A	Played a SIRT1-independent neuroprotective role by activating AMPK.	[55]