myloid plaques and microgliosis in the brain of Alzheimer’s mice fed
with GSE were also reduced by 49% and 70%, respectively
Curcumin also significantly reduced brain Aβ burden and microglia
activation
polyphenol-rich GSE prevents the Aβ deposition and attenuates the inflammation in the brain of a
transgenic mouse model, and this thus is promising in delaying development of AD.
Our results indicate that long-term EGCG treatment attenuated the development of obesity, symptoms associated with the metabolic syndrome, and fatty liver. Short-term EGCG treatment appeared to reverse preexisting high-fat-induced metabolic pathologies in obese mice. These effects may be mediated by decreased lipid absorption, decreased inflammation, and other mechanisms.
cancer stem cells may also contribute to tumor formation, metastasis, and treatment resistance
Studies have shown that some agents (such as metformin) can selectively target cancer stem cells and that dietary polyphenols, curcumin, peperine, and sulforaphane, which are derived from broccoli/broccoli sprouts, are able to target breast cancer stem cells via inhibition of the Wnt signaling, which affects mammosphere size and colony formation
niclosamide inhibits tumor growth and reduces tumor weight
Niclosamide treatment inhibited the expression of cyclin D1, Hes1, and PTCH by 33%, 57%, and 79%, respectively
The mechanism via which niclosamide, a protonophoric anthelmintic drug, induces stem-like-cell-specific toxicity in breast cancer is interesting. It is an old drug that has been used to treat tapeworms in animals
Niclosamide is known to uncouple mitochondrial oxidative phosphorylation during tapeworm killing
A screening of autophagy modulators revealed that niclosamide is a novel inhibitor of mTORC1 signaling
A recent work also demonstrated that niclosamide induces the apoptosis of myelogenous leukemic cells via the inactivation of NF-kappaB and reactive oxygen species generation
Niclosamide was also reported to inhibit Wnt signaling [31]–[33] in colon cancer cells
Our recent work demonstrated that niclosamide disrupts multiple metabolic pathways in ovarian-cancer-initiating cells
The present study showed that niclosamide treatment resulted in the downregulation of target genes involved in the self-renewal of cancer stem-like cells and inhibited breast SPS