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Curcumin is a natural compound with potency of anticancer. It is currently under clinical investigation for cancer chemoprevention. There is a variety of biochemical mechanisms of this anticancer function. The targets of Curcumin are involved in signaling pathways include transcription factors, growth factors,
inflammatory cytokines, receptors, and enzymes. Phase I trials have tested the toxicity and tolerability of Curcumin and found that Curcumin has no toxicities at doses up to 12 g/day. However, the bioavailability of Curcumin is quite poor. It is about ~1% after oral administration in phase I/II clinical trials and this hinders Curcumin‘s use in the clinic [2].
It is also reported that Curcumin reduces the generation of amloid beta (Aβ 40 and Aβ42) in SH-SY5Y neuroblastoma cells. It also down-regulates the expression of PS1 and GSK-3β in cells. All these cause the inhibition of Aβ formation and make Curcumin to be a potent therapeutic agent in AD [3].
References:
[1] Sachiko Shirota, Kouji Miyazaki, Ritsuo Aiyama, Minoru Ichioka and Teruo Yokokura. Tyrosinase inhibitors from crude drugs. Biol. Pharm. Bull. 1994, 17 (2): 266-269.
[2] Wungki Park, A.R.M Ruhul Amin, Zhuo Georgia Chen, and Dong M. Shin. New perspectives of curcumin in cancer prevention. Cancer Prev Res (Phila). 2013, 6(5): 387–400.
[3] Zhang Xiong, Zhang Hongmei, SiLu, LiYu. Curcumin mediates presenilin-1 activity to reduce β-amyloid production in a model of Alzheimer’s disease. Pharmacological Reports. 2013, 63: 1101-1108.
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