Abstract
Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) is a is an important consituitents present in Curcuma longa L (turmeric) rhizome. It is also a lipophilic molecule that rapidly permeates cell membrane. Curcumin has been used as pharmacological traditional medicinal agent in Ayurvedic medicine for similar to 6000 years. Being chemopreventive agent, curcumin has been found to modulate multiple molecular pathways through several mechanisms, e.g. induction of apoptosis, inhibition survival signals, and prevention from reactive oxidative species (ROS). Curcumin significantly caused reduction in lung cancer stem cells markers (CD133, ALDHA1, CD44, Nanog, and Oct4) and the number of CD133-positive cells as well as efficiently decreased the tumorsphere formation, inhibited proliferation, and induced apoptotic cell death. It also suppressed the activation of both Wnt/beta-catenin and Sonic Hedgehog pathways. Curcumin has been also reported to diminish renal hypertrophy, reduce mesangial matrix expansion, and cause a lower level of albuminuria. It also inhibited the upregulated protein and mRNA expressions of collagen IV and fibronectin in the renal cortices as well as significantly reduced the mature interleukin-1 beta, cleaved caspase-1, and NLRP3 protein levels in the renal cortices of db/db mice as well as in HK-2 cells. It also ameliorated the defective insulin signalling pathway by upregulating insulin-like growth factor (IGF)-1R, IRS-2, PI3K, p-PI3K, Akt and p-Akt protein expression while downregulating IR and IRS-1. Besides, curcumin lowered the heart MDA and DNA fragmentation levels, increased concentration of SOD, catalase, and gluathione levels, decreased the percentage of TUNEL-positive cells and gamma H2AX protein expression, while it lowered the percentage (%) of capspase 3 positive cells and improved the percentage of Bcl-2 positive cells. The current review article presents effective role of curcumin against cancer, diabetes, oxidative stress, cardiovascular, obesity, and aging.