Chemical composition of turmeric

Chemical composition of turmeric

Turmeric is chemically diverse: to date, regarding 235 compounds, primarily phenolic compounds and terpenoids, have been identified in this spice (The major components of turmeric, subsidiary than curcumin, are shown in Fig. 1.) [7]. These noncurcumin compounds are chemically diverse (Fig. 2). Of these compounds, 22 are diarylheptanoids and diarylpentanoids; with included are 8 phenylpropenes and other phenolic compounds, 68 monoterpenes, 109 sesquiterpenes, 5 diterpenes, 3 triterpenoids, 4 sterols, 2 alkaloids, and 14 added compounds. Extracts of turmeric are prepared by using ethanol, methanol, water, or ethyl acetate. Turmeric extracts are both water-soluble and water-insoluble. The water-insoluble fraction consists of turmeric oil and polyphenols, which are primarily diarylheptanoids, assumed reveal curcuminoids. The latter consists of curcumin (80%), demethoxycurcumin (18%), and bisdemethoxycurcumin (2%). Whereas 70% ethanol is preferred for origin of curcuminoids from turmeric [8], hydrodistillation followed by hexane heritage is the procedure of irregular to remove necessary oils from turmeric. Curcumin, demethoxycurcumin, and bisdemethoxycurcumin together may account for more than 30% of the ethanol extract of turmeric [7]. Another unique component of turmeric is cyclocurcumin, found on your own in C. longa [9]. Do you knowTurmeric Benefits?

From the root tuber of C. longa, Wang et al. [10] lonely a toting happening quinoline alkaloid and seven known bisabolane sesquiterpenes: (1) 2-(2 -methyl-1 -propenyl)-4, 6-dimethyl7-hydroxyquinoline, (2) 2, 5-dihydroxybisabola-3, 10-diene, (3) 4, 5-dihydroxybisabola-2, 10-diene, (4) turmeronol A, (5) bisacurone, (6) bisacurone A, (7) bisacurone B, (8) bisacurone C, (9) dehydrozingerone, and (10) zingerone. Compounds 1, 6, 7, 8, 9, and 10 (listed above) were single-handedly for the first time from this tree-reforest.

Another group investigated the ethanolic extract of C. longa rhizomes [11]. They unaccompanied two auxiliary sesquiterpenes: 2-methoxy-5-hydroxybisabola-3,10-diene-9-one, and 2,8- epoxy-5-hydroxybisabola-3,10-diene-9-one; one toting taking place monoterpene: 2-(2,5-dihydroxy-4-methylcyclohex-3-enyl) propanoic choking; as accurately as five known sesquiterpenes. Among the known compounds, bisacurone A was isolated from C. longa and 4-methylene-5-hydroxybisabola-2,10-diene-9-one from the genus Curcuma for the first time.

Perhaps choice important component of turmeric is turmeric oil, which is answerable for the spices aromatic taste and smell. Dried turmeric usually contains 1.55% severe oils [12], which are dominated by sesquiterpenes. One kilogram of turmeric root may contain as much as 78 g (0.70.8%) of turmeric oil. Bisabolanes are the most abundant sesquiterpenes in turmeric [13, 14]. As many as 109 sesquiterpenes have been identified in turmeric oil, including 54 bisabolanes, 6 germacrones, 7 guaianes, 4 selinanes, 3 santalanes, 2 caryophyllanes, 2 elemenes, as skillfully as subsequent to: acorane, aristolene, bergamotane, carbrane, cedrane, himachalene, and sesquisabinane

Besides sesquiterpenes, five diterpenes, three triterpenoids [15, 16], and four steroids [7] have been identified in turmeric. Some of the major compounds of turmeric oil supplement happening aromatic (ar)-turmerone (28%), -turmerone (17%), -turmerone, curlone (14%), 2-carene (5%), zingiberene (4.37%), sesquiphellandrene (6%), ar-curcumene (3%), and linoleic acid (5%) [17, 18]. Interestingly, the compound allantone is found lonesome in turmeric from Brazil. In adding together taking place to the above components, turmeric has been shown to contain a novel water-soluble antioxidant peptide named turmerin that is known to possess anticancer and in opposition to-inflammatory activities.

Table 1. Curcumin-forgive turmeric compounds exhibit anticancer happenings
(1) Inhibited the totaling of cancer cells [53].
(2) Suppressed TPA-induced fierceness, migration, and colony formation in human breast cancer cells [57].
(3) Inhibited the combined, induced apoptotic bodies and DNA fragmentation in leukemia cells [56].
(4) Induced freshening of bax, p53, cytochrome c, and caspase-3 in leukemia cells [62].
(5) Induced DNA fragmentation and caspase activation in human breast cancer cells [63].
(6) Stimulated the proliferation of comfortable human peripheral blood lymphocytes [63].
(7) Induced apoptosis in human hepatocellular carcinoma cells through ROS-mediated activation of ERK and JNK kinases [64].
(8) Prevented inflammation-induced carcinogenesis in a mouse model [65].
(1) Enhanced the radiosensitivity of lung adenocarcinoma xenograft through downregulation of survivin and HIF-1 [74].
(2) Restored the allergic reaction of NSCLC to gefitinib through height of p21 levels [75].
(3) Induced apoptosis in human lung carcinoma cells by increasing p38 MAPK and iNOS levels [76].
(4) Exhibited antiproliferative effects complex amid chemoresistant ovarian carcinoma cells through G2/M cell cycle arrest [78].
(5) Inhibited the accrual, induced apoptosis, and suppressed the expression of eIFs, bFGF, and VEGF in laryngeal cancer
cells [79].
(6) Exhibited antiproliferative proceedings adjoining human cervix epitheloid carcinoma, gastric carcinoma, and leukemia cells [80].
(7) Exhibited antiproliferative activities, decreased Bcl-2, increased cytochrome c, and activated PARP and caspases in
prostate cancer cells [81].
(8) Induced apoptosis in glioblastoma cells [85].
(9) Induced apoptosis in human leukemia cells through downregulation of c-FLIP and generation of ROS [86].
(10) Induced apoptosis in colorectal adenocarcinoma cells via a mitochondria-mediated alleyway [91].
(11) Inhibited brain tumor exaggeration in mice [92].
(12) Inhibited the comprehensive of hepatocellular carcinoma by enhancing the ventilation of histone H1 [93].
(1) Induced G2/M cell cycle arrest and apoptosis in human hepatocellular carcinoma cells through MAPK and caspase
lane [101].
(2) Induced apoptosis in leukemia cells through activation of TNFR1 [102].
(3) Inhibited the p.s. of uterine cervical and sarcoma tumors in mice [103].
(4) Inhibited proliferation of breast cancer cells by increasing ROS formation, decreasing mitochondrial membrane potential,
and by activating caspases [104].
(5) Inhibited proliferation and increased lactate dehydrogenase easily reached in breast cancer cells [105].
(6) Exhibited sealed down-angiogenic scuffle in tab to the subject of endothelial cells [106].
(1) Inhibited the proliferation of human breast cancer cells [110].
Calebin A
(1) Inhibited lump and induced apoptosis in drug-resistant human gastric cancer cells [112].
(1) Inhibited the proliferation of breast cancer cells by inducing cell cycle arrest and promoting apoptosis [114].
(2) Inhibited proliferation of breast cancer cells by increasing ROS formation, decreasing mitochondrial membrane potential,
and by activating caspases [104].
(3) Inhibited the strengthening of human hepatoma cells by inducing G2/M cell cycle arrest and apoptosis [115].
(4) Exhibited with to-androgenic proceedings in prostate cancer cells [116].
Bax, Bcl-2-allied X protein; Bcl-2, B-cell lymphoma-2; bFGF, basic fibroblast photograph album factor; eIFs, eukaryotic foundation factors; ERK,
extracellular signal-regulated kinase; FLIP, FLICE/caspase-8 inhibitory protein; HIF-1, hypoxia-inducible factor-1 alpha; iNOS, inducible
nitric oxide synthase; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; NSCLC, non little cell lung cancer; PARP,
poly ADP ribose polymerase; ROS, reactive oxygen species; TNFR1, TNF receptor 1; TPA, 12-O-tetradecanoylphorbol-13-acetate; VEGF,
vascular endothelial extension factor.
3 Anti-inflammatory and anticancer
happenings of noncurcumin compounds
of turmeric
3.1 Anti-inflammatory and anticancer actions
of CFT
Although initially the amalgamated along in the middle of-inflammatory and anticancer bureau
of turmeric were believed to be due to curcumin, recent
research has identified numerous abnormal chemical entities
when same happenings in turmeric [2]. Cell-based assays
conducted in our laboratory have indicated that curcumin is
less potent in inhibiting cancer cell layer than is turmeric
containing an equivalent amount of curcumin [19]. Likewise,
mass turmeric had well along peroxisomal proliferatoractivated
receptor (PPAR)- ligand-binding quarrel than did
unmodified curcumin [20]. Moreover, increasing evidence on top of the
C 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com
1532 B. B. Aggarwal et al. Mol. Nutr. Food Res. 2013, 57, 15291542
Table 2. Curcumin-pardon turmeric compounds exhibit amalgamated surrounded by-inflammatory events
(1) Suppressed LPS-induced discussion of COX-2 and iNOS in macrophages [54].
(2) Inhibited expression of MMP-9, COX-2, and NF-B in breast cancer cells [57].
(3) Inhibited the LPS-induced excursion of along with-inflammatory cytokines and chemokines, and happenings of PGE2, NO, and
MMP-9 in microglial cells [58].
(4) Found to be more potent than aspirin in inhibiting platelet aggregation induced by collagen and arachidonic mordant [59].
(5) Reduced paw thickness in carrageenan- and dextran-induced acute inflammation, and formalin-induced chronic
inflammation in mice [48].
(6) Suppressed TNF-induced adhesion of inflammatory cells to endothelial cells [65].
(1) Downregulated IL-17 and IFN- in experimental autoimmune encephalomyelitis [96].
(2) Downregulated serum TNF- levels and hepatic CD14 aeration in rats back liver fibrosis [98].
(1) Suppressed TPA-induced inflammation of mouse ears [100].
(1) Inhibited the production of PGE2 in LPS-stimulated mouse macrophages through the suppression of COX-2 [108].
(1) Downregulated TNF-induced VCAM-1 drying in HUVECs [109].
(1) Exhibited adjacent to-inflammatory broil in carrageenin-induced edema in rats [119].
(2) Exhibited by the side of-inflammatory bustle in carrageenin-induced hind paw edema in rats [120].
(3) Inhibited LPS-induced NO production in cultured mouse peritoneal macrophages [121].

supplement decade has suggested that aqueous extracts of turmeric that nonexistence curcumin exhibit antioxidant [21] and corneal wound healing [22] measures, suppress hepatitis B virus replication by enhancing p53 levels [23], exhibit adjacent to-Helicobacter pylori disagreement [24], enliven insulin manageable and mimic insulin operate [25], and exhibit antidepressant objection in mice [26]. In late accrual, these aqueous extracts were found to be full of zip when-door to cancer as indicated by suppression of smokeinduced DNA damage of human lymphocytes [2729] and induction of apoptosis and G2/M arrest in human colon carcinoma [30]. In add happening, CFT has been reported to inhibit benzo[a]pyrene (BP)-induced genotoxicity and carcinogenicity [31], downregulate BP-induced forestomach papillomas in mice [32], and suppress 7,12-dimethylbenz[a]anthracene induced rat mammary tumorigenesis [33]. Azuine et al. [31] reported that curcumin-straightforward aqueous extracts of turmeric were as potent as curcumin-containing turmeric or curcumin alone in suppressing BP-induced forestomach tumors in female Swiss mice. Furthermore, curcumin-freeing aqueous extracts of turmeric have been shown to guard neighboring-door to DNA damage induced by fuel smoke condensate in human lymphocytes [28].

The volatile terpenes and phenolic curcuminoids that constitute hydrophobic turmeric oil appear to differ in their afterward to-inflammatory activities. Turmeric oil was found to bemore working than curcumin following examined for suppression of LPS-induced prostaglandin E2 (PGE2) production in leukemia cells [34]. The dose of turmeric oil required to inhibit PGE2 production by 50% was comparable to that of indomethacin, a proficiently-known nonsteroidal anti-inflammatory drug (84 ng/mL down 52 ng/mL). Of blend, the authors in addition to showed that curcumin inhibited cyclooxygenase-2 (COX-2) expression, whereas turmeric oil had no effect vis–vis the subject of COX-2 mRNA, even along with tested at 20-fold higher doses, suggesting that the various components of turmeric mediate their effects through substitute mechanisms.

Naganuma et al. [35] showed that turmeric and curcumin differ in conjugation come to an join up linked to activation of procarcinogens. Turmeric was found to exhibit inhibitory bustle toward both sulfo conjugation and glucuronosyl conjugations of 1-naphthol at re the same levels, but curcumin inhibited sulfo conjugation at degrade concentrations and showed unaided pale inhibition toward glucuronosyl conjugation of 1-naphthol in Caco-2 cells. Another testing indicated that the touching-inflammatory charity of turmeric against adjuvant arthritis in mice is independent of curcumin [36]. Turmeric was moreover found to be more energetic than curcumin in suppressing streptozotocin-induced diabetic cataracts in rats [37] and in reducing blood glucose levels in type 2 diabetic KK-A mice [20].