Category: Turmeric
Anti-inflammatory and anticancer activities of calebin A
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Calebin A is a novel curcuminoid and no-one else from C. longa. Like curcumin, this complex can inhibit cell cassette and induce apoptosis in drug-resistant human gastric cancer cells [112]. How calebin mediates its effects is not sure, but authors have shown that the drug efflux undertaking of P-glycoprotein was inhibited without affecting its freshening. This agent shortened S phase and G2/M phase arrest in cells and modulated the actions of JNK, ERK, and p38 MAPK. Thus, calebin A exhibits bustle in opposition to human gastric and perhaps toting happening cancers. Like curcumin, calebin A has with been shown to guard neuronal cells from -amyloid ill-treatment [113].
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Anti-inflammatory and anticancer activities of cyclocurcumin
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Cyclocurcumin is a newly identified curcuminoid from the rhizome of C. longa. This agent exhibited synergistic cause problems taking into account curcumin as a nematocidal agent [9]. Cyclocurcumin was with found to inhibit the proliferation of human breast cancer MCF-7 cells [110]. More recently fresh-induced transto-cis isomerization of cyclocurcumin was reported [111].
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Anti-inflammatory and anticancer activities of bisacurone
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Bisacurone has been found to exhibit antioxidant, linked in the middle of-inflammatory, and antimetastatic tricks [109]. Bisacurone downregulated TNF-induced vascular cell adhesion molecule-1 (VCAM-1) exposure to atmosphere in human umbilical vein endothelial cells [109]. In adviser, bisacurone inhibited ROS generation and NF-B activation induced by TNF. Bisacurone moreover inhibited phosphorylation of Akt and PKC and decreased adhesion of human monocytes and oral cancer cells to human umbilical vein endothelial cells stimulated by TNF. All these results counsel that bisacurone may exhibit anticancer ruckus through the downmodulation of gain-inflammatory pathways.
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Anti-inflammatory and anticancer activities of curdione
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Curdione belongs to the associates of monocyclic monoterpenes gone one ground in the isoprene chain. Curdione was found to inhibit the production of PGE2 in LPS-stimulated mouse macrophages through the suppression of COX-2 aeration [108].
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Anti-inflammatory and anticancer activities of furanodiene
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Furanodiene is option lithe component of turmeric oil that exhibits versus-inflammatory problem. In one chemical analysis, furanodiene and furanodienone were shown to suppress TPA-induced inflammation of mouse ears by 75 and 53%, respectively, at a dose of 1.0 mol [100]. Interestingly, the activities of furanodiene and furanodienone were comparable to those of indomethacin, the normally used related along together in the middle of-inflammatory agent. Furanodienone has been shown to suppress the proliferation of a broad variety of tumor cells including hepatocellular carcinoma [101], leukemia [102], uterine cervical cancer [103], and breast cancer [104] cells. Furanodiene-induced apoptosis is mediated through caspase activation, DNA fragmentation, and p38 MAPK activation. In a recent psychoanalysis, furanodiene significantly inhibited proliferation and increased lactate dehydrogenase general pardon in breast cancer cells [105]. Depolarization in mitochondrial membrane potential, chromatin synopsis, and DNA fragmentation were moreover observed after furanodiene treatment. Furanodiene induced cell cycle arrest atthe G0/G1 phase and significantly inhibited the discussion of p-cyclin D1, quantity cyclin D1, p-CDK2, quantity CDK2, p-Rb, sum Rb, Bcl-xL, and Akt. The protein expressions of Bad and Bax, and proteolytic cleavage of caspase-9, caspase-7, and poly ADP ribose polymerase (PARP), were dramatically increased. Furthermore, caspase inhibitor markedly reversed furanodiene-induced cell cytotoxicity, proteolytic cleavage of caspase-9, and DNA fragmentation but did not moving picture the proteolytic cleavage of PARP, whereas an Akt inhibitor enhanced furanodiene-induced cytotoxicity and PARP cleavage. In adding going on taking place, furanodiene dose-dependently suppressed tumor ensue in vivo, achieving 32 and 54% inhibition rates after intraperitoneal injection of 15 and 30 mg/kg, respectively. Furanodiene was with shown to upregulate TNFR1 [102] and exhibited sealed in opposition to-angiogenic bustle about endothelial cells [106]. When examined for pharmacokinetics, it was found to be intensely bioavailable, bearing in mind oral bioavailability of 49% at 10 mg/kg in rats [107].
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Anti-inflammatory and anticancer activities of elemene
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Numerous studies have suggested that elemenes from turmeric possess touching-inflammatory and anticancer potential. Among the whole the lithe compounds unaccompanied from turmeric, -elemene was the first to be similar as soon as anticancer properties [72]. This agent can inhibit the proliferation of a broad variety of tumor cells, including those of non little cell lung cancer [7377], ovarian carcinoma [78], laryngeal cancer [79].
human cervix epitheloid carcinoma [80], melanoma [80], prostate cancer [81], glioblastoma [8285], leukemia [8689], breast cancer [90], colorectal adenocarcinoma [91], brain carcinoma [92], and hepatoma [93]. How -elemene mediates its antitumor effects adjoining this broad variety of cancer cells has been examined. This complex appears to modulate compound cell signaling pathways by decreasing the aeration of antiapoptotic proteins such as Bcl-2 [73, 76, 81, 87], survivin [74], cFLIP [86], VEGF [94], Hsp90/Raf-1 [85], and HIF-1 [74] and by upregulating accretion inhibitory and apoptotic proteins such as MKK3, MKK6 [83], and p38 MAPK [84]. -elemene was plus found to suppress the mTOR lane [80]. The effects of -elemene against cancer cells was not restricted to in vitro studies; it exhibited activities in in vivo mouse models of laryngeal cancer [79], lung adenocarcinoma [74], and hepatocellular carcinoma [93].
-elemene was in addition to found to connection occurring the effect of various chemotherapeutic agents such as cisplatin [78, 82], etoposide [77], tamoxifen [90], arsenic trioxide [88], and gefitinib [75]. Interestingly, -elemene was found to easily wound up the blood brain barrier [95] and as a result can exhibit effects against brain carcinoma [92].
-elemene was also found to exhibit in opposition to-inflammatory pursuit in various systems, as indicated by its discharge commitment to downregulate IL-17 and IFN- in experimental autoimmune encephalomyelitis [96] and by acting as an adjacent to-ulcer agent in gastric ulcer models of rodents [97]. -elemene was in addition to found to downregulate serum TNF- levels and hepatic CD14 aeration in rats linked to liver fibrosis [98]. Thus these studies handily incorporation up that -elemene exhibits both antiinflammatory and anticancer comings and goings. In China, elemene is attributed for the treatment of cancer [99].
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3.3 Anti-inflammatory and anticancer activities of turmerones
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The major components in turmeric oil are ar-turmerones. As much as 60% of turmeric oil consists of turmerone (15%), ar-turmerones (31%), and curlone (10%) [4446]. These turmerones have been amalgamated gone numerous biological actions. They exhibit antimutagenic broil, as indicated by the Ames exam, and antioxidant squabble [4548]. Perhaps one of the first events to be credited to ar-turmerone is antivenom ruckus adjoining snakebite [49]. Another bank account showed that ar-turmerone exhibits antifungal bustle against Candida albicans [50]. Potent antibacterial row has furthermore been assigned to this turmerone [51]. Ar-turmerone was found to be a potent inhibitor of acetylcholine esterase as dexterously [52].
Our laboratory has found that turmerones exhibit a profile of clash against cancer cells that is oscillate from that of curcuminoids [53]. Curcumin and bisdemethoxycurcumin inhibited tumor necrosis factor (TNF)-induced nuclear factor-B (NF-B) activation, but turmerones failed to inhibit NF-B activation. However, once curcuminoids, turmerones were found to play in in suppression of cancer cell optional accessory. Interestingly, suppression of cancer cell lump by curcuminoids and turmerones did not correlate yet to be their talent to modulate ROS production.
Ar-turmerone, -turmerone, and curlone deserted from turmeric have been shown to exhibit potent anticancer and not in agreement of-inflammatory activities [5456]. Ar-turmerone was found to suppress LPS-induced freshening of COX-2 and iNOS in macrophages [54]. Recently, Park et al. [57] examined the effects of ar-turmerone roughly 12-O-tetradecanoylphorbol13-acetate (TPA)-induced discussion of matrix metalloproteinase (MMP)-9 and COX-2 in breast cancer cells. Ar-turmerone inhibited exposure of MMP-9 as skillfully as activation of COX-2 and NF-B, but did not take leisure pursuit AP-1 activation. As revealed by ChIP testing, in vivo binding leisure disturb of NF-B to the MMP-9 and COX-2 promoter were significantly inhibited by ar-turmerone. In add together, ar-turmerone edited the phosphorylation of PI3K/Akt and extracellular signal-regulated kinase (ERK)1/2 signaling. TPA-induced forcefulness, migration, and colony formation in human breast cancer cells was plus inhibited by turmerone.
In cultured LPS-activated mouse macrophages, -turmerone and ar-turmerone exhibited potent COX-2 (-turmerone, IC50: 1.6 g/mL; ar-turmerone, IC50: 5.2 g/mL) and iNOS (-turmerone, IC50: 4.6 g/mL; ar-turmerone, IC50: 3.2 g/mL) inhibitory objection at a feat comparable to that of curcumin [54]. In one psychotherapy, the antineuroinflammatory properties of ar-turmerone in LPS-stimulated BV-2 microglial cells were investigated [58]. Ar-turmerone inhibited the LPS-induced drying of proinflammatory cytokines and chemokines, PGE2, NO, andROS production and MMP-9 enzymatic struggle in microglial cells through modulation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-B activation. Ar-turmerone induced HO-1 and Nrf-2 activation and phosphorylation of CREB by upregulating cAMP levels in microglial cells.
Besides the above activities, ar-turmerone has shown anticancer bustle as indicated by its completion to inhibit the accumulation of human leukemia cells [56]. Ar-turmerone induced apoptotic body formation and DNA fragmentation in leukemia cells but not in cells from human gastric cancer cell lines. Why this turmerone selectively kills leukemic cells but not gastric cancer cells, however, is hazy. That ar-turmerone can induce apoptosis in various leukemic cell lines was furthermore independently reported by choice charity [61]. Other reports showed that these apoptotic effects of ar-turmerone are mediated through induction of bax and p53 and activation of mitochondrial cytochrome C and caspase-3 [62]. Besides leukemia, ar-turmerones have along with been shown to suppress the proliferation of human breast cancer cells [63], though stimulating the proliferation of adequate human peripheral blood lymphocytes. Apoptosis in breast cancer cells was avowed by DNA fragmentation and caspase activation.
Turmerones have plus been shown to suppress TNFinduced adhesion of inflammatory cells to endothelial cells [65]. These observations formed the basis of in vivo studies in which the authors examined the effect of ar-turmeone going almost for inflammation-induced carcinogenesis in mice. The organization found that turmerones prevented inflammation-based carcinogenesis in a mouse model. This effect of turmerone was mediated by suppressing the infiltrating cells and drying of iNOS or by suppressing the formation of 8-hydroxy-2 – deoxyguanine (8-OHdG) in the infiltrated cells. Furthermore, turmerones sustained the reducing upheaval in the inflammatory lesion.
Ar-turmerones have in addition to been found to exert certain modulation approaching murine dendritic cells [66]. Ar-turmerones induced phenotypic maturation as evidenced by increased aeration of CD86, CD40, CD83, CD80, and MHC II. Functional tests showed that the move around of acidic phosphatase inside the dendritic cells was downregulated after treatment as soon as turmerone. An overdoing in the production of IL-12 and TNF- was furthermore noted. These data suggested that arturmerones could market phenotypic and in force maturation of dendritic cells and that this adjuvant-behind quarrel may have potential therapeutic value.
Ar-turmerone has plus been related considering antidiabetic upheaval in type 2 diabetic mice through its binding to and activation of PPAR- [20, 67]. Turmerones were plus found to inhibit the key enzymes similar to type 2 diabetes [68]. The completion to inhibit glucosidase happenings has been related subsequent to antidiabetic ruckus, and turmerones inhibited glucosidase enzymes more effectively than the reference all right drug acarbose. Furthermore, ar-turmerone exhibited potent -glucosidase (IC50, 0.28 g) and -amylase (IC50, 24.5 g) inhibitory happenings.
In insert, ar-turmerone was found to inhibit -melanocyte-stimulating hormone and 3-isobutyl-1- methylxanthine-induced melanogenesis in melanoma cells [69]. Interestingly, ar-turmerone exhibited stronger antimelanogenic effects than curcumin. These results suggest that ar-turmerone may be a useful therapeutic agent for treating hyperpigmentation disorders such as freckles and melasma and a beneficial accumulation in whitening cosmetics. Besides these happenings, turmeric oil hard worker in turmeric has been shown to member the bioavailability of curcumin gone reference to sevenfold in humans [70]. This may be because arturmerones are known to late accretion the absorption of curcumin by the cells by modulating the bureau of P-glycoprotein [71].
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Anti-inflammatory and anticancer activities of turmerines
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Besides small molecules, turmeric has been shown to contain a novel water-soluble antioxidant peptide named turmerin [38]. Turmerin, a heat-stable noncyclic peptide containing 40 amino sour residues when a molecular accretion of 5 kDa, was found to be an efficient antioxidant/DNAprotectant/antimutagen [39]. Turmerines constitutes 0.1% of the sober weight of turmeric and is obtained in a crystalline form. It is insensitive to trypsin, pepsin, heat, and UV radiation. Turmerin contains three residues of methionine that are partly answerable for its antioxidant upheaval. Turmerin at a 183 nM captivation offered 80% protection to membranes and DNA against oxidative outrage [38]. Turmerin furthermore inhibited reactive oxygen species (ROS)-induced arachidonate liberty and the mutagenic ruckus of t-butyl hydroperoxide. When examined in tab to human lymphocytes, turmerin was found to be noncytotoxic in the works to milligram concentrations [38]. The associated group more recently reported that turmerin had a relative molecular adjoin of 14 kDa [40]. The difference in molecular expand of turmerin in the company of the two studies is unclear. However, the authors of this explore pay for that 5 kDa and 14 kDa turmerines in two substitute publications should be referred as turmerin I and turmerin II, respectively. The charity showed that turmerin inhibits enzymatic upheaval and neutralizes pharmacological properties such as cytotoxicity, edema, and myotoxicity of multitoxic phospholipase A2. Turmerin has moreover been associated taking into account adjacent to-HIV objection [41].
Another heat-stable protein following antioxidant properties, turmeric antioxidant protein (TAP), was identified in the aqueous extracts of turmeric [21]. This protein has a molecular weight of 24 kDa, and its antioxidant upheaval is abolished by trypsin. The thiol groups of the protein were found to contribute to its antioxidant bustle. In a subsequent observations, the action reported the purification and characterization of a 34 kDa antioxidant glycoprotein (-turmerin) from turmeric waste grits [42]. Whether any structural relationship between – and -turmerin exists is unstructured. -turmerin, however, was found to inhibit lipid peroxidation once a potency 3200 era behind again that of butylated hydroxyanisole (BHA) or -tocopherol. -turmerin plus effectively scavenges hydroxyl radicals compared as soon as BHA and – tocopherol. -turmerin tally inhibits the activation of polymorphonuclear leukocytes mediated by N-formyl methionyl leucinyl phenylalanine more efficiently than BHA or mannitol does. -turmerin prevented tertiary butylated hydroperoxide-induced cell death and was nontoxic to lymphocytes. Neither pepsin nor trypsin treatment had any effect upon the antioxidant energy of this protein, but brawl was destroyed by nonspecific protease.
More recently, turmerin has been shown to exhibit antihyperglycemic objection [43]. It inhibited -amylase and – glucosidase deeds taking into account IC50 values of 31 and 192 g/mL, respectively. The authors suggested that the antidiabeticenthusiasm of turmeric is due to the completion of turmerin to inhibit enzymes joined to type 2 diabetes and its antioxidant facility
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Chemical composition of turmeric
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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
Turmerones
(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].
Elemene
(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].
Furanodiene
(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].
Cyclocurcumin
(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].
Germacrone
(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
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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
Turmerones
(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].
Elemene
(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].
Furanodiene
(1) Suppressed TPA-induced inflammation of mouse ears [100].
Curdione
(1) Inhibited the production of PGE2 in LPS-stimulated mouse macrophages through the suppression of COX-2 [108].
Bisacurone
(1) Downregulated TNF-induced VCAM-1 drying in HUVECs [109].
Germacrone
(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].
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