Cancer Anti-inflammtory IBS, Crohn's disease, ulcerative colitis, diabetes, dementia, alzheimer's disease, rheumatoid arthritis, high cholesterol, cancer preventative, and liver restorative

Curcumin 95%
Quercetin 95%


Objective By adopting MRC-5 induced by transforming growth factor 1 (TGF-b1), to explore the effect and mechanisms of curcumin on pulmonary fibrosis from molecular level in vitro and discuss the preventing and treating effect of curcumin on pulmonary fibrosis. Methods The MRC-5 were divided into four groups: normal group, curcumin group, TGF-b group, TGF-β?cucurmin group. The expression of TGF-b R I, TGF-b R II were tested by the Real-time PCR and Western blotting. Results The expression of TGF-b R I and TGF-b RII in TGF-β?cucurmin group was significantly decreased compared with normal group and TGF-β1 group. Conc?usions Curcumin can inhibit the MRC-5’s collagen deposition which may have important role in delaying lung fibrosis forming progress. Its mechanism may be related with inhibiting TGF-b R I and TGF-b R II.
--ZHANG Hui-cun, LI Ya-dong, WANG Ji-feng, et al. Effect of Curcumin on TGF-b Receptor of Human Embryo Lung Fibroblast. Zhong Guo Zhong Yi Yao Xin Xi Za Zhi. 2010; 17 (12): 23-25.
Objective To investigate the proliferation inhibitory effect and to explore the molecular mechanism of curcumin on pulmonary fibroblasts. Methods Fibroblasts derived from lung tissue of patients with idiopathic pulmonary fibrosis (IPF) was cultured in vitro and incubated with curcumin at different concentrations for different time. Fibroblasts were randomized into 5 groups, ie. a control group and 4 curcumin groups (intervened by 5, 10, 20, 40 umol/L curcumin, respectively). MTF assay was used to determine the inhibitory rate of curcumin on the proliferation of pulmonary fibroblasts. Apoptosis and the Caspase-3 expression of pulmonary fibroblasts were identified by flow cytometry (FCM). Variables were compared with One-Way ANOVA. The correlations between variables were analyzed using Pearson’s correlation coefficient. Results Curcumin inhibited pulmonary fibroblasts proliferation in a dose-dependent and time-dependent manner (r=0.886, r=0.832, respectively, all P<0.01). Apoptosis rate of pulmonary fibroblasts in 4 curcumin groups was (29.58±2. 13)%, (64.36±3.92)%, (72.98±4.42)%, (83.14±2.51)%, respectively, which was significantly higher than that in the control group [(3.84±1.88)%, P< 0.01]. The positive expression rate of apoptosis-regulating protein caspase-3 was (26.24±3.64)%, (44.87±5.31)%, (57.44±4.23)%, (73.65±5.01)%, respectively, which was significantly higher than that of the control group [ (4.02±0.62)%, P< 0.01]. Conclusions In vitro, curcumin can significantly inhibit proliferation and induce apoptosis of pulmonary fibroblasts of patients with IPF. The mechanism may be associated with up-regulating expression of Caspase-3.
--GAO Wei, ZHANG De-ping, CHEN Bi. Mechanism of Pulmonary Fibroblasts Apoptosis Induced by Curcumin. Zhong Guo Hu Xi Yu Wei Zhong Jian Hu Za Zhi. 2009; 8 (2): 186-189.

Curcuminoids inhibit enzymes, which participate in the synthesis of inflammatory substances in the body. The natural anti-inflammatory activity of curcuminoids is comparable in strength to steroidal drugs, and such nonsteroidal drugs as indomethacin and phenylbutazone, which have dangerous side effects.
Inflammation results from a complex series of actions and/or reactions triggered by the body's immunological response to tissue damage. This damage may be caused by physical traumas including various diseases and surgery. Moderate inflammation is necessary for the healing process; however, continuous inflammation leads to chronic conditions like arthritis and its associated pain. In a double blind, controlled study, three groups of patients received either curcumin (400 mg), the anti-inflammatory prescription drug phenylbutazone (100 mg), or a placebo (250 mg of lactose powder) three times daily for five consecutive days after surgery. They had been admitted for either a hernia condition or an accumulation of fluid in the scrotum. The results: curcumin was just as effective as phenylbutazone in reducing post-operative inflammation.
Curcuminoids prevent the synthesis of several inflammatory prostaglandins and leukotrienes
An overview of the good properties of curcumin related to cancer in general, which includes prostate cancer. (Some properties are mentioned more than once in the list A to N).
A) Curcumin selectively inhibits phosphorylase kinase, a key regulatory enzyme involved in the metabolism of glycogen. This has important implications for the anti-proliferative effects.
B) Curcumin reduces activity of xanthine oxidase [XO] activity, one of the major causative elements in PMA-mediated tumor promotion.
C) Curcumin inhibits epidermal growth factor (EGF) receptor intrinsic kinase activity up to 90%, and also inhibited EGF-induced tyrosine phosphorylation of EGF receptors. These findings demonstrate that curcumin is a potent inhibitor of a growth stimulatory pathway, the ligand-induced activation of EGF-R, and may potentially be useful in developing anti-proliferative strategies to control tumor cell growth.
D) Curcumin induces cell shrinkage, chromatin condensation, and DNA fragmentation, characteristics of apoptosis.
E) Curcumin inhibits protein kinase C (PKC) activity.
F) Curcumin inhibits tyrosine protein kinase activity.
G) Curcumin, Sulindac and PEMC significantly increase the percentage of apoptosis.
H) Curcumin and Genistein show synergistic inhibitory effects on the growth of human breast cancer MCF-7 cells induced by estrogenic pesticides.
I) Curcumin induced cell shrinkage, chromatin condensation, and DNA fragmentation.
J) Curcumin significantly reduced membranous protein tyrosine
kinase activity.
K) Curcumin caused a concentration-dependent inhibition of T-cell and may have novel adjuvant immunosuppressive properties.
L) Curcumin inhibits ""tyrosine kinase activity"" of p185neu and also depletes p185neu. The growth of several breast cancer cell lines was inhibited.
M) Curcumin and Genistein block TGF-beta 1-induced u-PA expression and migratory and invasive phenotype in mouse epidermal keratinocytes.
N) Curcumin inhibits tyrosine kinase activity of epidermal growth factor receptor and depletes the protein. Curcumin can induce apoptosis in both androgen-dependent (AD) and androgen-independent (AI). It can interfere with the signal transduction pathways of the prostate cancer cell and prevent it from progressing to its hormone-refractory state.

QUERCETIN is widely distributed in the plant kingdom and is the most abundant of the flavonoid molecules. It is found in many often-consumed foods, including apple, onion, tea, berries, and brassica vegetables, as well as many seeds, nuts, flowers, barks, and leaves. It is also found in medicinal botanicals, including Ginkgo biloba, Hypericum perforatum ( St. John's Wort), Sambucus canadensis (Elder), and many others. It is often a major component of the medicinal activity of the plant, and has been shown in experimental studies to have numerous effects on the body.
All flavonoids have the same basic chemical structure, a three-ringed molecule with hydroxyl (OH) groups attached. A multitude of other substitutions can occur, giving rise to the many types of flavonoids. Flavonoids often occur in foods as a glycoside, meaning they have a sugar molecule (rhamnose, glucose, galactose, etc.) attached to the center (C) ring. Quercetin is the aglycone (meaning minus the sugar molecule) of a number of other flavonoids, including rutin, quercetin, isoquercetin, and hyperoside. These molecules have the same structure as quercetin except they have a specific sugar molecule in place of one of quercetin's hydroxyl groups on the C ring, which dramatically changes the activity of the molecule. Activity comparison studies have identified other flavonoids as often having similar effects as quercetin; but quercetin usually has the greatest activity.
Quercetin appears to have many beneficial effects on human health, including cardiovascular protection, anti-cancer activity, anti-ulcer effects, anti-allergy activity, cataract prevention, antiviral activity, and anti-inflammatory effects."
Flavonoids, as a rule, are antioxidants, and a number of quercetin's effects appear to be due to its antioxidant activity. Quercetin scavenges oxygen radicals, inhibits xanthine oxidase, and inhibits lipid peroxidation in vitro. As another indicator of its antioxidant effects, quercetin inhibits oxidation of LDL cholesterol in vitro, probably by inhibiting LDL oxidation itself, by protecting vitamin E in LDL from being oxidized or by regenerating oxidized vitamin E. By itself, and paired with ascorbic acid, quercetin reduced the incidence of oxidative damage to neurovasculature structures in skin, and inhibited damage to neurons caused by experimental glutathione depletion.
Quercetin's anti-inflammatory activity appears to be due to its antioxidant and inhibitory effects on inflammation-producing enzymes (cyclooxygenase, lipoxygenase) and the subsequent inhibition of inflammatory mediators, including leukotrienes and prostaglandins. Inhibition of histamine release by mast cells and basophils also contributes to quercetin's anti-inflammatory activity.
Aldose reductase, the enzyme that catalyzes the conversion of glucose to sorbitol, is especially important in the eye, and plays a part in the formation of diabetic cataracts. Quercetin is a strong inhibitor of human lens aldose reductase.
Quercetin exerts antiviral activity against reverse transcriptase of HIV and other retroviruses, and was shown to reduce the infectivity and cellular replication of Herpes simplex virus type 1, poliovirus type 1, parainfluenza virus type 3, and respiratory syncytial virus (RSV).
Early studies on quercetin reported that administration to rats caused an increased incidence of urinary bladder tumors. Subsequent studies on rats, mice, and hamsters were unable to confirm the potential carcinogenicity of this molecule. In fact, much of the recent research on quercetin has shown it to be an anticarcinogen to numerous cancer cell types, including breast, leukemia, colon, ovary, squamous cell, endometrial, gastric, and non-small-cell lung.
Quercetin: Works like an antihistamine, treats allergies, prevents heart disease and Cancer.
Speed up healing of recurrent heartburn, or gastroesophogeal reflux disorder (GERD)
Epstein-Barr virus may be suppressed.
Diabetic neuropathies.
Allergies: Quercetin's mast-cell-stabilizing effects make it an obvious choice for use in preventing histamine release in allergy cases, similar to the synthetic flavonoid analogue cromolyn sodium. Absorption of the pure aglycone quercetin is poor (see below); however, much of quercetin's anti-allergy effects may be due to anti-inflammatory and anti-histaminic effects in the gut.
Cardiovascular Disease Prevention: Quercetin's cardiovascular effects center on its antioxidant and anti-inflammatory activity, and its ability to inhibit platelet aggregation ex vivo. The Zutphen Elderly Study investigated dietary flavonoid intake and risk of coronary heart disease. The risk of heart disease mortality decreased significantly as flavonoid intake increased. Individuals in the upper 25 percent of flavonoid intake had a relative risk of 0.42 compared to the lowest 25 percent in this 5-year follow-up study of men ages 65-84. Interestingly, the flavonoid-containing foods most commonly eaten in this study contain a high amount of quercetin (tea, onions, apples). In a cohort of the same study, dietary flavonoids (mainly quercetin) were inversely associated with stroke incidence.
Anti-ulcer/Gastroprotective effects: Animal studies have shown quercetin to be protective of gastric ulceration caused by ethanol, probably by inhibiting lipid peroxidation of gastric cells and/or by inhibition of gastric acid secretion. An interesting aspect of quercetin's anti-ulcer effect is that it has been shown to inhibit growth of Helicobacter pylori in a dose-dependent manner in vitro.
Cancer: As mentioned above, quercetin has been investigated in a number of animal models and human cancer cell lines, and has been found to have antiproliferative effects. It may also increase the effectiveness of chemotherapeutic agents. More clinically oriented research needs to be done in this area to discover effective dosage ranges and protocols.
Diabetic Complications: Quercetin's aldose reductase-inhibiting properties make it a useful addition to diabetic nutritional supplementation, to prevent cataract and neurovascular complications.
Viral Infections: Quercetin may be useful in viral infections; however, none of the research so far is clinically based. Even so, concentration on ingesting quercetin-rich foods or supplementation with the pure substance may be helpful during viral illnesses."
Few human quercetin absorption studies exist. A recent study of absorption in "healthy" ileostomy patients revealed an absorption of 24 percent of the pure aglycone and 52 percent of quercetin glycosides from onions. However, no intestinal permeability values were obtained in this group, and thus the results might not be reliable. Quercetin undergoes bacterial metabolism in the intestinal tract, and is converted into phenolic acids. Absorbed quercetin is transported to the liver bound to albumin, where some may be converted via methylation, hydroxylation, or conjugation.

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