Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, causes chronic abdominal pain, vomiting, diarrhea, weight loss and rarely death. Numerous treatments for IBD target the transcription factor NF-kappaB. This factor controls many genes involved in inflammation including those of cytokines and chemokines. These researchers looked at whether curcumin was able to affect the degree of inflammation of the colon (colitis) in mice treated with dinitrobenzene sulfonic acid (DNB). DNB was used to produce a predictable colitis in these mice. Curcumin was given by mouth 5 days before the DNB treatment. It reduced the amount of visually apparent damage in the colon. It also reduced NF-kappaB activation and the activity of the enzyme myeloperoxidase. Myeloperoxidase is a known marker for the accumulation of inflammatory cell infiltration in mouse models of colitis. They also measured the message for IL-1beta. This is one of the cytokines most important in IBD. The amount of this message, usually induced by DNB, was decreased in the curcumin treated mice. DNB reproducibly activated p38 mitogen-activated protein kinase measured in intestine cells of these mice. This level of activation was reduced by curcumin. They look under the microscope to see where this kinase activation was most reduced. They found that it was most reduced in cell of the intestinal mucosa. They concluded that curcumin is able to prevent the severity of this experimental colitis. They suggest that curcumin may be of value in treating human inflammatory bowel disease.
Helicobacter pylori, a cause of stomach and colon cancer, is inhibited by both tumeric and curcumin.June 7th, 2009
Curcumin is the primary chemical part of the spice turmeric (Curcuma longa). It has been shown to prevent stomach and colon cancers in rodents. Scientists have many theories as to how curcumin prevents cancer. But so far they have not reported whether curcumin affects the growth of the bacteria, Helicobacter pylori. This bacterium is a Group 1 carcinogen. It is linked with the growth of stomach and colon cancer. Two forms of tumeric were tested against 19 strains of H. pylori, including 5 cagA+ strains. These forms were the pure chemical, curcumin and an extract. The extract was made in the alcohol, methanol, from the dried powdered roots of the plant Curcuma longa. Both forms inhibited the growth of all strains of H. pylori grown in culture. The minimum inhibitory concentration ranged from 6.25-50 micrograms per milliliter. They concluded that curcumin inhibits the growth of H. pylori cagA+ strains grown in culture. They suggest that inhibition of H. pylori may be one of the ways by which curcumin prevents cancer.
The Indian spice tumeric (Curcuma longa) is a well-known traditional herbal medicine. These scientists evaluated it role in treating a mouse model for depression. In these models the animals become immobilized (still) by the despair caused by an inescapable external physical stress. Antidepressants reduce the duration of immobility. They extracted tumeric into water. They gave mice from 140 to 560 milligrams per kilogram body weight of the extract by mouth for 14 days. They found that greater doses of tumeric produced less immobility of the stressed mice. They used the tail suspension test and the forced swimming test. The effect of 560 milligrams per kilogram of the extract was greater than the comparison antidepressant fluoxetine (Prozac). The extracts, at the dose of 140 mg/kg or greater for 14 days, significantly inhibited the enzyme monoamine oxidase A (MAO) activity in mouse whole brain. In contrast only the highest dose of the extract, 560 mg/kg inhibited MAO B activity in mouse brains. MAO inhibitors are an important class of currently used antidepressants. Fluoxetine (Prozac) showed only a tendency to inhibit MAO A and B activity in animal brain in the study. Fluoxetine is in the class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). Neither the extract nor fluoxetine, at the doses tested, reduced locomotor activity. These scientists concluded that that C. longa had antidepressant effects in this mouse model. They suggest that this effect of tumeric may be due to its inhibition of MAO A.
Antidepressant activity of aqueous extracts of Cur…[J Ethnopharmacol. 2002]
Tumeric is an Indian spice made from the roots of the plant Curcuma longa. These researchers were interested in turmeric’s role in atherosclerosis, hardening of the arteries. Atherosclerosis leads to illnesses of the blood vessels and heart. These include heart attacks and stroke. They studied how an extract of Curcuma longa affected experimental atherosclerosis (fatty streak) in rabbits. They also measured its interaction with other antioxidants in the plasma (liquid part of the blood). This is because in humans oxidative stress has a role in the development of atherosclerosis. Two groups of male New Zealand White rabbits, a control group and a treatment group, were fed a diet known to cause atherosclerosis. The treatment group was also given curcuma extracted in alcohol and water, by mouth. Six animals from each group were killed after 10, 20, and 30 days. At each interval (10, 20, and 30 days) the treatment group had significantly lower plasma lipid peroxide compared with the controls. The treatment group showed significantly higher levels of the antioxidants, alpha-tocopherol and coenzyme Q at 20 and 30 days. They looked under the microscope for the earliest sign of atherosclerosis, called fatty streak. This type of damage in the largest blood vessel, the aorta, in the chest and abdomen was significantly less in the treatment group than in the controls after 30 days. This extract of Curcuma longa reduced oxidative stress and lessened the early signs of atherosclerosis in rabbits fed a high cholesterol diet.
Curcumin, the main chemical part of turmeric, has raised interest because of its activity against inflammation and cancer. These scientists were concerned that curcumin could interfere with anti-cancer drugs. This is because curcumin inhibited two steps in the pathway of these drugs. These steps are, making of reactive oxygen species (ROS) and the c-Jun NH (2)-terminal kinase (JNK) pathway. They are how many cancer drugs start programmed cell death, a process called apoptosis. In their experiments, curcumin inhibited the apoptosis of human breast cancer cells (MCF-7, MDA-MB-231, and BT-4) caused by chemotherapy by up to 70%. They used the anti-cancer drugs; camptothecin-, mechlorethamine-, and doxorubicin. This inhibition was greater when cells were treated with more and longer curcumin. But they saw this inhibition even with short, 3 hours, durations of curcumin. Even the low amount of curcumin, 1 micromole, found in Phase I clinical trials of human, inhibited this apoptosis. In these studies curcumin was an antioxidant. It blocked the activation of JNK and mitochondrial release of cytochrome c in a concentration-dependent manner. They also looked at curcumins effect in mice injected with human breast cancer cells. Curcumin in mouse diets reduced the tumor decreasing effect of the anti-cancer drug, cyclophosphamide. It also blocked the cyclophosamide caused events, activation of apoptosis and JNK. They concluded that curcumin in the diet can interfere with cancer chemotherapy by inhibiting apoptosis. They suggest that additional studies should look at whether curcumin should be avoided by breast cancer patients undergoing chemotherapy.
In the traditional system of healing in India, Ayurveda, they believe several spices and herbs can heal illnesses. For instance, the roots spice turmeric (Curcuma longa. Linn.) is used to flavor and color foods in Indian everyday. These scientists studied both tumeric and its principal chemical, curcumin, in diabetes mellitus. They gave rats the chemical alloxan to make them have diabetes. Giving them turmeric or curcumin significantly lowered blood sugar, hemoglobin and glycosylated hemoglobin levels. Glycosylated hemoglobin reflects the average level of glucose. It is used to monitor glucose control in diabetes. Turmeric and curcumin in the diet also decreased the oxidative stress of these rats. This was shown the lower levels of TBARS (thiobarbituric acid reactive substances). Also, treatment with turmeric or curcumin the significantly lowered the activity of sorbitol dehydrogenase. This enzyme effects the change of the sugar sorbitol into fructose. Finally they observed that curcumin may be more effective in controlling diabetes mellitus than turmeric.
Efficacy of turmeric on blood sugar and polyol pat…[Plant Foods Hum Nutr. 2002]
Curcumin, part of the spice turmeric, prevents cancers in rodent intestines. It is being studied in clinical trials of humans to prevent colon cancer. Very little of dietary curcumin goes into the blood stream. These researchers further evaluated the notion that curcumin is metabolized in the intestine. They compared its metabolism in parts intestinal cells with the same parts of liver cells from humans and rats. They also studied the metabolism of curcumin in rat intestinal sacs grown in test tubes. Curcumin conjugates and reduction products were identified using high-performance liquid chromatography. Curcumin glucuronide was found in microsomes of liver and intestine cells. Curcumin sulfate, tetrahydrocurcumin, and hexahydrocurcumin found as curcumin metabolites in the cytosol of these cells. Cytosol is fluid part of the cell. In cells from the intestine, curcumin was conjugated more in human cells than in rat cells. The opposite occurred in cells from the liver. The cytosol of human intestinal and liver cells reduced curcumin 18 and 5 fold more, respectively, than did the same type of cell from rats. The intact rat gut sacs produced curcumin sulfate from curcumin. They concluded that curcumin is metabolized greatly, both conjugated and reduced, in the in the gastrointestinal tract and metabolized more by human than by rat intestines. The metabolism of curcumin should be taken into consideration in planning trials of curcumin given by mouth.
Long term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with less risk of Alzheimer’s disease. Also, lengthy use of ibuprofen lessened inflammation and plaque-related damage in a mouse model (Tg2576) of Alzheimer’s disease. But too much use of the NSAIDs that inhibit the enzyme cyclooxygenase I can cause gastrointestinal, liver, and liver damage. Curcumin, a part of the curry spice turmeric, may be a less toxic NSAID alternative. These researchers studied whether curcumin could reduce the brain damage in this same mouse model. They tested a low (160 parts per million) and a high dose of dietary curcumin (5000 parts per million). Both doses of curcumin significantly lowered oxidized proteins and interleukin-1beta. This is a proinflammatory cytokine elevated in the brains of these mice. Three indicators of Alzheimer’s disease were significantly decreased by 43-50%, but only with the low dose. These indicators were; astrocytic marker, glial fibrillary acidic protein, insoluble beta-amyloid (Abeta), soluble Abeta, and number of plaques. Amyloid plaques in the brains of Alzheimer’s disease patients contain lots of Abeta, a peptide. Microgliosis was also suppressed in neuronal layers but not adjacent to plaques. However, levels of amyloid precursor in the membrane fraction were not reduced. They concluded that curcumin is likely to help in the prevention of Alzheimer’s disease because of its efficacy in this mouse model and its low toxicity.
Curcumin, the chemically active part of the spice turmeric, inhibits cancer cells from starting, growing and spreading. These researchers studied the steps by which curcumin inhibited breast cancer cells in the test tube. They looked at genes, proteins and enzymes related to the features of malignant cancer. These included uncontrolled cell multiplication, invasion and spread throughout the body (metastasis). They found that curcumin inhibited H-ras-induced invasive phenotype in MCF10A human breast cells. Ras and ras-related proteins are often uncontrolled in cancers, leading to invasion, spread, and decreased apoptosis. Apoptosis is planned cell suicide, an organized process in which the cells corpses and fragments are safely disposed. Too little apoptosis leads to cells multiplying uncontrollably, such as in cancer. Curcumin downregulated the enzyme, matrix metalloproteinase 2. This enzyme is thought to be important in metastasis of cancer. Curcumin was poisonous to H-ras MCF10A cells. A higher amount of curcumin was more toxic. Curcumin-induced cell death was mainly due to apoptosis. Curcumin caused these breast cancer cells to make reactive oxygen species. These small molecules are highly reactive. They can result in significant damage to cell structures and a situation known as oxidative stress. The antioxidant, N-acetyl-L-cysteine, inhibited the apoptosis causes by curcumin. This may mean that redox signaling is the way curcumin starts apoptosis, cell death, in these breast cancer cells. These scientists concluded that curcumin inhibits cancer invasion and starts a type of controlled cell death, apoptosis and that these findings prove that curcumin has potential to prevent cancer.
This was a clinical trial of tumeric to treat patients with symptoms of peptic ulcer. Peptic ulcers in humans occur in the stomach and the duodenum (small intestine attached to the stomach). Forty-five patients, 24 males and 21 females, aged between 16-60 years were included. Twenty-five patients, 18 males and 7 females, were endoscoped; their ulcers located in the duodenal bulb (DB) and gastric (stomach) angulus (GA). The ulcers ranged from 0.5 to 1.5 centimeters in width. Capsules filled with turmeric (300 milligrams each) were given by mouth. They gave 2 capsules five times daily, one half to an hour before the three meals, at 4 pm and at bedtime. After 4 weeks of treatment ulcers were absent in 48% or 12 cases (DB 9 and GA 3). After 8 weeks eighteen cases (DB 13 and GA 5) had no ulcers. Nineteen cases (76%) (DB 14 and GA 5) did not have ulcers after 12 weeks of treatment. The rest, 20 cases, were not found to have ulcers even before treatment. Some were not endoscoped. These 20 seemed to have erosions, gastritis and dyspepsia. They were treated with turmeric capsules for 4 weeks. Their abdominal pain and discomfort satisfactorily lessened in the first and second week. After treatment they could take normal foods instead of soft meals. Blood studies of all patients, before and after treatment, showed no significant changes in the blood cells, nor in the chemicals and enzymes used to measure liver and kidney health.