Curcumin is a biologically active component of the popular Indian spice turmeric and is purported to have several beneficial therapeutic properties to combat illnesses, such as cancer, Alzheimer's disease and cirrhosis of the liver. Several scientific studies have been conducted confirming its antitumor, anti-inflammatory and hepatoprotective, or protecting the liver, properties; however, a specialist should always be consulted before using herbs to treat life-threatening conditions, such as cirrhosis.
Medicinal Effects of Curcumin
Curcumin acts as a free radical scavenger and antioxidant, inhibiting lipid, or fat, deposition, necessary for fibrosis formation, and it can induce metabolic pathways that are potent inhibitors of enzymes in lipid formation. Although many studies suggest curcumin may be useful for the prevention and treatment of numerous diseases, the efficacy of curcumin has not yet been fully established in randomized and controlled clinical human trials.
Cirrhosis
The liver plays a vital role in synthesis of proteins, detoxification and storage of vitamins in addition to the metabolism of lipids and carbohydrates. Cirrhosis is a consequence of chronic liver disease most commonly caused by alcoholism, hepatitis B and C, and fatty liver disease and is characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules, or lumps, leading to loss of normal function. Recent research illustrates the crucial role of the liver stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis leading to structural breakdown and replacement of tissue. Hepatic stellate cells, or HSCs, are relevant effectors during hepatic fibrogenesis, or scar tissue formation, and experimental evidence supports the proposal that inhibiting the accumulation of lipids would inhibit HSC activation and alleviate further liver damage.
Current Reseach Supporting Usage of Curcumin
A November 2010 article appearing in the "British Journal of Pharmacology," documented a study designed to explore the molecular mechanisms of glucose accumulation in HSCs, necessary for the cells' proliferation. The authors hypothesized that stimulated HSCs, activated by increasing intracellular glucose concentrations, could be eliminated by curcumin-inhibition of glucose transporters in the membrane of the cells. The intracellular glucose levels were measured in rat HSCs and human hepatocytes, or liver cells. Data were analyzed and signaling pathways were assessed by comparing enzymatic activity. Researchers found that curcumin prevented levels of intracellular glucose to increase in activated HSCs by inhibiting glucose transport proteins. In a September 2010 article published in the medical journal "Endocrinology," researchers discovered one of the mechanisms by which HSCs were activated to deplete intracellular lipids, necessary for fibrogenesis. They observed reduced levels of intracellular fatty acids and triglycerides in HSCs, purportedly reduced by curcumin treatment. They concluded that curcumin eliminated the effects of HSC activation and lead to inhibiting expression of genes relevant to intracellular accumulation of lipids.
Further Clinical Studies
An April 2010 issue of the medical periodical "Gut" published a study designed to document whether curcumin could ease hepatic damage of chemically induced liver injury in mice. The researchers investigated potential anti-inflammatory and antifibrotic mechanisms of curcumin. They found that liver damage and related fibrosis were reduced in experimental mice after curcumin feeding and illustrated that curcumin may have multiple targets in the liver, thereby identifying several metabolic pathways that could be useful for further therapies.
References
- "British Journal of Pharmacology"; Curcumin Prevents Leptin Raising Glucose Levels in Hepatic Stellate Cells ... ; Y. Tang, et al.; November 2010.
- "Endocrinology"; Curcumin Protects Hepatic Stellate C ... ; Y Tang, et al.; September 2010.
- "Gut"; Curcumin Improves Sclerosing Cholangitis ... ; A Baghdasaryan, et al.; April 2010.
