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Health Nutrition Ingredients price What is pure UDCA powder?
Pure UDCA powder,the main component is 3a,7尾~dihydroxy~5尾~cholestane~24~acid, is an organic compound, odorless and bitter in taste. This product is soluble in ethanol, insoluble in chloroform; soluble in glacial acetic acid, soluble in sodium hydroxide test solution. In medicine, it is used to increase the secretion of bile acids, change the composition of bile, reduce cholesterol and cholesterol lipids in bile, and help the cholesterol in gallstones to gradually dissolve.UDCA is a commonly used choleretic agent in gastroenterology, and it is also a gallstone dissolving agent, so it can be used in the treatment of gallstones under normal circumstances, provided that the contraction function of the gallbladder is normal. The course of treatment lasts from 6 to 24 months, and the oral dose is 10 milliliters per kilogram of body weight per day. In addition, the drug can treat cholestatic liver disease, such as primary cholestatic cirrhosis. At the same time, it can also treat bile reflux gastritis, 250 mg each time, once a day, orally before going to bed.
UDCA has previously been used to treat gallstone disease, dissolves cholesterol stones, and is now used to treat cholestatic disease. Domestic UDCA is less pure, which contains chenodeoxycholic acid, which can dissolve gallstones, but its protective effect on hepatocytes is far less than that of UDCA. It is clinically used for hepatocyte cholestasis, and its effect seems to be inferior to foreign reports. So good. It has a higher cure rate for non-calcified floating cholesterol stones.
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Pure UDCA powder (3伪,7尾-dihydroxy-5尾-cholanoic acid, UDCA) is a dihydroxycholic acid that constitutes 3% of total human bile. It was first named by Shoda of Okayama University in Japan isolated from Chinese bear bile. In 1985, Leuschner et al. used it to treat gallstones complicated with hepatitis and found that serum transaminases decreased. Since then, a large number of clinical studies have also confirmed that UDCA has definite treatment for some liver diseases. effect. Its mechanism of action and efficacy are briefly described as follows:
Mechanism
Cholestatic liver disease is associated with the accumulation of chenodeoxycholic acid, deoxycholic acid, and lithocholic acid, which cause liver cell damage due to their detergent action. UDCA is a non-toxic hydrophilic cholic acid that competitively inhibits the absorption of toxic endogenous cholic acid in the ileum. By activating the signaling network composed of calcium ions and protein kinase C, and by activating the split-active protein kinase to enhance the secretion ability of cholestatic hepatocytes, the concentration of endogenous hydrophobic cholic acid in blood and hepatocytes is reduced, and the anti-cholestasis effect is achieved. effect. UDCA can also competitively replace toxic bile acid molecules on cell membranes and organelles, preventing hepatocytes and bile duct cells from being damaged by more toxic bile acids. The above effects are embodied in: (1) Cell protection. UDCA conjugates can significantly alleviate hydrophobic bile acid-induced hepatocyte lysis and reduce toxic bile acid-induced apoptosis in cultured murine and human hepatocytes. (2) Membrane stabilization. UDCA prevents bile acid-induced changes in mitochondrial membrane permeability, that is, prevents toxic bile acid-induced damage to mitochondrial membranes, basement membranes, and small bile duct membranes through membrane stabilization. (3) Antioxidant effect. UDCA can inhibit the activation of Kupffer cells caused by toxic bile acids, and can also increase the levels of glutathione and thiol-containing proteins in hepatocytes, preventing oxidative damage to hepatocytes. (4) Immunomodulatory effects. UDCA indirectly inhibits the stimulatory effects of hydrophobic cholic acids and directly inhibits the expression of histocompatibility complex (MHC) class I and II genes by activating glucocorticoid receptors.
Clinical application
Primary biliary cirrhosis (PBC). PBC is a chronic progressive cholestatic liver disease that mainly occurs in middle-aged women and may be related to immune factors. In a trial conducted by Pares et al, the mean interval between biopsies was 4.5 years. It was found that UDCA did prevent the progression of histological staging of PBC. In 1999, Angulo et al reported that in a long-term treatment trial of UDCA in non-cirrhotic PBC patients (average 6.6 years), the time to develop cirrhosis in the treatment group was delayed compared with the patients in the ineffective treatment group. In most trials of UDCA treatment, doses of 13 to 15 mg/kg per day were used. Two recent studies aimed at investigating appropriate doses of UDCA found that daily doses of 13 to 15 mg/kg and 20 to 25 mg/kg were superior to 10 to 15 mg/kg or less daily. The efficacy of UDCA combined with methotrexate or colchicine in the treatment of PBC is not better than that of UDCA alone; however, the efficacy of UDCA in combination with prednisone or prednisone plus azathioprine is significantly better than that of UDCA alone.
Primary sclerosing cholangitis (PSC). PSC is a rare cholestatic disease characterized by stenosis and dilation of intrahepatic and extrahepatic bile ducts. A recent prospective randomized placebo-controlled trial of 105 patients treated for a mean duration of 2.2 years (UDCA 13 to 15 mg/kg daily) showed significant improvement in biochemical parameters, clinical symptoms and liver histology There were no significant changes. However, for obvious bile duct strictures, the addition of UDCA to endoscopic therapy can improve the prognosis of patients.
Intrahepatic cholestasis of pregnancy (ICP). ICP often occurs in the third trimester of pregnancy. The main symptoms are itching and jaundice in pregnant women, which can lead to complications such as premature birth, stillbirth, and stillbirth. It is believed that it is related to the increase of estrogen in the body on the basis of heredity. A randomized, double-blind, placebo-controlled trial of UDCA in the treatment of IPC included 15 patients with improvement in pruritus and liver biochemical markers in the treatment group, and 8 pregnant women (receiving UDCA 1.0 g/day) who delivered at or near their due date; and placebo Of the 7 pregnant women treated, 5 delivered at 36 weeks of gestation, 1 of which was stillborn. No maternal or infant side effects occurred during the treatment. Therefore, UDCA appears to be effective and safe for the treatment of ICP.
Gallbladder fibrosis (CF). In a follow-up double-blind placebo-controlled trial of 55 patients, Colom-bo et al compared UDCA treatment (15 mg/kg daily) with placebo after 1 year. The results showed that the symptoms, nutritional status and biochemical indicators of the treatment group were significantly improved. VandeMeeberg and SulliVan et al. reported that higher doses of UDCA (20 mg/kg daily) were more effective than lower doses (5鈥?5 mg/kg daily).
Chronic hepatitis C. In 2001, several randomized placebo-controlled trials of UDCA combined with alpha-interferon in the treatment of chronic hepatitis C reported that biochemical indicators improved after treatment, but the clearance of hepatitis C virus (HCV)-RNA was ineffective, and liver histological characteristics did not change. .
other. Studies have shown that UDCA combined with cyclosporine A and methotrexate in the treatment of heterogeneous bone marrow transplantation, UDCA can prevent venous occlusion and the occurrence of acute graft-versus-host disease. UDCA at 15 mg/kg daily improves cholestasis symptoms and biochemical markers in progressive familial intrahepatic cholestasis, bile duct atresia, and total parenteral nutrition-related liver disease. UDCA has also been studied for the treatment of other liver diseases, such as alcoholic liver disease, non-alcoholic fatty liver disease, benign recurrent intrahepatic cholestasis, congenital intrahepatic cystic dilatation of the bile duct, autoimmune hepatitis and acute hepatitis, etc. , its efficacy needs to be further evaluated
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