Preparation Of Liver Targeting β-estradiol Nanoparticles And Its Anti-hepatic Fibrosis Activity

Liver fibrosis is a result of chronic hepatocellular damage due to a variety of liver diseases including viral hepatitis, alcoholic hepatitis, schistosomiasis, primary and secondary biliary cirrhosis, primary sclerosing cholangitis, etc. Increased deposition of extracellular matrix (ECM) and reduced matrix degradation are the major character of liver fibrosis. Hepatic stellate cells (HSCs) is playing the central role in the pathogenesis of liver fibrosis. There are a lot of growth factors, cytokines and oxidative stress involved in the activation of HSCs, including transforming growth factor (TGF-β), interleukin (IL-1, IL-6), tumor necrosis factor (TNF-α), connective tissue growth factor (CTGF). Liver fibrosis is reversible, but liver cirrhosis is irreversible which is one of the common and main death causes of diseases in our country .Epidemiological studies found that chronic HBV infection was a common cause of cirrhosis and hepatocellular carcinoma (HCC), particularly in endemic countries. Three independent factors are associated with a faster fibrosis progression: age, alcohol consumption and male gender. Chronic liver diseases, such as hepatic fibrosis or cirrhosis, are more common in men than in women. Fibrosis progression is slower in females as compared to males in chronic hepatitis C and hepatitis B. It was found that oestradiol suppressed hepatic fibrosis in an animal liver fibrosis model induced by CCl₄, and decreased proliferation of HSCs which led to less progression of fibrosis. These studies indicated that the progression of fibrosis in the liver was determined by gender. Estrogens exert the effects of less progression of fibrosis and preventing hepatic damage. However the liver was not the main effect organ of...