Halting production of additional fibrosis may be half the battle... Stop laying down new fibrosis and allow the liver to begin healing itself.
http://www.ncbi.nlm....pubmed/11749858
Effect of genistein and quercetin on proliferation, collagen synthesis, and type I procollagen mRNA levels of rat hepatic stellate cells.
"CONCLUSION: GE and QU inhibited hepatic stellate cell proliferation and collagen synthesis that might have a protective role against liver fibrosis"
http://www.ncbi.nlm....les/PMC2241785/
Curcumin: potential for hepatic fibrosis therapy?
"The beneficial antioxidative, anti-inflammatory and antitumorigenic effects of curcumin have been well documented in relation to cancer and other chronic diseases. Recent evidence suggests that it may be of therapeutic interest in chronic liver disease. Hepatic fibrosis (scarring) occurs in advanced liver disease, where normal hepatic tissue is replaced with collagen-rich extracellular matrix and, if left untreated, results in cirrhosis. Curcumin inhibits liver cirrhosis in a rodent model and exerts multiple biological effects in hepatic stellate cells (HSCs), which play a central role in the pathogenesis of hepatic fibrosis. In response to liver injury, these cells proliferate producing pro-inflammatory mediators and extracellular matrix. Curcumin induces apoptosis and suppresses proliferation in HSCs. In addition, it inhibits extracellular matrix formation by enhancing HSC matrix metalloproteinase expression via PPARγ and suppressing connective tissue growth factor (CTGF) expression. In this issue, Chen and co-workers propose that curcumin suppresses CTGF expression in HSC by inhibiting ERK and NF-κB activation. These studies suggest that curcumin modulates several intracellular signalling pathways in HSC and may be of future interest in hepatic fibrosis therapy."
Coffee Anyone? http://www.ncbi.nlm....pubmed/23808892
Caffeine attenuates liver fibrosis via defective adhesion of hepatic stellate cells in cirrhotic model
"Caffeine increased HSCs apoptosis and intracellular F-actin and cyclic adenosine monophosphate expression. Caffeine also inhibited procollagen type Ic and α-SMA expression in a dose- and time-dependent manner. In rat model, caffeine decreased periportal inflammation, levels of inflammatory cells (1.4 ± 0.52 vs 2.6 ± 0.46, P < 0.05), and fibrosis (2.1 ± 0.35 vs 2.9 ± 0.84, P < 0.05). Transforming growth factor-β and α-SMA expressions were also reduced by caffeine.
CONCLUSION:
Caffeine attenuates the progression of liver fibrosis by inhibiting HSCs adhesion and activation."
And of course, keep iron low (through chelation or blood donation) to avoid progression of disease! The liver is the primary storage site for excess iron, & iron is the flam in liver inflammation! Give these titles a google for more on this.
Iron-dependent activation of NF-kappaB in Kupffer cells: a priming mechanism for alcoholic liver disease
Iron Overload: An Important Co-Factor In The Development of Liver Disease in Alcoholics
Iron accumulation in alcoholic liver diseases
The Role of Iron in Alcoholic Liver Disease
Liver Iron is Predictive of Death in Alcoholic Cirrhosis
Serum ferritin concentration predicts mortality in patients awaiting liver transplantation
http://www.ncbi.nlm....pubmed/12957300
Iron chelators and iron toxicity
"Iron chelation may offer new approaches to the treatment and prevention of alcoholic liver disease. With chronic excess, either iron or alcohol alone may individually injure the liver and other organs. In combination, each exaggerates the adverse effects of the other. In alcoholic liver disease, both iron and alcohol contribute to the production of hepatic fibrosis through their effects on damaged hepatocytes, hepatic macrophages, hepatic stellate cells, and the extracellular matrix. The pivotal role of iron in these processes suggests that chelating iron may offer a new approach to arresting or ameliorating liver injury"
EDIT
"These agents may provide new pharmacological means of averting or ameliorating liver damage in alcoholic liver disease by binding, inactivating, and eliminating the reactive forms of iron that contribute to oxidative injury of cellular components, are involved in signal transduction, or both."
Helpful Hints: Curcumin and Quercetin are both iron chelators.
Iron chelation in the biological activity of curcumin
"Consistent with the hypothesis that curcumin acts as an iron chelator, mice that were fed diets supplemented with curcumin exhibited a decline in levels of ferritin protein in the liver. These results suggest that iron chelation may be an additional mode of action of curcumin."
Role of Quercetin on iron homeostasis
"after longer oral treatment with quercetin, animals became iron deficient as both liver and spleen iron levels decreased significantly"
Edited by synesthesia, 26 March 2016 - 05:34 AM.
