Information presented on this website is for educational purposes only.
Materials presented have not been evaluated by the U.S. Food & Drug Administration and are not in any way a replacement or substitute for professional medical diagnosis and treatment. 

 
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Information presented on this website is for educational purposes only.
Materials presented have not been evaluated by the U.S. Food & Drug Administration and is not meant to diagnose or treat medical illnesses.
 

 


Philosophical Differences Between Western and Chinese Medicine:

Part 1: Western Medicine
Part 2: Traditional Chinese Medicine
Part 3: Modern Chinese Medicine

 
Liver Disorders
Hepatitis C
Liver Fibrosis
Alcoholic Hepatitis
Non-Alcoholic Steatohepatitis (NASH) or Fatty Liver  
Auto-Immune Hepatitis
Cholestatic Hepatitis
 

Chronic Lyme Disease


IBS/Crohn's Disease


 

Modern Chinese Medicine and Supportive Therapies for Cancer Patients
Artemisinin and its Derivatives
 



 



 

Modern Chinese Medicine (MCM) Anti-Liver-Fibrosis Treatments

What is liver fibrosis?

Classifications of Liver Fibrosis

Pathophysiology of Liver Fibrosis

Diagnosis and Staging of Liver Fibrosis

What is liver cirrhosis?

Is Fibrosis reversible?

MCM Anti-Fibrosis Treatments

 

Pathophysiology of Liver Fibrosis

Fibrosis is a complicated pathophysiological process in which different liver cells, cytokines secreted by these liver cells, and extra-cellular matrix (ECM) are involved. The liver cell injury triggers this process. The pathophysiological center of liver fibrosis is centered around the activities of hepatic stellate cells (HSC), which are the main producers of ECM. Fibrosis is a dynamic pathogenesis and ECM accumulation is the result of the imbalance between synthesis and decomposition. There are three basic phenomena related to liver fibrosis and liver inflammation:

1. HSC activation and transferred to become fibroblastic cells: First phase, before inflammation, injury by (HBV, HCV, alcohol, bile retention, parasites, chemical intoxication, etc.) liver cells secrete stimulating factors to activate the activity of hepatic stellate cell (HSC) and suppress the inhibitory factors' activity.

2. Reduction of Retinoid in the HSC: Second phase, during the liver inflammation, Kupffer calls, inflammatory cells and HSC secrete cytokines such as TGFb1 (transforming growth factor-beta 1), PDGF (platelet delivered growth factor), PAI (Plasminogen activator inhibitor), ET-1 and Retinoid reduction in HSC and all these transfer HSC to become fibroblastic cells, which is the main type of cell to produce extra cellular matrix (ECM).

3. The synthesis of ECM increases and the decomposition of ECM decreases: Third phase, post-inflammation stage, fibroblastic cells secrete more cytokines such as TGFb1, PDGF, and TIMP (tissue inhibitor of metalloproteinases), which can continuously activate HSC to make more fibroblastic cells, and increase the amount of ECM. TIMP combines with MMP (Matrix metalloproteinases) can suppress HSC's ECM-decomposing action, which resulting in ECM synthesis increase and decomposition decrease. TGFb1 suppresses the production of HGF (hepatocellular growth factor) and promotes the liver cell apoptosis. HSC can also secrete many other cytokines, which further promote fibrotic activities.

In short, inflammation is the motivating force that pushes fibrosis progression, and the central role is played by
hepatic stellate cells (HSC).

 

Information presented on this website is for educational purposes only.
Materials presented have not been evaluated by the U.S. Food & Drug Administration and are not in any way a replacement or substitute for professional medical diagnosis and treatment. 

 

Information presented on this website is for educational purposes only.
Materials presented have not been evaluated by the U.S. Food & Drug Administration and are not in any way a replacement or substitute for professional medical diagnosis and treatment. 

 

Copyright  2005 Sinomed Research Institute

Medical Information Resources:
http://www.nih.gov/
http://www.nlm.nih.gov/

http://nccam.nih.gov/


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