Hepatic fibrosis is an early event of cirrhosis. Alcoholic hepatic fibrosis is a process of damage and repair of the liver after long-term alcohol exposure, accompanied by the excessive accumulation and rearrangement of the extracellular matrix, the development of AH, and the formation of pseudolobules. These pathological changes cause damage to the liver structure and ultimately progress to liver cirrhosis. A previous study showed that the expression of the C5 gene is involved in liver fibrogenesis, and inhibition of the C5aR1 attenuates liver fibrosis in mice [43]. Moreover, C5 has a causal role in fibrogenesis across species between humans and mice. A number of studies have confirmed a decrease in the level of serum complement proteins, including C1, C3, C4, C5, and FB, in patients with alcoholic cirrhosis [44-47]. Other studies further revealed that serum concentrations of C3, C4a, and C5a had a negative relationship with liver fibrosis stages and the Child-Pugh score [48-50]. These studies show that the levels of complement components may be an indicator of liver fibrosis or cirrhosis stage [51]. There are two possible mechanisms: the
