Table 2.

The function of neutrophils granule component in liver disease.

Factors	Models of liver disease	Pathogenesis	References
The granule components of neutrophils
MPO	IRI	Oxidative damage to the tissue	(27)
	NAFLD	Modulate the infiltration of neutrophils and T cells, induce pro-inflammatory factors Increase liver cholesterol Promote NAFLD toward advanced stages with fibrosis	(54)
	ALD	Act as a marker for the infiltration of neutrophils, and predict the prognosis in patients with alcoholic cirrhosis	(55)
	Fibrosis	Activate HSCs, upregulate fibrosis-related genes, and induce the oxidative stress in vitro Induce the hepatocyte death in vivo	(56)
	HCC	Expedite the HCV infection to HCC	(57)
NE	IRI	Adherence and extravasation of leukocyte via basement membrane degradation Stimulates the production of MCP-1 by macrophages in vitro Decreases endothelial production of prostacyclin and insulin-like growth factor-I in rats	(31, 32, 58, 59)
	NAFLD	Insulin resistance Induces the activation of pro-inflammatory factors	(49, 50)
	ALD	Induces proteolytic damage	(60)
	Fibrosis	Induces proteolytic tissue damage	(61)
	HCC	Induces proteolytic damage	(62)
MMP9	IRI	Promotes recruitment and MPO activation of neutrophils	(28)
	NAFLD	Elevated MMP9 drives the NASH and fibrosis progress	(63)
	ALD	Regulates homeostasis of the liver microenvironment	(64)
	Fibrosis	Degrades ECM and basement membrane components	(65)
	HCC	Decreases cell apoptosis and promote tumor metastasis Acts as a strong angiogenic stimulant	(66, 67)