Table 2.
Cell source | Experimental model | Administration rout | Result | References |
---|---|---|---|---|
Bone marrow |
Hepatic ischemia Reperfusion injury |
Intravenous | Repression of the transcription of inflammation-associated genes | Anger et al. [141] |
Bone marrow | Liver injury | Intravenous | Enhancement of anti-inflammatory cytokines and T regulatory cells | Tamura et al. [142] |
Bone marrow |
Hepatic ischemia Reperfusion injury |
Intravenous | A decrease in the number of recruiting macrophages and neutrophils as well as a reduction in TNF-α and IL-6 levels | Haga et al. [149] |
Umbilical cord | Acute liver injury | Intravenous | Reduced expression of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and TGF-β and number of Kuppfer cells | Ohara et al. [147] |
Umbilical cord |
Hepatic ischemia Reperfusion injury |
Intravenous |
Inhibition of neutrophil inflammatory response |
Yao et al. [143] |
Adipose tissue | Acute liver injury | Intravenous | Reduction in inflammatory activation in Kuppfer cells | Liu et al. [145] |
Umbilical cord | Acute liver injury | Intravenous | Reduction in NLRP3, Casp-1, IL-1, and IL-6 expressions in the macrophage | Jiang et al. [132] |
Embryonic stem cell | Chronic liver injury | Intravenous | Upregulation of anti-inflammatory cytokines (TGF-β1 and IL-10) and downregulation of pro-inflammatory cytokines (TNFα and IL-2) | Mardpour et al. [148] |
Bone marrow | Experimental autoimmune epatitis | Intraperitoneal | Regulation of NLRP3 and caspase-1 | Chen et al. [140] |
Bone marrow | Autoimmune hepatitis | Intraperitoneal | Reduction in inflammatory responses | Lu et al. [144] |
Liver tissue | Liver fibrosis | Intravenous | Modulating the inflammatory response | Bruno et al. [146] |
Adipose tissue | NASH model | Intravenous | Increase in anti-inflammatory macrophages in the liver | Watanabe et al. [148] |