Abstract
Mesenchymal stem cells (MSCs) have been increasingly applied into clinical therapy. Exosomes are small (30–100 nm in diameter) membrane vesicles released by different cell types and possess the similar functions with their derived cells. Human umbilical cord MSC-derived exosomes (hucMSC-Ex) play important roles in liver repair. However, the effects and mechanisms of hucMSC-Ex on liver injury development remain elusive. Mouse models of acute and chronic liver injury and liver tumor were induced by carbon tetrachloride (CCl4) injection, followed by administration of hucMSC-Ex via the tail vein. Alleviation of liver injury by hucMSC-Ex was determined. We further explored the production of oxidative stress and apoptosis in the development of liver injury and compared the antioxidant effects of hucMSC-Ex with frequently used hepatic protectant, bifendate (DDB) in liver injury. hucMSC-Ex alleviated CCl4-induced acute liver injury and liver fibrosis and restrained the growth of liver tumors. Decreased oxidative stress and apoptosis were found in hucMSC-Ex-treated mouse models and liver cells. Compared to bifendate (DDB) treatment, hucMSC-Ex presented more distinct antioxidant and hepatoprotective effects. hucMSC-Ex may suppress CCl4-induced liver injury development via antioxidant potentials and could be a more effective antioxidant than DDB in CCl4-induced liver tumor development.
Highlights
The imbalance between oxidant and antioxidant results in oxidative stress
Our previous studies demonstrated that the protective effect of human umbilical cord MSCs (hucMSCs)-derived exosomes on tissue repair including acute renal injury (AKI), cutaneous wound, and liver fibrosis [20,21,22] and even illuminated that hucMSC-Ex delivered GPX1 could promote the recovery of oxidatively injured liver [23]
We demonstrated that hucMSC-Ex could suppress CCl4-induced acute and chronic liver injury and liver tumor growth in mice
Summary
The imbalance between oxidant and antioxidant results in oxidative stress. Most chronic liver diseases, such as alcoholic liver disease, nonalcoholic fatty liver disease, liver fibrosis, and viral hepatitis, possess the increased oxidant stress [1]. Our previous studies have successfully isolated the MSCs from human umbilical cord and demonstrated that human umbilical cord MSCs (hucMSCs) could ameliorate mouse hepatic injury and acute renal failure [8,9,10,11]. Studies have suggested that mechanism of MSC in tissue repair may prefer secreting soluble factors to alter the tissue microenvironment rather than differentiation solely [14]. Our previous studies demonstrated that the protective effect of hucMSC-derived exosomes (hucMSC-Ex) on tissue repair including acute renal injury (AKI), cutaneous wound, and liver fibrosis [20,21,22] and even illuminated that hucMSC-Ex delivered GPX1 could promote the recovery of oxidatively injured liver [23]. We compared the antioxidative and antiapoptotic effects of hucMSC-Ex with that of bifendate (DDB) in CCl4-induced acute liver injury
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