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Bilirubin improves the quality and function of hypothermic preserved islets by its antioxidative and anti-inflammatory effect.

BACKGROUND
Islet transplantation is a promising option for the treatment of type 1 diabetes. However, the current lack of practical techniques for the isolated islets preservation still hampers the advancement of life-saving islet transplantation. Islet suffers from internal or external stimuli induced oxidative stress and subsequent inflammation during preservation, which leads to disappointing outcomes regarding islet yield, survival and function. ROS overproduction is the primary cause of oxidative stress that induces islet loss and dysfunction. Thus, in this paper, we hypothesized that an endogenous antioxidant, bilirubin, that could efficiently scavenge ROS and inhibit inflammatory reactions could be beneficial for islet preservation.


METHODS
Herein, we studied the effect of bilirubin on the hypothermic preserved (4°C) islets, and evaluate the islets viability, insulin secretory function, oxidative stress levels, and in vivo transplantation performance.


RESULTS
Bilirubin could prevent cellular damages during short-term preservation, and maintain the co-cultured islets viability and function. The protective role of bilirubin is associated with its antioxidative ability, which dramatically increased the activities of antioxidant enzymes (SOD and GSH-Px), and decreased the levels of ROS and MDA. Diabetic mice transplanted with bilirubin preserved islets were normoglycemic for 28 days, even overmatched the diabetic mouse transplanted with fresh islets. Mice receiving bilirubin co-cultured islets required the least time to achieve normoglycemia among all groups and exhibited minimum inflammatory responses during the early transplantation stage.


CONCLUSIONS
By utilizing bilirubin, we achieved highly viable and functional islets after hypothermic preservation to reverse diabetes in mice.