In addition, Compound C (an AMPK inhibitor) decreased the expression of Occludin and ZO-1 in ECs following LPS combined with adenosine treatment. Moreover, the inhibition of adenosine to LPS-induced inactivation of AMPK/AKT signaling pathway was partly recused by A2AR suppression. However, inhibition the A2A receptor (A2AR) could attenuate the influence of adenosine on LPS-treated ECs, indicating that adenosine alleviated LPS-induced BLB damage by activating A2AR. Meantime, LPS-induced increasing in reactive oxygen species (ROS) production and ECs permeability also was rescued by adenosine treatment. LPS treatment obviously suppressed the expression of Occludin and Zonula occludens-1 (ZO-1) in ECs, which was partly recused by adenosine treatment. Our data showed that adenosine at dosage of 1, 10, and 20 μM had no influence on the cell viability of ECs. In our study, ECs were treated with LPS to mimic BLB damage in vitro. The aims of our study was to explore the role and action mechanism of adenosine in LPS-induced endothelial cells (ECs) damage, which are one of the major principal cell type for blood-labyrinth barrier (BLB), and so as to assess the potential of adenosine to be used in the treatment of BLB disruption in animal experiment. Blood-labyrinth barrier (BLB) disruption plays a crucial role in the development of otitis media.
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