Abstract: Objective To study the signaling pathways associated with lipopolysaccharide (LPS)-induced inflammation in islet
microendothelial cells (IMECs) and the mechanism of pravastatin intervention. Methods IMECs exposed to LPS, SB203580,
pravastatin, or SB203580 + pravastatin were examined for cell apoptosis with Hoechst staining and flow cytometry and for
expression levels of total-p38, photophosphorylation-p38 (p-p38) and iNOS with Western blotting. Results The apoptosis rate
and expression levels of total-p38, p-p38, iNOS in IMECs all increased after LPS exposure. Pravastatin, SB203580, and their
combination significantly attenuated LPS-induced enhancement of cell apoptosis and total-p38, p-p38, and iNOS expressions
in IMECs. Conclusion LPS-induced inflammatory toxicity in IMECs is associated with the activation of P38MAPK and iNOS/
NO signaling pathways. Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve
the cell inflammatory injuries.