PTGS2 and hyperlipidemia: Additionally, LPC 18:0 protects against endotoxemia and experimental sepsis by inhibiting lipopolysaccharide-mediated caspase-11 activation (14), and LPC 16:0 and LPC 20:4 increased the transcription and protein levels of cyclooxygenase-2 (COX-2) to maintain basal endothelial COX-2 expression, which led to an excess of proinflammatory and vasoconstricting prostanoids in hyperlipidemia (15).