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Overexpression of cyclooxygenase\u20102 (COX\u20102), a major intravascular source of ROS production, has been observed in LSECs of cirrhotic liver. However, the links between low NO bioavailability and COX\u20102 overexpression in LSECs are unknown. This study has confirmed the link between low NO bioavailability and COX\u20102 overexpression by COX\u20102\u2010dependent PGE2\u2010EP2\u2010ERK1\/2\u2010NOX1\/NOX4\u00a0signalling pathway in LSECs <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic>. In addition, the regulation of COX\u20102\u2010independent LKB1\u2010AMPK\u2010NRF2\u2010HO\u20101\u00a0signalling pathway on NO homeostasis in LSECs was also elucidated. The combinative effects of celecoxib on diminishment of ROS via COX\u20102\u2010dependent and COX\u20102\u2010independent signalling pathways greatly decreased NO scavenging. As a result, LSECs capillarisation was reduced, and endothelial dysfunction was corrected. 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