Dibutyl phthalate (DBP) promotes Epithelial-Mesenchymal Transition (EMT) to aggravate liver fibrosis into cirrhosis and portal hypertension (PHT) via ROS/TGF-β1/Snail-1 signalling pathway in adult rats.

Objective: The primary objective of this study was to investigate the toxicological impact of Dibutyl phthalate (DBP) on the process of liver fibrosis transitioning into cirrhosis and the subsequent development of portal hypertension (PHT) through the mechanism of epithelial-mesenchymal transition (EMT) mediated by the ROS/TGF-β/Snail-1 signaling pathway.

Method: Carbon tetrachloride (CCl) (1 mg/kg) was introduced in adult rats by oral feeding in CCl and CCl+DBP groups twice a week for 8 weeks, and twice for another 8 week in CCl group. DBP was introduced by oral feeding in the CCl+DBP group twice over the following 8 weeks.

Cediranib ameliorates portal hypertensive syndrome via inhibition of VEGFR-2 signaling in cirrhotic rats.

Portal hypertension (PHT) is a syndrome caused by systemic and portal hemodynamic disturbances with the progression of cirrhosis. However, the exact mechanisms regulating angiogenesis-related responses in PHT remain unclear. Cediranib is a potent inhibitor of vascular endothelial growth factor receptor (VEGFR) tyrosine kinases, exhibiting a greater affinity for VEGFR-2.

Telmisartan relieves liver fibrosis and portal hypertension by improving vascular remodeling and sinusoidal dysfunction.

Backgrounds: Telmisartan(TEL) has demonstrated anti-fibrotic and blood pressure lowering effect in various diseases. In this study, we aimed to explore the beneficial effects of TEL on portal hypertension(PHT).

Methods: Two models of cirrhosis-induced PHT were involved including carbon tetrachloride injection(CCl) and bile duct ligation(BDL).