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Portal hypertension is an increased in the blood pressure within portal venous system, liver damage may block blood vessels in the liver this prevents proper flow of blood in the liver and leads to portal hypertension. Treatment with aleglitazar, a dual peroxisome proliferator-activated receptor-alpha/gamma (PPARα/γ) agonist, reduced inflammation, vasoconstriction, angiogenesis, mucosal disruption, and tumor necrosis factor (TNF)-α overproduction in cirrhotic rats with PH.
Nonselective beta-blockers, which lack splanchnic and intestinal effects, have been the mainstay of drug therapy for PH but are limited by their potential for adverse effects. Cirrhosis of the liver is a serious condition in which the liver is permanently scarred, as a result of liver disease, hepatitis C virus, or alcohol or drug use. Cirrhosis is the most common cause of PH and can result in fluid accumulation, increased spleen size, and swollen veins around the esophagus and intestines.
Treatment with aleglitazar for 21 days produced changes in cirrhotic rats. In the liver, aleglitazar suppressed hepatic fibrogenesis, neoangiogenesis, and vasoconstrictor responsiveness. In the splanchnic system, aleglitazar reduced neoangiogenesis, vasodilatation, and portosystemic shunts. It also decreased intestinal mucosal injury and hyper-permeability. The dual composition of aleglitazar expand its effectiveness. PPARγ is activated in the liver, PPARα is activated in the intestine, and both PPARα and PPARγ mediate effects in the splanchnic system.
haleplushearty.org