Effectiveness of antiplatelet drugs against experimental non-alcoholic fatty liver disease

Abstract

Antiplatelet agents, especially cilostazol, offer the promise of becoming key agents for the treatment of NAFLD.

Hepatic sinusoidal endothelium avidly binds platelets in an integrin-dependent manner, leading to platelet and endothelial activation and leukocyte recruitment

“…Our findings explain how platelets bind to hepatic vessels and suggest that such interactions promote immune cell recruitment by triggering chemokine secretion and providing an adhesive substrate for circulating leukocytes. These findings provide further evidence that antiplatelet therapy might modify liver injury in inflammatory liver disease (18,61).…”

“…Platelets promote liver injury in models of hepatitis, and antiplatelet therapy is under investigation for treatment of chronic diseases such as nonalcoholic steatohepatitis (18). However, platelets also serve key hemostatic roles (51) and help neutrophils clear pathogens during sepsis (43).…”

The protective and therapeutic effect of phenoxy-2-methyl-2-propionic acid on experimental fatty liver in rats

“…A significant elevation was reported in serum urea levels in a DOX study in rabbits (11). Insignificant changes were seen in serum triglyceride levels in both rat and rabbit studies (22,24). Increased serum triglyceride levels were detected in rabbit and rat studies in which CCl 4 and a high fat diet were used (14,17).…”

“…Triglyceride levels were significantly higher in PMPA-administered Holstein cows compared to those not given PMPA (8). Cholesterol level was insignificant in an experimental rat study (24). High cholesterol levels were found to be significant in diet studies of rats and rabbits (15,22).…”

Novel Findings for the Development of Drug Therapy for Various Liver Diseases: Liver Microsomal Triglyceride Transfer Protein Activator May Be a Possible Therapeutic Agent in Non-alcoholic Steatohepatitis

“…Although both are well-established animal models of NAFLD, the former involves only fatty liver, not steatohepatitis, while the latter includes both steatohepatitis and liver cirrhosis (9). The mechanisms of fatty liver pathogenesis also differ in that lipids accumulate in the liver because of increased fatty acid (FA) inflow in the former model and because of the blockage of VLDL secretion in the latter (7,8).…”