Adenosine A2A receptors play a role in the pathogenesis of hepatic cirrhosis

摘要: 1. Adenosine is a potent endogenous regulator of inflammation and tissue repair. Adenosine, which released from injured hypoxic or in response to toxins medications, may induce pulmonary fibrosis mice, presumably via interaction with specific adenosine receptor. We therefore determined whether its receptors contribute the pathogenesis hepatic fibrosis. 2. As other tissues cell types, vitro fibrogenic stimuli ethanol (40 mg dl(-1)) methotrexate (100 nM). 3. A(2A) are expressed on rat human stellate lines receptor occupancy promotes collagen production by these cells. Liver sections mice treated hepatotoxins carbon tetrachloride (CCl(4)) (0.05 ml oil, 50 : v v, subcutaneously) thioacetamide kg(-1) PBS, intraperitoneally) more than those untreated when cultured ex vivo. 4. receptor-deficient, but not wild-type A(3) protected development following CCl(4) exposure. 5. Similarly, caffeine (50 day(-1), po), nonselective antagonist, ZM241385 (25 bid), selective antagonist receptor, diminished exposed either thioacetamide. 6. These results demonstrate that play an active role fibrosis, suggest novel therapeutic target treatment prevention cirrhosis.