Liver cirrhosis reversion is improved in hamsters with a neurointermediate pituitary lobectomy

Regulating mechanisms of fibrosis is an important goal in the treatment of fibrosis and liver cirrhosis. The role of arginine vasopressin (AVP) in promoting fibrosis in several organs has been well documented. However, the result of an AVP deficiency during liver fibrosis has not been reported. We herein study the effects of an AVP deficiency, which was induced by neurointermediate pituitary lobectomy (NIL), on liver cirrhosis and liver cirrhosis reversion. Hamsters were intact (control) or underwent CCl₄-induced cirrhosis, the latter animals divided into four groups: Cirrhotic, NIL-cirrhotic, Cirrhotic-reversion (R) and NIL-cirrhotic-R. Liver function, liver histopathology (including the fibrosis area and collagen types) and liver expression of MMP-13 and TIMP-2 were assessed. Results show that the AVP deficiency decreased the levels of alkaline phosphatase in serum and the expression of type I collagen and TIMP-2, and increased type III collagen deposition, MMP-13 expression and the size of regeneration nodules in NIL-cirrhotic and NIL-cirrhotic-R animals. A significantly greater recovery was found in the NIL-cirrhotic-R than the Cirrhotic-R group. We conclude that an AVP deficiency participates importantly in hamster liver regeneration by: 1) prompting the fibroblasts to produce type III collagen deposit, 2) influencing the activity of AP from bile duct cells, and 3) inhibiting TIMP-2 expression while favoring the fibrolytic activity of MMP-13.