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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, METHODS, METHODS, METHODS, RESULTS. Meshes: Animals, Antithrombins, Apoptosis, Insulin-Like Growth Factor I, Liver, Male, Mice, Reperfusion Injury.
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Does antithrombin prevent reperfusion-induced hepatic apoptosis by enhancing insulin-like growth factor-I production in mice? Context: Antithrombin (AT) reduces ischemia/reperfusion-induced liver injury by increasing release of calcitonin gene-related peptide (CGRP) from sensory neurons. Because CGRP increases the production of insulin-like growth factor-I (IGF-I), an antiapoptotic factor, it is possible that AT prevents apoptosis by increasing IGF-I production. We examined this possibility in the present study. Prospective, randomized, controlled study. University laboratory. Male C57BL/6 wild-type mice and alphaCGRP-deficient mice weighing 16-23 g. AT (250 units/kg) was intravenously administered to mice subjected to hepatic ischemia/reperfusion. Liver injury was evaluated by determining changes in serum levels of alanine aminotransferase after ischemia/reperfusion. Hepatic apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining. AT reduced ischemia/reperfusion-induced liver injury and enhanced increases in hepatic tissue levels of IGF-I in wild-type mice, although it did not reduce liver injury or enhance increases in hepatic tissue levels of IGF-I in alphaCGRP-deficient mice. Reperfusion-induced hepatic apoptosis was markedly suppressed by AT in wild-type mice, but not in alphaCGRP-deficient mice. Pretreatment with anti-IGF-I antibody completely reversed therapeutic effects of AT in wild-type mice. Both CGRP and IGF-I showed therapeutic effects similar to those of AT in wild-type and alphaCGRP-deficient mice.
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: These observations suggested that AT may prevent reperfusion-induced hepatic apoptosis by enhancing IGF-I production through promotion of sensory neuron activation, thereby reducing ischemia/reperfusion-induced liver injury. Final Decision: yes