Inhibition of GHRH aggravated acetaminophen-induced acute mice liver injury through GH/IGF-I axis

摘要: The aim of the current study is to investigate effects growth hormone releasing (GHRH) antagonist on acetaminophen (APAP)-induced acute liver injury in mice. Healthy C57/B6L mice were orally treated with 200 mg/kg APAP or without a 30-min pre-treatment 300 µg/kg GHRH MZ-5-156. After 12 hours, serum, plasma, and samples from each mouse collected for analyses. Our results showed that twelve-hour treatment caused obvious injury, elevated serum alanine aminotransferase (ALT) aspartate (AST) levels, increased oxidative stress, reduced expressions antioxidant enzymes, accumulated expression pro-inflammatory cytokines, circulating levels (GH) insulin-like factor-I (IGF-I). Pre-treatment MZ-5-156 aggravated further ALT AST exacerbated stress inflammation induced by APAP. Treatment also blocked phosphorylation form total Janus kinase 2 (JAK2) signal transducer activator transcription 5 (STAT5). super-agonist JI-38 immediately after partly reversed In conclusion, plays essential protective role APAP-induced vivo. properties are partially through GH/IGF-I axis JAK/STAT pathway.