Hydrogen protects against liver injury during CO 2 pneumoperitoneum in rats

// Mingzi Chen 1 , Lihong Jiang 1 , Yue Li 1 , Ge Bai 1 , Jinghua Zhao 1 , Ming Zhang 1 and Jiantao Zhang 1 1 Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China Correspondence to: Jiantao Zhang, email: zhangjiantao@neau.edu.cn Keywords: hydrogen, CO 2 pneumoperitoneum, liver, ischemia-reperfusion Received: July 18, 2017      Accepted: October 05, 2017      Published: December 15, 2017 ABSTRACT The aim of the current study was to identify the protective effect of hydrogen gas against liver injury during CO 2 pneumoperitoneum. Rats were randomly divided into three groups: control group (C group), pneumoperitoneum group (P15 group) and hydrogen group (H 2 group). Rats in the C group were subjected to anesthesia for 90 min. Rats in the P15 group received an abdominal insufflation of CO 2 for 90 min at an intra-abdominal pressure of 15 mmHg. Rats in the H 2 group received a hypodermic injection of hydrogen gas (0.2 mL/kg) and after 10 min they received an abdominal insufflation of CO 2 for 90 min at an intra-abdominal pressure of 15 mmHg. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured to evaluate liver function. Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) content were measured to evaluate oxidative stress. Nuclear factor E2-related factor 2 (Nrf2) and Nrf2 downstream target genes, apoptosis-related genes and inflammatory cytokine mRNA and protein expression were detected. Liver injury was detected under the microscope. Our results revealed that liver function, antioxidants content, inflammation and liver injury were improved after hydrogen preconditioning in H 2 group compared with P15 group. Overall, our results revealed that subcutaneous hydrogen injection could exert a protective effect against liver injury during CO 2 pneumoperitoneum through reducing oxidative stress, cell apoptosis and inflammatory cytokines release.