Objective To explore the protective effect of hydrogen-rich saline on liver ischemiareperfusion (IR) in mice and the possible mechanisms. Methods Twenty-four C57BL/6 mice were randomly divided into 3 groups: sham-operated group, control group (mice were injected with 5 ml/kg saline by tail vein just before ischemia induction) and hydrogen-rich saline group (mice were injected with 5 ml/kg hydrogen-rich saline). Six hour after reperfusion, the mice were sacrificed and the serum and liver samples undergoing IR injury were collected. The ALT and AST levels in serum were determined and liver histiological damage was also evaluated with Suziki's criteria. Malondialdehyde (MDA) contents in liver samples were measured using specific kits. The infiltration of F4/80 positive macrophage cells was detected by using immunohistochemistry and that of neutrophils with myeloperoxidase (MPO) kits. The mRNA expression of TNF-α, IL-6, ICAM-1 and IP-10 was assayed by using real-time reverse transcription PCR. The activation of transcription factor NF-κB was measured by using Western botting analysis. Results As compared with control group, at the 6th h following reperfusion, mice in hydrogen-rich saline group exhibited lower levels of ALT and AST (P＜0. 05) in serum, milder histological damage (P＜0. 01) and less MDA contents in liver samples (P＜0. 01). The infiltration of macrophages, neutrophils and the mRNA expression of TNF-α, IL-6,ICAM-1 and IP-10 in the liver tissue in hydrogen-rich saline group were reduced as compared with IR group (P＜0. 05 or P＜0. 01). The activation of NF-κB in hydrogen-rich saline group was significantly down-regulated as compared with control group. Conclusion Injection of hydrogen-rich saline via the tail vein can alleviate liver IR injury probably by inhibiting oxidant stress and inflammatory response induced by reperfusion.

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Pulmonary hypertension (PH) is an extremely malignant pulmonary vascular disease of unknown etiology. ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine, thereby affecting RNA expression. However, the role of ADAR1 in PH development remains unclear. In the present study, we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling. Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs). Conversely, inhibition of ADAR1 produced opposite effects. High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH. CircCDK17 level was significantly lowered in the serum of PH patients. The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17. ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from m1A modification. We demonstrate for the first time that ADAR1 contributes to the PH development, at least partially, through m1A modification of circCDK17 and the subsequent PASMCs proliferation. Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.