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To explore the efficacy and safety of endoscopic resection and open surgery for treating thyroid diseases using meta-analysis. Related data in computer retrieval of Cochrane Library, American National Library of Medicine Biomedical Information Retrieval System (Pub Med), Dutch Medicine Abstracts (Embase), China Biomedical Literature Database (CBM), China Academic Journals Full-text Database (CNKI), Chinese Science and Technology Journal Database (VIP), and Western Language Biomedical Journal Literature Database (EMC) from December 2019 to April 2020 were retrieved. Relevant journals and included references were manually searched. Randomized controlled trials regarding the effects of endoscopic thyroid surgery and open thyroid surgery on the immune response of thyroid diseases were included. Two reviewers conducted independent data extraction, quality evaluation and cross-checking according to inclusion and exclusion criteria. RevMan 5.1.4 software was employed. Eight non-randomized controlled retrospective cohort studies were finally included. The curative rate (168/185, 90.81 % vs. 194/383, 50.65 %, p

The small intestine is known to be particularly sensitive to radiation, and the major limiting factor of radiotherapy is the gastrointestinal syndrome that subsequently develops after its administration. The detrimental effects of radiation are mostly mediated via the overproduction of reactive oxygen species (ROS), especially the hydroxyl radical (·OH). Because hydrogen is a selective ·OH scavenger, we hypothesized that hydrogen might exert a protective effect against radiation-induced intestinal damage. Herein, radiation models were built both in mice and in an intestinal crypt epithelial cell (IEC-6) line. In the animal experiment, we demonstrated that hydrogen-rich saline significantly reduced radiation-induced intestinal mucosal damage, improved intestinal function, and increased the survival rate. In addition, radiation-induced oxidative stress damage and systemic inflammatory response were also mitigated by hydrogen treatment. Moreover, hydrogen treatment decreased cell apoptosis and maintained intestinal epithelial cell proliferation in mice. In vitro experiments using the IEC-6 cell line showed that hydrogen-rich medium significantly inhibited ROS formation, maintained cell viability, and inhibited cell apoptosis. Importantly, hydrogen treatment prevented mitochondrial depolarization, cytochrome c release, and activity of caspase-3, caspase-9, and PARP. Moreover, the decreased expression of Bcl-xl and Bcl-2 and the increased expression of Bax protein were also blocked by hydrogen treatment. In conclusion, our study concurrently demonstrated that hydrogen provides an obviously protective effect on radiation-induced intestinal and cell injuries. Our work demonstrated that this protective effect might be due to the blockage of the mitochondrial apoptotic pathway.