title: Hydrogen-rich saline protects against mitochondrial dysfunction and apoptosis in mice with obstructive jaundice.
abstract: Previous studies have demonstrated that hydrogen-rich saline (HS) protects against bile duct ligation (BDL)-induced liver injury by suppressing oxidative stress and inflammation. Mitochondria, which are targets of excessive reactive oxygen species and central mediators of apoptosis, have a pivotal role in hepatic injury during obstructive jaundice (OJ); however, the implications of HS in the hepatic mitochondria of BDL mice remain unknown. The present study investigated the hypothesis that HS could reduce OJ‑induced liver injury through the protection of mitochondrial structure and function, as well as inhibition of the mitochondrial apoptotic pathway. Male C57BL/6 mice were randomly divided into three experimental groups: Sham operation group, BDL injury with normal saline (NS) treatment group, and BDL‑injury with HS treatment group. Mitochondrial damage and apoptotic parameters were determined 3 days post‑BDL injury and treatment. The results demonstrated that mitochondria isolated from the livers of NS-treated BDL mice exhibited increased mitochondrial swelling, cytochrome c release, and oxidative damage. In addition, liver samples from NS‑treated BDL mice exhibited significant increases in B‑cell lymphoma 2 (Bcl‑2)‑associated X protein expression, caspase activities, and hepatocyte apoptosis compared with livers from sham‑operated controls. Notably, treatment with HS reduced the levels of these markers and alleviated morphological defects in the mitochondria following injury. In addition, HS markedly increased the antioxidant potential of mitochondria, as evidenced by elevated adenosine triphosphate levels, mitochondrial respiratory function, and increased levels of active Bcl‑2. In conclusion, HS attenuates mitochondrial oxidative stress and dysfunction, and inhibits mitochondrial-mediated apoptosis in the livers of BDL mice.
authors.affiliation: Department of Surgical Oncology, The General Hospital of Chinese People's Liberation Army, Beijing 100853, P.R. China.
authors.forename: Qu
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Department of General Surgery, People's Liberation Army No. 254 Hospital, Nankai University, Tianjin 300141, P.R. China.
authors.forename: Bao-Shan
authors.initials: BS
authors.lastname: Li
authors.affiliation: Department of Cell Biology, Beijing Institute of Basic Medical Sciences, Academy of Military Medicine, Beijing 100850, P.R. China.
authors.forename: Yu-Jiao
authors.initials: YJ
authors.lastname: Song
authors.affiliation: Department of Surgical Oncology, The General Hospital of Chinese People's Liberation Army, Beijing 100853, P.R. China.
authors.forename: Ming-Gen
authors.initials: MG
authors.lastname: Hu
authors.affiliation: Department of General Surgery, People's Liberation Army No. 254 Hospital, Nankai University, Tianjin 300141, P.R. China.
authors.forename: Jian-Yue
authors.initials: JY
authors.lastname: Lu
authors.affiliation: Department of General Surgery, People's Liberation Army No. 254 Hospital, Nankai University, Tianjin 300141, P.R. China.
authors.forename: Ang
authors.initials: A
authors.lastname: Gao
authors.affiliation: Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Xue-Jun
authors.initials: XJ
authors.lastname: Sun
authors.affiliation: Department of Cell Biology, Beijing Institute of Basic Medical Sciences, Academy of Military Medicine, Beijing 100850, P.R. China.
authors.forename: Xi-Ming
authors.initials: XM
authors.lastname: Guo
authors.affiliation: Department of Surgical Oncology, The General Hospital of Chinese People's Liberation Army, Beijing 100853, P.R. China.
authors.forename: Rong
authors.initials: R
authors.lastname: Liu
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D045304:Cytochromes c / Q000378:metabolism; D004195:Disease Models, Animal; D006859:Hydrogen / Q000737:chemistry* / Q000494:pharmacology; D041781:Jaundice, Obstructive / Q000378:metabolism / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; D019253:Proto-Oncogene Proteins c-bcl-2; D012462:Saline Solution, Hypertonic; D051028:bcl-2-Associated X Protein; D006859:Hydrogen; D000255:Adenosine Triphosphate; D045304:Cytochromes c