title: [Proanthocyanidin protects H9C2 cells against hypoxia/reoxygenation injury via JAK2/STAT3 signaling pathway].
abstract: The present study was aimed to investigate the underlying mechanisms of the protective effect of proanthocyanidin (Pro) against hypoxia/reoxygenation (H/R) injury in H9C2 cells with a focus on Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. H9C2 cells were randomly assigned to 5 groups, including the control group (Con), the H/R-injured group (H/R), the Pro-treated group (H/R+Pro), the JAK2 siRNA-treated group (H/R+Pro+JAK2 siRNA) and the JAK2 siRNA control group (H/R+JAK2 siRNA). The cells were pretreated with Pro (40 µmol/L) for 8 h before 2 h of hypoxia and 4 h of reoxygenation. Cellular viability and apoptosis rate were detected by MTT and TUNEL methods, and superoxide generation was measured. JAK2/STAT3 signaling, oxidative stress markers and endoplasmic reticulum stress markers were also detected by Western blot. We found that Pro treatment significantly improved cellular viability and reduced apoptosis rate in H/R-treated H9C2 cells. In addition, Pro treatment significantly up-regulated the phosphorylation levels of JAK2 and STAT3, down-regulated the superoxide generation, gp91phox, glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP) and caspase-12 expression. However, these protective effects of Pro were all attenuated by JAK2 siRNA administration. Taken together, we demonstrated that Pro protects H9C2 cells against H/R-induced oxidative stress and endoplasmic reticulum stress injury via JAK2/STAT3 signaling pathway.
authors: Emergency Department of Jiangsu Research Institute of Traditional Chinese Medicine, Nanjing 210028, China.|Experimental Teaching Center, The Fourth Military Medical University, Xi'an 710032, China.
authors: Chen-Bin
authors: CB
authors: Yu
authors: Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China.
authors: Guo-Long
authors: GL
authors: Zhao
authors: Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China.
authors: Li-Ming
authors: LM
authors: Yu
authors: Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China.
authors: Shi-Qiang
authors: SQ
authors: Yu
authors: Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China. duanweixun@126.com.
authors: Wei-Xun
authors: WX
authors: Duan
authors: Experimental Teaching Center, The Fourth Military Medical University, Xi'an 710032, China. hfzhang@fmmu.edu.cn.
authors: Hai-Feng
authors: HF
authors: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D015687:Cell Hypoxia; D002460:Cell Line; D002470:Cell Survival; D059865:Endoplasmic Reticulum Stress; D020287:In Situ Nick-End Labeling; D053616:Janus Kinase 3; D010084:Oxidation-Reduction; D010766:Phosphorylation; D044945:Proanthocyanidins; D020011:Protective Agents; D034741:RNA, Small Interfering; D051381:Rats; D050796:STAT3 Transcription Factor; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: C507936:Jak3 protein, rat; D044945:Proanthocyanidins; D020011:Protective Agents; D034741:RNA, Small Interfering; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat; C013221:proanthocyanidin; D053616:Janus Kinase 3