@article{Li2017, 
author = {Yijie Li and Xiaolan Su and Peng Wu and Jifeng Wang and Yu Guo and Jiajie Zhu and Qingguo Wang and Jiande Chen and Fuquan Yang and Wei Wei},
title = {Proteomics analysis of IBS-D with spleen and kidney yang deficiency},
year = {2017},
journal = {Journal of Traditional Chinese Medical Sciences},
volume = {4},
number = {1},
pages = {39-49},
keywords = {Spleen and kidney yang deficiency, IBS-D, Proteomics, Mechanism},
url = {https://www.sciopen.com/article/10.1016/j.jtcms.2017.05.006},
doi = {10.1016/j.jtcms.2017.05.006},
abstract = {ObjectiveTo investigate the molecular mechanism underlying the development of diarrhea-predominant irritable bowel syndrome (IBS-D) with spleen and kidney yang deficiency (SKYD) using a proteomics approach.MethodsMale Sprague–Dawley rats (n = 22) were divided into IBS-D (n = 12) and normal control (n = 10) groups. SKYD was then modeled in IBS-D rats by a combination of acetic acid enema, bondage, rectal dilation, tail stimulation, and Senna gavage. Colon tissue samples were subsequently collected and examined by Q Exactive mass spectrometry to identify differentially expressed proteins between the two groups.ResultsThe occurrence of SKYD/IBS-D was associated with ribosomal protein S23 (Rps23), protein phosphatase 2 catalytic subunit alpha (Pp2a), and growth factor receptor-bound protein 2 (Grb2), which are involved in the ribosome, neurotrophin signaling, and Janus kinase–signal transducer and activator of transcription (JAK–STAT) signaling pathways.ConclusionThese data suggest that SKYD/IBS-D pathophysiology likely involves inflammation, cell growth, apoptosis, stress granule formation, immune activation, loss of epithelial cell integrity, and visceral hypersensitivity.}
}