期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 96, 期 1, 页码 138-150出版社
WILEY
DOI: 10.1002/jnr.24098
关键词
diabetic encephalopathy; cognitive dysfunction; tryptophan; serotonin; 3-hydroxykynurenine; LC-MS; MS
资金
- Natural Science Foundation of China [81403001]
- China Postdoctoral Science Foundation [2016T90510, 2015M580474]
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [13KJB350007]
- Open Project Program of Jiangsu Key Laboratory of Drug Metabolism & Pharmacokinetics, China Pharmaceutical University [k-201402]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
Diabetic encephalopathy (DE), one of the most prevalent chronic complications of diabetes mellitus, is short of effective prevention and formidable therapeutic strategies. The aim of the present study is to reveal the imbalance of tryptophan (Trp) and its metabolites in streptozotocin (STZ)-induced experimental DE rats to underscore their critical values in clinical diagnosis of the disease. For this purpose, we first developed an accurate and appropriate simultaneous method for measuring Trp and its metabolites using liquid chromatography-tandem mass spectrometry, which was in accordance with the requirements of biological sample analysis. Secondly, a single STZ intraperitoneal injection was administered to male Sprague-Dawley rats, and their cognitive function was detected by Morris water maze tests. Cerebrospinal fluid (CSF), serum, and brain tissue were then collected for the determination of Trp and its metabolites. Compared with age-matched control rats, the levels of neuroprotective serotonin decreased significantly in the samples of cortices, hippocampi, striatum, CSF, and serums in the STZ-induced DE rats, while the levels of neurotoxic 3-hydroxykynurenine increased significantly. Moreover, analogous changes of both compounds were found in the central nervous system and peripheral blood of the STZ-induced DE rats. In conclusion, we established a quantitative method for the simultaneous detection of Trp and its metabolites, and we also present a critical elucidation of the nervous system dysfunction in DE.
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