Andrographolide derivative AL-1 reduces intestinal permeability in dextran sulfate sodium (DSS)-induced mice colitis model
| Autor: | Luchen Shan, Yun Cen, Yuke Wei, Pei Yu, Zaijun Zhang, Lipeng Xu, Nan Jiang, Yuqiang Wang |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Cell Membrane Permeability medicine.medical_treatment Andrographolide Anti-Inflammatory Agents Pharmacology 030226 pharmacology & pharmacy General Biochemistry Genetics and Molecular Biology Tight Junctions 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Western blot medicine Animals General Pharmacology Toxicology and Pharmaceutics Colitis Intestinal Mucosa Phosphorylation Myosin-Light-Chain Kinase Barrier function Intestinal permeability Tight junction medicine.diagnostic_test Chemistry Dextran Sulfate General Medicine medicine.disease Mucus Mice Inbred C57BL 030104 developmental biology Cytokine Diterpenes Signal Transduction |
| Zdroj: | Life sciences. 241 |
| ISSN: | 1879-0631 |
| Popis: | Aims This study was to assess whether andrographolide derivative (AL-1) could restore mucosal homeostasis and regulate tight junctions through MLCK-dependent pathway in DSS-induced colitis mice. Main methods Colitis mice model was induced by daily administration of 2.5% DSS for seven days. The therapeutic effect was determined by evaluating the histopathological changes and the pro-inflammatory cytokine level. In addition, the effects of AL-1 on tight junctions were examined by immunohistochemistry and Western blot. The expressions of factors in MLCK-dependent pathway were evaluated by immunofluorescence and Western blot. Key findings AL-1 protected the intestinal barrier function in DSS-induced colitis mice. These protective effects were achieved by maintaining the normal mucus secretion and preserving tight junctions via suppression of the MLCK-dependent pathway. Significance AL-1 could prevent the increase in the DSS-induced intestinal permeability. These data indicated that AL-1 could be a promising agent for UC treatment. |
| Databáze: | OpenAIRE |
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