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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Astragalus Plant, Cell Line, Enzyme Activation, Extracellular Signal-Regulated MAP Kinases, Gene Expression, Interleukin-8, JNK Mitogen-Activated Protein Kinases, Lipopolysaccharides, MAP Kinase Signaling System, Phosphorylation, Polysaccharides, Rats, Time Factors, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
user
Does astragalus mongholicus polysaccharide inhibit lipopolysaccharide-induced production of TNF-alpha and interleukin-8? Context: To explore the effect of Astragalus mongholicus polysaccharide (APS) on gene expression and mitogen-activated protein kinase (MAPK) transcriptional activity in intestinal epithelial cells (IEC). IEC were divided into control group, lipopolysaccharide (LPS) group, LPS+ 50 microg/mL APS group, LPS+ 100 microg/mL APS group, LPS+ 200 microg/mL APS group, and LPS+ 500 microg/mL APS group. Levels of mRNAs in LPS-induced inflammatory factors, tumor necrosis factor (TNF)-alpha and interleukin (IL)-8, were measured by reverse transcription-polymerase chain reaction. MAPK protein level was measured by Western blotting. The levels of TNF-alpha and IL-8 mRNAs were significantly higher in IEC with LPS-induced damage than in control cells. APS significantly abrogated the LPS-induced expression of the TNF-alpha and IL-8 genes. APS did not block the activation of extracellular signal-regulated kinase or c Jun amino-terminal kinase, but inhibited the activation of p38, suggesting that APS inhibits LPS-induced production of TNF-alpha and IL-8 mRNAs, possibly by suppressing the p38 signaling pathway.
assistant
APS-modulated bacterial product-mediated p38 signaling represents an attractive strategy for prevention and treatment of intestinal inflammation. Final Decision: yes