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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: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Anti-Inflammatory Agents, Antioxidants, Chemical Fractionation, Colitis, Colon, Curcuma, Cytokines, Dextran Sulfate, Disease Models, Animal, Gastric Juice, Gastrointestinal Agents, Gene Expression Regulation, Inflammation Mediators, Intestinal Secretions, Male, Oxidative Stress, Phytotherapy, Plant Extracts, Plants, Medicinal, Rats, Sprague-Dawley, Time Factors.
user
Does semi-bionic extraction of compound turmeric protect against dextran sulfate sodium-induced acute enteritis in rats? Context: Compound turmeric has been widely used as a remedy for infectious diseases in China. It is a classic multi-herb prescription in traditional Chinese medicine, commonly used in the treatment of enteritis, pneumonia, and abdominal pain for hundreds of years. However, throughout this history, the powder of multi-herbs was directly swallowed, which is currently difficult to administer to patients. The extract of Chinese herbal medicine is made by semi-bionic extraction technology, which is great progress in the modernization of powders of traditional Chinese medicine. The aim of this work is to investigate the protective effects of semi-bionic extraction of compound turmeric (SET) on acute enteritis (AE) induced by dextran sulfate sodium (DSS) in rats. SET was extracted in artificial gastric juice or artificial intestinal juice and mixed. After vacuum drying, the SET powder was dissolved in distilled water. Adult male Sprague-Dawley rats were randomly divided into six groups. Rats were given salazosulfapyridine (SASP, 175.0mg/kg) or SET (0.42 or 0.21g/kg) before intragastric administration of 5% DSS solutions (0.75g/kg). The treatments lasted 7 days. The food intake in 24h, disease activity index (DAI), and wet/dry (W/D) weight ratios and histological changes in colon tissue were measured. The tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, IL-8, and IL-10 in serum were determined at 1, 4, or 7 d after DSS challenge. Myeloperoxidase (MPO), malonaldehyde (MDA), diamine oxidase (DAO), and glutathione peroxidase (GSH-Px) activities in colon tissue were determined at 7 d. In addition, the nuclear factor-kappa (NF-κ B) and intercellular cell adhesion molecule-1 (ICAM-1) activations in colon tissue were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. In rats with AE, SET significantly reduced DAI at 7 d after DSS treatment, increased the body weight of rats and the food intake in 24h at 3 or 6 d after DSS challenge, and reduced the colon W/D ratio. SET also reduced the TNF-α, IL-6, IL-1β, and IL-8 in serum and increased IL-10 in serum at 4 and 7 d. In addition, SET decreased MPO, MDA, DAO, and GSH-Px activities in colon and attenuated histological changes in the colon at 7 d after DSS treatment. Further studies demonstrated that SET significantly inhibited NF-κB and ICAM-1 activations in colon tissue.
assistant
The current study demonstrated that SET has potent protective effects on DSS-induced AE in rats through its anti-inflammatory and anti-oxidant activities. Final Decision: yes