Gang Chen1, Yang Yang2, Moli Liu3, Zhiying Teng4, Juan Ye2, Yuehua Xu5, Xueting Cai2, Xiaolan Cheng2, Jie Yang2, Chunping Hu2, Min Wang6, Peng Cao7. 1. State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, Jiangsu, China; Laboratory of Cellular and Molecular Biology, Jiangsu Province Institute of Traditional Chinese Medicine, Nanjing 210028, Jiangsu, China. 2. Laboratory of Cellular and Molecular Biology, Jiangsu Province Institute of Traditional Chinese Medicine, Nanjing 210028, Jiangsu, China. 3. State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, Jiangsu, China. 4. School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, China. 5. State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu, China. 6. State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, Jiangsu, China. Electronic address: minwang@cpu.edu.cn. 7. Laboratory of Cellular and Molecular Biology, Jiangsu Province Institute of Traditional Chinese Medicine, Nanjing 210028, Jiangsu, China. Electronic address: pcao79@yahoo.com.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Banxia Xiexin decoction (BXD), one of a traditional Chinese medicine chronicled in Shang Han Lun, is commonly used to treat gastroenteritis, ulcerative colitis and diarrhea. In our study, we used current biomedical approaches to investigate the therapeutic efficacy of BXD and possible protective mechanism involved in inhibiting dextran sulfate sodium (DSS)-induced chronic ulcerative colitis model. MATERIALS AND METHODS: Chronic DSS colitis was induced in C57BL/6 male mice by three cycles of 5 days of 2% DSS in drinking water, alternating with 5 days of normal water, totaling 30 days. In BXD group, the mice were administered at a dose of 8.7g/kg BXD for 5 days before and during DSS treatment via oral gavage per day. Mice in vehicle group and DSS group were given orally the same volume of drinking water, instead. Body weight, stool characters and hematochezia were observed everyday. The colorectal tissues were used to detect levels of TNF-α, IL-4, IL-10, IL-1β, IL-17, IL-23 and MPO by ELISA or qRT-PCR. The expression of COX-2, 8-Oxoguanine and Nrf2 were examined by IHC, and p-p65 was examined by western blotting. ThOD and the content of MDA were measured according to kits respectively. RESULTS: BXD significantly protected against DSS-induced chronic ulcerative colitis by amelioration of body weight loss, DAI and histology score. The level of TNF-α, IL-1β, IL-17, IL-23, COX-2 and p-p65 were decreased significantly, while the level of IL-10 improved with the treatment of BXD. MDA, MPO and 8-Oxoguanine were decreased, meanwhile SOD activity and Nrf2 expression were elevated significantly by BXD. CONCLUSIONS: BXD possesses the potential of anti-inflammation and anti-oxidation to treat colitis. The protective mechanism of BXD may involve in inhibition of NF-κBp65 activation and increasement of Nrf2 expression in colorectums of mice.
ETHNOPHARMACOLOGICAL RELEVANCE: Banxia Xiexin decoction (BXD), one of a traditional Chinese medicine chronicled in Shang Han Lun, is commonly used to treat gastroenteritis, ulcerative colitis and diarrhea. In our study, we used current biomedical approaches to investigate the therapeutic efficacy of BXD and possible protective mechanism involved in inhibiting dextran sulfate sodium (DSS)-induced chronic ulcerative colitis model. MATERIALS AND METHODS: Chronic DSScolitis was induced in C57BL/6 male mice by three cycles of 5 days of 2% DSS in drinking water, alternating with 5 days of normal water, totaling 30 days. In BXD group, the mice were administered at a dose of 8.7g/kg BXD for 5 days before and during DSS treatment via oral gavage per day. Mice in vehicle group and DSS group were given orally the same volume of drinking water, instead. Body weight, stool characters and hematochezia were observed everyday. The colorectal tissues were used to detect levels of TNF-α, IL-4, IL-10, IL-1β, IL-17, IL-23 and MPO by ELISA or qRT-PCR. The expression of COX-2, 8-Oxoguanine and Nrf2 were examined by IHC, and p-p65 was examined by western blotting. ThOD and the content of MDA were measured according to kits respectively. RESULTS: BXD significantly protected against DSS-induced chronic ulcerative colitis by amelioration of body weight loss, DAI and histology score. The level of TNF-α, IL-1β, IL-17, IL-23, COX-2 and p-p65 were decreased significantly, while the level of IL-10 improved with the treatment of BXD. MDA, MPO and 8-Oxoguanine were decreased, meanwhile SOD activity and Nrf2 expression were elevated significantly by BXD. CONCLUSIONS: BXD possesses the potential of anti-inflammation and anti-oxidation to treat colitis. The protective mechanism of BXD may involve in inhibition of NF-κBp65 activation and increasement of Nrf2 expression in colorectums of mice.