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QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling.
Cell Prolif. 2019 Mar; 52(2):e12547.CP

Abstract

OBJECTIVE

Chinese Herb QingBai decoction (QBD) has been approved affective in the treatment of IBD patients in clinic. However, the underlying mechanism remains unknown. We aim to investigate the effect of QBD on the mouse model of ulcerative colitis and its possible mechanism.

METHODS

C57/bL mice were given 5% DSS to induce colitis and were divided as QBD and mesalazine group. Weight, faeces and mental status were recorded each day and the histopathological changes (goblet cells etc) of the colon were observed after sacrificed. Fluorescein isothiocyanate-dextran 4000 was measured to reflect the intestinal mucosal permeability. In addition, cell junction-related proteins and possible signal pathways were investigated.

RESULTS

QingBai decoction could significantly alleviate the inflammation and the protection effect of colitis is comparable as those in mesalazine enema group. It was found that the permeability reduced significantly with QBD treatment vs the control group, while no significant difference between the mesalazine and QBD groups. QBD treatment could upregulate the expression of tight junction complex(ZO-1, claudin-1 and occludin)and muc-2 expression. It significantly reduced the production and secretion of serials proinflammatory cytokines (IL-1β, IL-6, Kc and TNF-α) compared with the control group. Meanwhile, NF-κB and Notch pathways were regulated.

CONCLUSION

QingBai decoction can effectively alleviate intestinal inflammation and mucosal barrier function in colitis mice, and the mechanism may be related to the inhibition of inflammatory cascade as well as enhanced mucus layer barrier and mechanical barrier function by NF-κB and Notch signalling.

Authors+Show Affiliations

Department of Gastroenterology, Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shanxi, China.Department of Gastroenterology, Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shanxi, China.Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan, China.Department of Gastroenterology, Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shanxi, China.Department of Gastroenterology, Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shanxi, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. Department of Gastroenterology, NO. 307 Hospital of PLA, Beijing, China.Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan, China.Laboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, China.Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30657238

Citation

Lin, Jun-Chao, et al. "QingBai Decoction Regulates Intestinal Permeability of Dextran Sulphate Sodium-induced Colitis Through the Modulation of Notch and NF-κB Signalling." Cell Proliferation, vol. 52, no. 2, 2019, pp. e12547.
Lin JC, Wu JQ, Wang F, et al. QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling. Cell Prolif. 2019;52(2):e12547.
Lin, J. C., Wu, J. Q., Wang, F., Tang, F. Y., Sun, J., Xu, B., Jiang, M., Chu, Y., Chen, D., Li, X., Su, S., Zhang, Y., Wu, N., Yang, S., Wu, K., & Liang, J. (2019). QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling. Cell Proliferation, 52(2), e12547. https://doi.org/10.1111/cpr.12547
Lin JC, et al. QingBai Decoction Regulates Intestinal Permeability of Dextran Sulphate Sodium-induced Colitis Through the Modulation of Notch and NF-κB Signalling. Cell Prolif. 2019;52(2):e12547. PubMed PMID: 30657238.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling. AU - Lin,Jun-Chao, AU - Wu,Jie-Qiong, AU - Wang,Fang, AU - Tang,Feng-Ying, AU - Sun,Jia, AU - Xu,Bing, AU - Jiang,Mingzuo, AU - Chu,Yi, AU - Chen,Di, AU - Li,Xiaowei, AU - Su,Song, AU - Zhang,Yujie, AU - Wu,Nan, AU - Yang,Shaoqi, AU - Wu,Kaichun, AU - Liang,Jie, Y1 - 2019/01/18/ PY - 2018/07/12/received PY - 2018/09/20/revised PY - 2018/10/10/accepted PY - 2019/1/19/pubmed PY - 2019/4/16/medline PY - 2019/1/19/entrez KW - MMP-9 KW - Mucin-2 KW - Notch KW - QingBai decoction KW - intestinal permeability KW - ulcerative colitis SP - e12547 EP - e12547 JF - Cell proliferation JO - Cell Prolif. VL - 52 IS - 2 N2 - OBJECTIVE: Chinese Herb QingBai decoction (QBD) has been approved affective in the treatment of IBD patients in clinic. However, the underlying mechanism remains unknown. We aim to investigate the effect of QBD on the mouse model of ulcerative colitis and its possible mechanism. METHODS: C57/bL mice were given 5% DSS to induce colitis and were divided as QBD and mesalazine group. Weight, faeces and mental status were recorded each day and the histopathological changes (goblet cells etc) of the colon were observed after sacrificed. Fluorescein isothiocyanate-dextran 4000 was measured to reflect the intestinal mucosal permeability. In addition, cell junction-related proteins and possible signal pathways were investigated. RESULTS: QingBai decoction could significantly alleviate the inflammation and the protection effect of colitis is comparable as those in mesalazine enema group. It was found that the permeability reduced significantly with QBD treatment vs the control group, while no significant difference between the mesalazine and QBD groups. QBD treatment could upregulate the expression of tight junction complex(ZO-1, claudin-1 and occludin)and muc-2 expression. It significantly reduced the production and secretion of serials proinflammatory cytokines (IL-1β, IL-6, Kc and TNF-α) compared with the control group. Meanwhile, NF-κB and Notch pathways were regulated. CONCLUSION: QingBai decoction can effectively alleviate intestinal inflammation and mucosal barrier function in colitis mice, and the mechanism may be related to the inhibition of inflammatory cascade as well as enhanced mucus layer barrier and mechanical barrier function by NF-κB and Notch signalling. SN - 1365-2184 UR - https://www.unboundmedicine.com/medline/citation/30657238/QingBai_decoction_regulates_intestinal_permeability_of_dextran_sulphate_sodium_induced_colitis_through_the_modulation_of_notch_and_NF_κB_signalling_ L2 - https://doi.org/10.1111/cpr.12547 DB - PRIME DP - Unbound Medicine ER -