Baicalein inhibits acinar-to-ductal metaplasia of pancreatic acinal cell AR42J via improving the inflammatory microenvironment
- Pu, Wei-Ling Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Luo, Ying-Ying Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Bai, Ru-Yu Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Guo, Ao-Wei Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Zhou, Kun Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Chinese medicine, Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Prescription Compatibility, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Zhang, Yun-Sha School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Pathology Unit, Faculty of Sciences, Department of Medicine, University of Fribourg, Switzerland
- Miao, Lin Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Chinese medicine, Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Prescription Compatibility, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Department of Molecular Mechanisms of Disease, University of Zurich-Irchel, Zurich, Switzerland
- Rüegg, Curzio Pathology Unit, Faculty of Sciences, Department of Medicine, University of Fribourg, Switzerland
- Hottiger, Micheal O. Department of Molecular Mechanisms of Disease, University of Zurich-Irchel, Zurich, Switzerland
- Gao, Xiu-Mei Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Chinese medicine, Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Prescription Compatibility, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Sun, Li-Kang Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Chinese medicine, Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China - Laboratory of Prescription Compatibility, Tianjin University of Traditional Chinese Medicine, Tianjin, China - School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
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2018
Published in:
- Journal of Cellular Physiology. - 2018, vol. 233, no. 8, p. 5747–5755
English
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive cancers. Recent research has demonstrated that chronic pancreatitis (CP) is associated with an increased risk of PDAC, partly due to acinar-to-ductal metaplasia (ADM). Baicalein has been shown to exert anti-inflammatory and anti-tumor effects for CP or PDAC, respectively. The aim of our study was to investigate the effect of baicalein, and the putative underlying mechanism, on inflammatory cytokines-induced ADM of rat pancreatic acinar cell line AR42J. To investigate ADM and baicalein effects in vitro, AR42J were treated with recombinant rat Tumor Necrosis Factor alpha (rTNFα) with or without baicalein for 5 days. Results showed that rTNFα-induced AR42J cells switched their phenotype from dominantly amylase-positive acinar cells to dominantly cytokeratin 19-positive ductal cells. Moreover, expression of the transcripts for TNFα or Hes-1, a Notch target, was up-regulated in these cells. Interestingly, baicalein reduced the population of ADM as well as cytokines gene expression but not Hes-1. Baicalein inhibited NF-κB activation induced by rTNFα in AR42J, but no effect on Notch 1activation. Moreover, baicalein suppressed the secretion of TNFα and Nitric Oxide (NO) in macrophages stimulated with LPS and further inhibited ADM of conditional medium-treated AR42J cells. Baicalein also suppressed the inflammatory response of LPS-activated macrophages, thereby inhibited ADM of AR42J by altering their microenvironment. Taken together, our study indicates that baicalein reduces rTNFα-induced ADM of AR42J cells by inhibiting NF-κB activation. It also sheds new light on Chinese material medica therapy of pancreatitis and thereby prevention of PDAC.
- Faculty
- Faculté des sciences et de médecine
- Department
- Médecine 3ème année
- Language
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- English
- Classification
- Biological sciences
- License
- License undefined
- Identifiers
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- RERO DOC 309526
- DOI 10.1002/jcp.26293
- Persistent URL
- https://folia.unifr.ch/unifr/documents/306741
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