PMID- 33536916
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210206
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 11
DP  - 2020
TI  - Baicalin Ameliorates Pancreatic Fibrosis by Inhibiting the Activation of 
      Pancreatic Stellate Cells in Mice with Chronic Pancreatitis.
PG  - 607133
LID - 10.3389/fphar.2020.607133 [doi]
LID - 607133
AB  - Pancreatic inflammation and fibrosis are typical pathological features in chronic 
      pancreatitis (CP). Activated pancreatic stellate cells (PSCs) have been regarded 
      as the core event in the development of pancreatic fibrosis and are considered to 
      be the key target for treatment of CP. Baicalin (C(21)H(18)O(11)), the main 
      chemical composition of Baikal skullcap in the traditional Chinese medicines 
      Dachaihu decoction (DCHD) and Xiaochaihu decoction (XCHD), has shown significant 
      effects in the treatment of pancreatic fibrosis in CP mice; however, whether 
      baicalin can inhibit the activation of PSCs and its underlying mechanism remain 
      unclear. In this study, the influence of baicalin on activated PSCs in vitro and 
      in vivo was investigated, and the results showed that Baicalin could 
      significantly ameliorate the degree of pancreatic inflammation and fibrosis, 
      while decreasing the levels of alpha-smooth muscle actin (alpha-SMA), F4/80 (surface 
      markers of mouse macrophages), nuclear factor kappa-B (NF-kappaB), monocyte 
      chemotactic protein 1 (MCP-1), and collagen type I alpha 1 (COL1A1)in the 
      pancreas. Moreover, NF-kappaB and alpha-SMA were co-expressed in the pancreas of CP mice. 
      Baicalin treatment markedly reduced the expression of co-location of alpha-SMA and 
      NF-kappaB. In vitro, the protein expression levels of transforming growth factor-beta 
      receptor 1 (TGF-betaR1), phosphorylated TGF-beta activated kinase 1 p-TAK 1, and 
      NF-kappaBp65 in PSCs were all remarkably reduced after treatment with baicalin. In 
      addition, baicalin could inhibit MCP-1 mRNA expression in supernatant of 
      activated PSCs, as well as the excessive migration of macrophages. Taken 
      together, our findings indicated that baicalin could inhibit the 
      TGF-beta1/TGF-betaR1/TAK1/NF-kappaB signaling pathway of activated PSCs, reduce the 
      secretion of MCP-1, and further decrease the infiltration of macrophages and 
      inflammation cells of the local microenvironment of the pancreas. Thus, this 
      study provides a reliable experimental basis for baicalin in the prevention and 
      treatment of CP.
CI  - Copyright (c) 2021 Fan, Duan, Wu, Xu, Xin, Jiang, Zhang and Zhang.
FAU - Fan, Jianwei
AU  - Fan J
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
FAU - Duan, Lifang
AU  - Duan L
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
FAU - Wu, Nan
AU  - Wu N
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
FAU - Xu, Xiaofan
AU  - Xu X
AD  - Medical Experiment Center, Shaanxi University of Chinese Medicine, Xianyang, 
      China.
FAU - Xin, Jiaqi
AU  - Xin J
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
FAU - Jiang, Shengnan
AU  - Jiang S
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
FAU - Zhang, Cheng
AU  - Zhang C
AD  - Department of Hepatobiliary Surgery, Xianyang Central Hospital, Xianyang, China.
FAU - Zhang, Hong
AU  - Zhang H
AD  - Basic Medical Academy, Shaanxi University of Chinese Medicine, Xianyang, China.
AD  - Medical Experiment Center, Shaanxi University of Chinese Medicine, Xianyang, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20210118
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC7848203
OTO - NOTNLM
OT  - baicalin
OT  - nuclear factor-kappaB
OT  - pancreatic fibrosis
OT  - pancreatic inflammation
OT  - pancreatic stellate cells
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/02/05 06:00
MHDA- 2021/02/05 06:01
PMCR- 2021/01/18
CRDT- 2021/02/04 05:50
PHST- 2020/09/17 00:00 [received]
PHST- 2020/12/02 00:00 [accepted]
PHST- 2021/02/04 05:50 [entrez]
PHST- 2021/02/05 06:00 [pubmed]
PHST- 2021/02/05 06:01 [medline]
PHST- 2021/01/18 00:00 [pmc-release]
AID - 607133 [pii]
AID - 10.3389/fphar.2020.607133 [doi]
PST - epublish
SO  - Front Pharmacol. 2021 Jan 18;11:607133. doi: 10.3389/fphar.2020.607133. 
      eCollection 2020.