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CLC number: S854.8

On-line Access: 2019-09-06

Received: 2019-02-17

Revision Accepted: 2019-06-04

Crosschecked: 2019-08-08

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Journal of Zhejiang University SCIENCE B 2019 Vol.20 No.10 P.816-827


Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling

Author(s):  Hua Zhang, Zhi-Min Wu, Ya-Ping Yang, Aftab Shaukat, Jing Yang, Ying-Fang Guo, Tao Zhang, Xin-Ying Zhu, Jin-Xia Qiu, Gan-Zhen Deng, Dong-Mei Shi

Affiliation(s):  Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China; more

Corresponding email(s):   ganzhendeng@sohu.com, dongmeishi126@126.com

Key Words:  Catalpol, Endometritis, Inflammation, Toll-like receptor 4 (TLR4), Nuclear factor-κ, B (NF-κ, B)

Hua Zhang, Zhi-Min Wu, Ya-Ping Yang, Aftab Shaukat, Jing Yang, Ying-Fang Guo, Tao Zhang, Xin-Ying Zhu, Jin-Xia Qiu, Gan-Zhen Deng, Dong-Mei Shi. Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling[J]. Journal of Zhejiang University Science B, 2019, 20(10): 816-827.

@article{title="Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling",
author="Hua Zhang, Zhi-Min Wu, Ya-Ping Yang, Aftab Shaukat, Jing Yang, Ying-Fang Guo, Tao Zhang, Xin-Ying Zhu, Jin-Xia Qiu, Gan-Zhen Deng, Dong-Mei Shi",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling
%A Hua Zhang
%A Zhi-Min Wu
%A Ya-Ping Yang
%A Aftab Shaukat
%A Jing Yang
%A Ying-Fang Guo
%A Tao Zhang
%A Xin-Ying Zhu
%A Jin-Xia Qiu
%A Gan-Zhen Deng
%A Dong-Mei Shi
%J Journal of Zhejiang University SCIENCE B
%V 20
%N 10
%P 816-827
%@ 1673-1581
%D 2019
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1900071

T1 - Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling
A1 - Hua Zhang
A1 - Zhi-Min Wu
A1 - Ya-Ping Yang
A1 - Aftab Shaukat
A1 - Jing Yang
A1 - Ying-Fang Guo
A1 - Tao Zhang
A1 - Xin-Ying Zhu
A1 - Jin-Xia Qiu
A1 - Gan-Zhen Deng
A1 - Dong-Mei Shi
J0 - Journal of Zhejiang University Science B
VL - 20
IS - 10
SP - 816
EP - 827
%@ 1673-1581
Y1 - 2019
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1900071

catalpol is the main active ingredient of an extract from Radix rehmanniae, which in a previous study showed a protective effect against various types of tissue injury. However, a protective effect of catalpol on uterine inflammation has not been reported. In this study, to investigate the protective mechanism of catalpol on lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and mouse endometritis, in vitro and in vivo inflammation models were established. The toll-like receptor 4 (TLR4)/nuclear factor-κ;b (NF-κ;b) signaling pathway and its downstream inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), western blot (Wb), and immunofluorescence techniques. The results from ELISA and qRT-PCR showed that catalpol dose-dependently reduced the expression of pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, and chemokines such as C-X-C motif chemokine ligand 8 (CXCL8) and CXCL5, both in bEECs and in uterine tissue. From the experimental results of WB, qRT-PCR, and immunofluorescence, the expression of TLR4 and the phosphorylation of NF-κB p65 were markedly inhibited by catalpol compared with the LPS group. The inflammatory damage to the mouse uterus caused by LPS was greatly reduced and was accompanied by a decline in myeloperoxidase (MPO) activity. The results of this study suggest that catalpol can exert an anti-inflammatory impact on LPS-induced bEECs and mouse endometritis by inhibiting inflammation and activation of the TLR4/NF-κB signaling pathway.

梓醇通过抑制炎症反应和TLR4/NF-κB 信号通路改善脂多糖诱导的小鼠子宫内膜炎

方法:通过LPS的诱导,分别建立牛子宫内膜上皮细胞体外炎症模型和小鼠子宫内膜体内炎症模型,设置不同梓醇作用浓度梯度,采用酶联免疫吸附测定法(ELISA)、实时荧光定量聚合酶链式反应(qRT-PCR)、蛋白免疫印迹(western blot)和免疫荧光技术检测TLR4/NF-κB信号通路及其下游炎症因子的表达.
结论:梓醇可以显著抑制TLR4和p65 NF-κB信号通路的表达,降低炎性因子肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和白细胞介素6(IL-6)的水平以及趋化因子CXCL8和CXCL5的表达,同时降低子宫组织髓过氧化物酶水平.通过在体内外炎症模型中加入梓醇,可以显著降低牛子宫内膜上皮细胞的炎症反应,有效保护小鼠体内子宫内膜的组织损伤.


Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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