Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling.
- Author:
Hua ZHANG
1
;
Zhi-Min WU
1
;
Ya-Ping YANG
1
;
Aftab SHAUKAT
1
;
Jing YANG
1
;
Ying-Fang GUO
1
;
Tao ZHANG
1
;
Xin-Ying ZHU
1
;
Jin-Xia QIU
1
;
Gan-Zhen DENG
1
;
Dong-Mei SHI
2
Author Information
- Publication Type:Journal Article
- Keywords: Catalpol; Endometritis; Inflammation; Toll-like receptor 4 (TLR4); Nuclear factor-κB (NF-κB)
- MeSH: Animals; Cattle; Chemokines/genetics*; Cytokines/genetics*; Endometritis/drug therapy*; Epithelial Cells/drug effects*; Female; Inflammation/prevention & control*; Iridoid Glucosides/therapeutic use*; Lipopolysaccharides/pharmacology*; Mice; NF-kappa B/physiology*; Signal Transduction/drug effects*; Toll-Like Receptor 4/physiology*
- From: Journal of Zhejiang University. Science. B 2019;20(10):816-827
- CountryChina
- Language:English
- Abstract: 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-κB (NF-κB) 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.
