Protective effect and mechanism of deoxycholic acid(DCA)on Staphylococcus aureus induced mastitis in mice
10.16303/j.cnki.1005-4545.2025.02.14
- VernacularTitle:脱氧胆酸(DCA)对金黄色葡萄球菌诱导小鼠乳腺炎的治疗作用及机制
- Author:
Ziting DONG
1
;
Chaohui LIANG
1
;
Qingsong SUN
1
;
Yue ZHANG
1
;
Musen LI
1
Author Information
1. 吉林农业科技学院动物科技学院,吉林吉林 132109
- Publication Type:Journal Article
- Keywords:
deoxycholic acid;
mastitis;
TGR5 receptor;
inflammatory cytokines;
NF-κB;
mice
- From:
Chinese Journal of Veterinary Science
2025;45(2):274-280
- CountryChina
- Language:Chinese
-
Abstract:
Mastitis,as an important disease that endangers the development of the dairy industry,causes huge economic losses to the breeding industry.Staphylococcus aureus is one of the impor-tant pathogenic bacteria that cause mastitis in dairy cows.Previous studies have found that deoxy-cholic acid(DCA)plays an important role in many diseases,but its effect on mastitis has not been reported yet.In order to investigate the effect and mechanism of DCA on Staphylococcus aureus in-duced mouse mastitis,this study constructed a Staphylococcus aureus induced mouse mastitis model,mice were intraperitoneally injected DCA(0.01,0.02,0.03 mg/g),breast tissue were col-lected,and the protective effect and mechanism of DCA on mastitis were evalued.The results showed that DCA dose dependently reduced the pathological damage of mouse breast tissue in-duced by Staphylococcus aureus;DCA inhibited the expression of inflammatory cytokines TNF-α and IL-1β and MPO activity induced by Staphylococcus aureus;DCA significantly reduced the con-centration of MDA and iron ions,while upregulating the expression of GSH and GPX4,indicating that DCA could inhibit ferroptosis induced by Staphylococcus aureus;Western blot results showed that DCA could upregulate TGR5 receptors,thereby inhibiting the NF-κB signaling pathway.The above results indicate that DCA inhibits mastitis by regulating the TGR5-NF-κB signaling pathway to inhibit the inflammatory response and ferroptosis induced by Staphylococcus aureus.
