Carvacrol alleviates LPS-induced mammary epithelial cell inflammation and endo-plasmic reticulum stress in dairy cows
10.16303/j.cnki.1005-4545.2025.11.19
- VernacularTitle:香芹酚缓解LPS诱导的奶牛乳腺上皮细胞炎症与内质网应激
- Author:
Yue YANG
1
;
Ming LI
1
;
Jingyi WANG
1
;
Huijing ZHANG
1
;
Qingnian HUANG
1
;
Shihao SONG
1
;
Chuang XU
1
Author Information
1. 中国农业大学动物医学院,北京 100193
- Publication Type:Journal Article
- Keywords:
carvacrol;
NF-κB pathway;
endoplasmic reticulum stress;
bovine mastitis
- From:
Chinese Journal of Veterinary Science
2025;45(11):2447-2456
- CountryChina
- Language:Chinese
-
Abstract:
This study investigated the regulatory effects of carvacrol on lipopolysaccharide(LPS)-induced inflammatory response and endoplasmic reticulum(ER)stress in bovine mammary epithe-lial cells using in vitro cell culture techniques.Western blot analysis revealed significantly elevated expression levels of NF-κB pathway-related proteins and ER stress marker proteins in mastitis samples compared to healthy mammary tissues(P＜0.05).Cells were divided into a blank control group and carvacrol(CAV)treatment groups with varying concentrations(50,100,250,500,750,1 000 μmol/L).After 24 hours of culture,cell proliferation was assessed using the CCK-8 assay.An inflammatory model was established by stimulating MAC-T cells(a bovine mammary epithelial cell line)with LPS(10 mg/L)for 12 h,followed by measurement of the transcriptional levels of inflammatory-related genes(IL-6,IL-1β,and TNFα).MAC-T cells were pretreated with low,medi-um,and high doses of CAV for 12 h before LPS stimulation.Molecular docking analysis was per-formed to examine the interaction between CAV and GRP78,a key ER stress protein.Real-time quantitative PCR(qPCR)was used to analyze the mRNA expression levels of inflammatory cyto-kines(IL-6,IL-1β,TNFα),while Western blot was employed to assess the expression levels of NF-κB pathway proteins(p-IκB,p-NF-κB p65)and ER stress-related proteins(p-PERK,p-IRE1α,ATF6,GRP78,CHOP).The results from Western blot and qPCR demonstrated that CAV alleviated LPS-induced inflammatory response and cellular damage by inhibiting the NF-κB signa-ling pathway and ER stress.
