Salidroside alleviates LPS-induced inflammatory injury in MAC-T cells by promoting mitophagy and improving mitochondrial function via the AMPK/mTOR pathway
- 1College of Animal Science and Technology, Huazhong Agricultural University
- 2Xinjiang Academy of Animal Sciences
Abstract
Mastitis severely impairs dairy production, and lipopolysaccharide (LPS), a major endotoxin, induces mitochondrial dysfunction and inflammatory injury in bovine mammary epithelial cells (BMECs). Mitophagy, which is regulated by the AMPK/mTOR axis, removes damaged mitochondria to restrict excessive inflammation. Although salidroside (SAL) has anti-inflammatory activity, whether it protects against LPS-triggered inflammatory injury in mammary epithelial cells via this pathway remains unclear. Here, we investigated the protective effects of SAL on LPS-stimulated MAC-T cells. Pretreatment with 200 μM SAL markedly reduced the secretion of proinflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) induced by 5 μg/mL LPS. Mechanistically, SAL maintained mitochondrial function by restoring ATP levels, restoring mitochondrial membrane potential, and inhibiting abnormal mPTP opening. Moreover, SAL increased the LC3B-II/I ratio and Beclin-1 expression and promoted p62 degradation. Tandem mRFP-GFP-LC3 assays verified that SAL restored functional autophagic flux; moreover, SAL upregulated PINK1 and Parkin expression, indicating mitophagy activation. The results of inhibition experiments demonstrated that 3-methyladenine or cyclosporin A eliminated the protective effects of SAL. The inhibition of AMPK by Compound C blocked SAL-induced mitophagy and reversed its beneficial effects on mitochondrial homeostasis and inflammation. In summary, SAL protected MAC-T cells against LPS-induced inflammatory injury in an AMPK/mTOR-dependent manner by driving PINK1/Parkin-mediated mitophagy to eliminate damaged mitochondria and maintain mitochondrial homeostasis.
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BibTeX
@article{huang2026salidroside,
title = {{Salidroside alleviates LPS-induced inflammatory injury in MAC-T cells by promoting mitophagy and improving mitochondrial function via the AMPK/mTOR pathway}},
author = {Qixin Huang and Huiyuan Cao and Yang Geng and Zheng Peng and Xiaokai Lu and Shujun Zhang and Nongjiang Zu and Lijun Cao and Xinbao Zheng and Zhili Qi},
journal = {Animal Diseases},
year = {2026},
month = oct,
doi = {10.1186/s44149-026-00283-1},
url = {https://doi.org/10.1186/s44149-026-00283-1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Salidroside alleviates LPS-induced inflammatory injury in MAC-T cells by promoting mitophagy and improving mitochondrial function via the AMPK/mTOR pathway
AU - Qixin Huang
AU - Huiyuan Cao
AU - Yang Geng
AU - Zheng Peng
AU - Xiaokai Lu
AU - Shujun Zhang
AU - Nongjiang Zu
AU - Lijun Cao
AU - Xinbao Zheng
AU - Zhili Qi
PY - 2026
DA - 2026/10/25
JO - Animal Diseases
DO - 10.1186/s44149-026-00283-1
UR - https://doi.org/10.1186/s44149-026-00283-1
AB - Mastitis severely impairs dairy production, and lipopolysaccharide (LPS), a major endotoxin, induces mitochondrial dysfunction and inflammatory injury in bovine mammary epithelial cells (BMECs). Mitophagy, which is regulated by the AMPK/mTOR axis, removes damaged mitochondria to restrict excessive inflammation. Although salidroside (SAL) has anti-inflammatory activity, whether it protects against LPS-triggered inflammatory injury in mammary epithelial cells via this pathway remains unclear. Here, we investigated the protective effects of SAL on LPS-stimulated MAC-T cells. Pretreatment with 200 μM SAL markedly reduced the secretion of proinflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) induced by 5 μg/mL LPS. Mechanistically, SAL maintained mitochondrial function by restoring ATP levels, restoring mitochondrial membrane potential, and inhibiting abnormal mPTP opening. Moreover, SAL increased the LC3B-II/I ratio and Beclin-1 expression and promoted p62 degradation. Tandem mRFP-GFP-LC3 assays verified that SAL restored functional autophagic flux; moreover, SAL upregulated PINK1 and Parkin expression, indicating mitophagy activation. The results of inhibition experiments demonstrated that 3-methyladenine or cyclosporin A eliminated the protective effects of SAL. The inhibition of AMPK by Compound C blocked SAL-induced mitophagy and reversed its beneficial effects on mitochondrial homeostasis and inflammation. In summary, SAL protected MAC-T cells against LPS-induced inflammatory injury in an AMPK/mTOR-dependent manner by driving PINK1/Parkin-mediated mitophagy to eliminate damaged mitochondria and maintain mitochondrial homeostasis.
SN - 2731-0442
ER -