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Published on: May 26, 2023
Forsythiaside A attenuates mastitis via PINK1/Parkin-mediated mitophagy
Jingjing Liu1, Yingkui Gao1, Huaqiang Zhang1
1College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450000, Henan province, PR China; Ministry of Education Key Laboratory for Animal Pathogens and Biosafety, Zhengzhou 450000, Henan province, PR China.
Background:
Bovine mastitis is the most common animal production disease in the global dairy industry, which affects the health of dairy cows. When bovine mastitis occurs, the mitochondrial metabolism of breast tissue increases, and the relationship between inflammation and mitophagy has become a hot topic for many scholars. The abuse of antibiotics leads to the increase of resistance to bovine mastitis. FTA is one of the main effective components of Forsythia suspensa, which has anti-inflammatory, anti-infection, anti-oxidation and anti-virus pharmacological effects, and has broad application prospects in the prevention and treatment of bovine mastitis. However, the relationship between the anti-inflammatory effects of FTA and mitophagy is still unclear.
Purpose:
This study mainly explores the anti-inflammatory effect of FTA in bovine mastitis and the relationship between mitophagy.
Methods:
MAC-T cells and wild-type mice were used to simulate the in vitro and in vivo response of mastitis. After the pretreatment with FTA, CsA inhibitors and siPINK1 were used to interfere with mitophagy, and the mitochondrial function impairment and the expression of inflammatory factors were detected.
Results:
It was found that pre-treatment with FTA significantly reduced LPS induced inflammatory response and mitochondrial damage, while promoting the expression of mitophagy related factors. However, after inhibiting mitophagy, the anti-inflammatory effect of FTA was inhibited.
Conclusion:
This study is the first to suggest the relationship between the anti-inflammatory effect of FTA and mitophagy. PINK1/Parkin-mediated mitophagy is one of the ways that FTA protects MAC-T cells from LPS-induced inflammatory damage.
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