Mammary gland health is an important guarantee for the normal lactation function of cows.The high incidence and complex pathogenesis of mastitis in dairy cows can significantly reduce mammary gland health,lactation performance,reproductive performance and milk quality,and increase the culling rate of cows.Therefore,deeper exploration of the pathogenesis of mastitis in dairy cows and its prevention and control remains a major issue to be addressed in the dairy industry.Peroxisome proliferator-activated receptor γ coactivator 1α(PGC-1α)is a major regulator of mitochondrial biosynthesis and mitochondrial dynamics,which can regulate mitochondrial function,oxidative stress and various tissue metabolic pathways by Previous studies have focused on the involvement of PGC-1αas a regulatory factor in the regulation of mitochondrial homeostasis,but whether PGC-1α regulates the mammary inflammatory response in cows,and how PGC-1α exerts its anti-1αctation effect by enhancing the mitochondrial function of bovine mammary epithelial cells(bMECs).In the present study,PGC-1αwas used to control the mammary inflammatory response in dairy cows.Based on this,blood and milk samples were collected from 10 healthy cows and 10 cows with mastitis(SCC≥400,000-500,000/mL)in late lactation(200±20 d),with consistent body condition score(3.0-3.5)and litter size(2-3 litters).On this basis,lipopolysaccharide(LPS)was used to induce the construction of inflammatory injury bMECs model with and without the addition of resveratrol(RES)to construct CON,LPS,RES,and RES+LPS groups;to reveal whether RES played an anti-mastitis role in cows by mediating PGC-1α,this experiment interfered with PGC-1α(si-PGC-1α)to construct si-NC+LPS,si-PGC-1α+LPS,si-NC+RES+LPS,and si-PGC-1α+RES+LPS groups.The results showed that(1)compared with healthy cows,the levels of pro-inflammatory factors interleukin-6(IL-6)and interleukin-8(IL-8)were significantly increased in mastitis cows(P<0.05),the mRNA expression of malondialdehyde(MDA)was significantly up-regulated(P<0.05),mRNA expression of glutathione peroxidase(GSH-PX)was significantly downregulated(P<0.05),and mitochondria-related factor PGC-1α and its downstream mitochondrial transcription factor A(Tfam)were significantly reduced(P<0.05)was significantly reduced(P<0.05).(2)LPS upregulated the inflammatory factors tumor necrosis factor-α(TNF-α),IL-1βand IL-8,the oxidative factors reactive oxygen species(ROS)and malonaldehyde(MDA),the pro-apoptotic gene Bcl-2(B-cell lymphoma-2 associated X protein,BAX),down-regulation of superoxide dismutase(SOD)and GSH-PX,the mitochondrial genes PGC-1α and Tfam,and the apoptotic genes B-cell lymphoma-2(B cell lymphoma-2,BCL-2)mRNA expression,leading to oxidative stress,inflammatory stress,mitochondrial damage and apoptosis in bMECs;while RES reversed this response and significantly reduced LPS-induced oxidative stress,inflammatory stress,mitochondrial damage and apoptosis in bMECs with inflammatory damage;while interference with PGC-1α in bMECs with inflammatory damage After interfering with PGC-1α in inflammatory injury bMECs,it was found that RES could not alleviate LPS-induced oxidative stress,inflammatory stress,mitochondrial injury,or inhibit apoptosis in bMECs,indicating that RES serves to alleviate LPS-induced inflammatory injury and apoptosis in bMECs through activating the PGC-1α pathway.In conclusion,RES can alleviate LPS-induced mitochondrial damage,oxidative stress,inflammatory response and inhibit apoptosis in bMECs by activating the PGC-1α pathway,revealing the role of RES in alleviating inflammatory damage in bMECs and its mechanism,which can lay the technical support for promoting the application of RES in dairy production. |