ACAC-Induced Mitochondrial Damage in Bovine Mammary Epithelial Cells by Inhibiting the Nrf2
To investigate whether acetoacetic acid(ACAC)induced mitochondrial damage of bovine mammary epithelial cells by inhibiting the nuclear transcription factor NF-E2-related factor 2(Nrf2).Bovine mammary epithelial cells(MAC-T)were treated with 0,0.6,1.2 or 1.8 mmol·L-1 ACAC for 24 h;MAC-T cells were pretreated with 10 μmol·L-1 SFN for 24 h and then treated with 1.2 mmol·L-1 ACAC for 24 h.Flow cytometry was used to detect mitochondrial reactive oxygen species(ROS);JC-1 staining was used to detect mitochondrial membrane potential changes;the gene expression of mitochondrial oxidative phosphorylation complexⅠ-Ⅴ(COⅠ-Ⅴ)was determined by q-PCR,as well as the mitochondrial biosynthesis regulator Nrf2,peroxisome proliferator-activated receptor γ-γ activator 1-α(PGC-1α),mitochondrial transcription factor A(TFAM),Nuclear respirator-1(Nrf1),and mitochondrial DNA;the adenine nucleoside triphosphate(ATP)content was detected by the kit.The results showed that after ACAC treatment,the content of ROS was significantly increased(P<0.05),while the mitochondrial membrane potential decreased significantly(P<0.05),and the mRNA expression level of COⅠ,COⅡ,COⅢ,COⅣ and COⅤ were significantly decreased(P<0.05),the mRNA expression of PGC-1α,TFAM,Nrf1 and Nrf2 were decreased(P<0.05),and the mtDNA content was decreased(P<0.05),the ATP content was decreased(P<0.05),while SFN pretreatment alleviated the above effects.The results showed that ACAC induced mitochondrial damage in MAC-T cells by inhibiting the Nrf2 signaling pathway.
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