Allicin Promotes Mitochondrial Biogenesis through the Activation of Sirt1-PGC1α-Tfam Pathway
(A) The mRNA expression of SIRT1, Tfam, and NRF1 in BAT from control and allicin-treated DIO mice.
(B) Western blot analysis of the Sirt1, PGC1α, NRF1, and Tfam in BAT from control and allicin-treated DIO mice.
(C) Western blot analysis of Sirt1, PGC1α, NRF1, and Tfam in brown adipocytes treated with or without allicin.
(D) The phosphorylation levels of sirt1 in brown adipocytes treated with allicin at different concentrations.
(E) SIRT1 deacetylates PGC1α, and allicin treatment substantially increases the phosphorylation of sirt1 and SIRT1-mediated PGC1α deacetylation.
(F) In contrast, shSIRT1 treatment significantly diminishes allicin-mediated PGC1α deacetylation.
(G) Mitochondrial mtDNA copy number in BAT from control and allicin-treated DIO or Db/Db mice.
(H) Transmission electron microscopic (TEM) analysis of mitochondrial in BAT of control and allicin-treated DIO mice. Scale bars, 2 μm.
(I) shSIRT1 treatment significantly diminishes the allicin-mediated increase in mtDNA copy number.Values represent means ± SEM. Error bars represent SEM; significant differences compared with vehicle controls are indicated by ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 (assessed by Student's t test).