Research Paper Volume 11, Issue 22 pp 10356—10373

Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism

Figure 5. FA supplementation regulated telomere–p53–mitochondria pathway in brain of SAMP8 mice. Mice were assigned to treatment groups as described in Figure 1. (A) The relative mRNA levels of PGC-1α, Nrf1 and Tfam quantified by qPCR were normalized to β-actin and expressed as fold changes relative to the FA-N group [F(5,54) = 30.274, P<0.001; F(5,54) = 36.428, P<0.001; F(5,54) = 34.239, P<0.001]. (B) The protein expressions of PGC-1α, Nrf1 and Tfam quantified by western blot were normalized to β-actin [F(5,12) = 21.689, P<0.001; F(5,12) = 39.452, P<0.001; F(5,12) = 38.230, P<0.001]. (C) The level of phospho-p53 quantified by western blot was normalized to p53 [F(5,12) = 51.308, P<0.001]. (D) Representative western blot of phospho-p53, p53, PGC-1α, Nrf1, Tfam and β-actin. Data are expressed as mean ± SD (n= 10 mice/group for qPCR, and n= 3 mice/group for western blot). *P<0.05 compared with FA-N group. #P<0.05 compared with Con-Y group. &P<0.05 compared between FA-L and FA-H groups.