Protective effect of taurine on skin aging caused by deficiency of B cell-specific Moloney MLV insertion site-1.

Bmi-1 deficiency leads to elevated oxidative damage and premature aging, making it a suitable model for studying the mechanisms of intrinsic skin aging. Taurine is abundant in the skin and has been shown to have various health benefits. However, it is unclear whether taurine can inhibit intrinsic aging by protecting skin from oxidative damage and suppressing cellular senescence(definition). In the current study, Bmi-1 homozygous mice were fed with or without taurine. We constructed siRNA plasmids specifically targeting Bmi-1 and transfected them into human dermal fibroblasts (HDFs). HDFs were then treated with or without taurine. The changes in dermal morphology of mice, HDF function, proliferation, oxidative stress, DNA damage, and cell senescence were compared to observe whether taurine can inhibit skin aging caused by Bmi-1 deficiency. Results showed that, in Bmi-1 homozygous mice drinking normal water, the vertical thickness of skin, the positive area of collagen bundles, type I collagen and elastic fiber, the percentage of PCNA-positive cells, and SOD1 and SOD2 proteins levels were significantly reduced. ROS levels, the proportion of 8-OHdG positive cells, p53, Chk2, p-Chk2, γ-H2AX and MMP3 proteins levels, as well as the percentage of SA-β-gal, MMP1 and MMP3-positive areas were upregulated dramatically. However, taurine supplementation reversed these changes. <i>In vitro</i>, compared to the control group, dramatic increases of γ-H2AX-positive HDFs, p16 mRNA levels, and SA-β-gal-positive areas were observed in the si-Bmi-1 group, while taurine treatment significantly decreased these expression levels. These results demonstrated that taurine could prevent Bmi-1 deficiency-induced skin aging.