LBP1C Extracted From Lycium barbarum Delays Aging by Activating TFEB

Objective This study aims to explore the effects and mechanisms of LBP1C extracted from Lycium barbarum on delaying the natural aging of human fibroblasts and nematodes, and provide scientific evidence and explanation for the anti-aging and skin whitening effects recorded in the "Ben Cao Gang Mu (Compendium of Materia Medica)". Methods Human fibroblasts and C. elegans were used as natural aging models and treated with LBP1C. The expression levels of P16, P21 and the number of SA-(3-gal staining positive cell were used to indicate the cell senescence level. The levels of GATA4, indicators related to the senescence associated secretory phenotype (SASP), transcription factor EB (TFEB) targeting genes and autophagy marker protein LC3 were detected by qPCR or Western-blot. The level of nuclear transcription of TFEB, a key regulatory factor for lysosomal biogenesis and autophagy, was detected by immunofluorescence in fibroblasts. The effects of LBP1C on lipofuscin levels in fibroblasts and C. elegans were respectively detected by lipofuscin kit and fluorescence microscope. The motor ability of LBP1C to C. elegans was evaluated through body bends and pumping analysis. Results Human fibroblasts and C. elegans were used as natural aging models in this study. Aging related indicators (P16, P21 expression levels and the number of SA-(3-gal staining positive cell) in the LBP1C treatment group decreased markedly compared with the control group, which indicated that LBP1C delayed cell senescence. The proportion of TFEB nuclear translocation significantly increased in the LBP1C treated groups and activated autophagy. Detection of TFEB downstream genes showed that mRNAs of lysosomal enzymes, lysosomal membrane proteins and functionally related vesicular ATPases were all significantly upregulated in the LBP1C treatment groups. The increase in autophagy level autophagy reduced the level of SASP transcription factor GATA4, thereby reducing the levels of SASP related IL-1(3 and iNOS. Besides, the increase in autophagy level accelerated the degradation of lipofuscin, and reduced the accumulation of lipofuscin in cells and C. elegans. LBP1C reduced the accumulation of lipofuscin in cells and C. elegans and improved the motor ability of C. elegans, which suggested that LBP1C promotes healthy aging of C. elegans. Conclusion This study investigated the new function and mechanism of LBP1C extracted from Lycium barbarum, which delays cell senescence by promoting autophagy to achieve the effects of anti-aging and skin whitening. LBP1C increased autophagy level by activating TFEB, thereby reducing the accumulation of SASP and lipofuscin, delaying aging and promoting healthy aging. This study reveals the effects and mechanisms of Lycium barbarum in anti-aging and skin whitening aspects, and provides scientific and theoretical basis for further application research, which provides exciting translational opportunities ahead.