Abstract
Gradual accumulation of oxidatively damaged cell structures along with impairment of redox homeostasis has been suggested as a key factor in ageing and cellular senescence. Anti-ageing effects were reported for a number of phenol- and quinone-type compounds. By using a model of senescent human fibroblasts (strain VH-10), potential beneficial effects of semisynthetic compound, 4-O-(2-chloro-1,4-naphtoquinone-3-yloxy) quercetin (CHNQ) were investigated. CHNQ significantly suppressed senescence markers, SAβ-galactosidase activity and lipofuscin-related autofluorescence. Moreover, CHNQ, more efficiently than its precursors, restored mitochondrial membrane potential linked probably to observed decrease in ROS levels. In addition, CHNQ-treated cells showed increased LC3 turnover pointing to improvement of autophagy flux. By contrast, the compounds tested restored neither the gradual decline in proliferation, nor the cell cycle arrest at G2/M phase. Yet, modulation of p21 and p53 proteins dependently on the persistence time of senescent cells in culture was found. In conclusion, the result of our study point to protective effect of CHNQ on functionalities of senescent fibroblasts, without influencing their proliferative lifespan [VEGA 2/0041/17,2/0029/16,APVV-15–0308, ITMS 26240220040].
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