Protective Action of SIRT1 Activator Aptamer in Human Skin Cell Line

Main Article Content

Rana Faris Salman
Basma Talib Al-Sudani
Bahir Abdul Razzaq Mshimesh

Keywords

Reactive oxygen species, Human keratinocytes cell line (HaCaT), SIRT1 aptamer, Apoptosis

Abstract

The skin is the largest organ of the body. The general aging process, which is genetically fixed and happens solely with the passage of time, is referred to as the intrinsic skin aging process. The skin aging process caused by external causes is referred to as extrinsic skin aging. The skin must endure a continual bombardment from the outside by reactive oxygen species, or ROS, which are given to the skin by the environment and created within the skin itself, either as a reaction to incoming UV radiation or made when mitochondria aerobic respiration. An increase in the levels of ROS lead to damage the mtDNA, affecting cell signaling and inducing the apoptosis responses, such as senescence, fibrosis, calcification, and hypertrophy. During the past decade, investigators have reported the relationship between disturbance of SIRT1 activation and the onset of aging. Sirtuin1 is indispensable for DNA repair which make it good anti-senescence/anti-ageing targets and because ROS and SIRT1 are disturbed in the aging process. Because of its enhancing effect on reactive oxygen species and apoptotic pathways, an aberrant increase in NO generation has been linked to early skin aging. We'll look at how SIRT1 aptamer (as a SIRT1 activator) can protect cells against sodium nitroprusside-induced cell death (SNP), employing a human keratinocyte cell line to study a well-known NO generating chemical with suspected harmful and apoptotic effects on keratinocytes (HaCaT). As a result, the primary goal of this research is to discover and define the protective effects of SIRT1 activators in human skin cells. Finally, the findings imply that SIRT1 aptamer might be effective in preventing skin aging caused by reactive oxygen species (ROS).

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