Abstract
In this study, the effects of Chlorella vulgaris (CV) on replicative senescence of human diploid fibroblasts (HDFs) were investigated. Hot water extract of CV was used to treat HDFs at passages 6, 15, and 30 which represent young, presenescence, and senescence ages, respectively. The level of DNA damage was determined by comet assay while apoptosis and cell cycle profile were determined using FACSCalibur flow cytometer. Our results showed direct correlation between increased levels of damaged DNA and apoptosis with senescence in untreated HDFs (P < 0.05). Cell cycle profile showed increased population of untreated senescent cells that enter G0/G1 phase while the cell population in S phase decreased significantly (P < 0.05). Treatment with CV however caused a significant reduction in the level of damaged DNA and apoptosis in all age groups of HDFs (P < 0.05). Cell cycle analysis showed that treatment with CV increased significantly the percentage of senescent HDFs in S phase and G2/M phases but decreased the population of cells in G0/G1 phase (P < 0.05). In conclusion, hot water extract of Chlorella vulgaris effectively decreased the biomarkers of ageing, indicating its potential as an antiageing compound.
Highlights
Regardless of the persons’ official age, senescence is associated with appearance of age-related phenotypes, decline in protein homeostasis, and accumulation of DNA damage which alters individual lifespan
Was subsequently lyophilized to obtain C. vulgaris extracts (CVE) which was added to cell culture growth medium as supplementation
Presenescent, and senescent human diploid fibroblasts (HDFs) were treated with 400 μg/mL, 200 μg/mL and 100 μg/mL of Chlorella vulgaris, respectively for 24 h before determination of aging biomarkers which include morphological analysis, senescence-associated β-galactosidase (SA-B-gal) expression, DNA damage, apoptosis, and cell cycle profile
Summary
Regardless of the persons’ official age, senescence is associated with appearance of age-related phenotypes, decline in protein homeostasis, and accumulation of DNA damage which alters individual lifespan. The stochastic theories rely on the accumulation of cell damages and their inefficient repair as the main reason of ageing [3]. We can do nothing with ageing based on the genetic theories, but it is reversible based on the stochastic theories by improving the cellular defense system or decreasing cell damages. Based on the free radical theory of ageing, accumulation of free radicals over times leads to cellular damages and progressive deterioration of cells functions, tissues, and organ systems [4]. Due to their instability, the free radicals will attack the neighboring molecules to balance their unpaired electrons. The mitochondria, for instance, are major contributors of reactive oxygen species (ROS) in the cells [4], and any dysfunction in this organelle can result in energy shortage and other cellular deficiency that give rise to age-related disorders such as muscular and neurological degeneration, heart failure, strokes, and other degenerative diseases and death
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