Abstract
Piper betle (PB) is a traditional medicine that is widely used to treat different diseases around Asian region. The leaf extracts contain various bioactive compounds, which were reported to have antidiabetic, antibacterial, anti-inflammatory, antioxidant, and anticancer effects. In this study, the effect of PB aqueous extracts on replicative senescent human diploid fibroblasts (HDFs) was investigated by determining the expressions of senescence-associated genes using quantitative PCR. Our results showed that PB extracts at 0.4 mg/ml can improve cell proliferation of young (143%), presenescent (127.3%), and senescent (157.3%) HDFs. Increased expressions of PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were observed in senescent HDFs compared to young and/or presenescent HDFs. Treatment with PB extracts modulates the transcriptional profile changes in senescent HDFs. By contrast, expressions of SOD1 increased, whereas GPX1, PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were decreased in PB-treated senescent HDFs compared to untreated senescent HDFs. In conclusion, this study indicates the modulation of PB extracts on senescence-associated genes expression of replicative senescent HDFs. Further studies warrant determining the mechanism of PB in modulating replicative senescence of HDFs through these signaling pathways.
Highlights
In 1961, Hayflick and Moorhead discovered the finite cell growth of fibroblasts after multiple division, later called replicative senescence, which serves as model to study aging [1]
The results showed that Piper betle (PB) extracts significantly increased the cell proliferation of young human diploid fibroblasts (HDFs) compared to control (p < 0.05) at concentration ranging from 0.2 mg/ml to 0.8 mg/ml (Figure 1)
Our results in this study showed that expressions of MAPK14, TP53, PAK2, and CDKN2A were increased in senescent cells, suggesting that p53 and p16 pathways may be involved in the cell growth arrest of replicative senescent HDFs
Summary
In 1961, Hayflick and Moorhead discovered the finite cell growth of fibroblasts after multiple division, later called replicative senescence, which serves as model to study aging [1]. Replicative senescence is an irreversible growth arrest due to limited cell expansion number which was observed in human diploid fibroblasts (HDFs) and other cell types including astrocytes [2] and smooth muscle cells [3]. A balance between production of free radicals and cellular antioxidants defence is required in preventing oxidative stress. Elevated free radicals generation and ineffective antioxidant defence have been observed with increasing age. Antioxidant supplementation becomes popular, with the intention to improve the redox balance, achieve the desired longevity, and increase health span. Does this antioxidant supplementation work as expected as antiaging agents and what is the mechanism involved?
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