Abstract
Dermal fibroblast aging contributes to aging-associated functional defects in the skin since dermal fibroblasts maintain skin homeostasis by interacting with the epidermis and extracellular matrix. Here, we found that puerarin, an isoflavone present in Pueraria lobata (Kudzu), can prevent the development of the aging-phenotype in human dermal fibroblasts. Normal human dermal fibroblasts (NHDFs) were subcultivated and high-passage cells were selected as senescent cells, whereas low-passage cells were selected as a young cell control. Puerarin treatment increased cell proliferation and decreased the proportion of senescence-associated beta-galactosidase-positive cells in a high-passage culture of NHDFs. Moreover, puerarin treatment reduced the number of smooth muscle actin (SMA)-positive myofibroblasts and the expression of a reticular fibroblast marker, calponin 1 (CNN1), which were induced in high-passage NHDFs. Fulvestrant, an estrogen receptor antagonist, blocked the puerarin-mediated downregulation of SMA and CNN1. Our results suggest that puerarin may be a useful functional food that alleviates aging-related functional defects in dermal fibroblasts.
Highlights
Skin aging is affected by diet and nutrition as well as other intrinsic factors such as chronological aging, and extrinsic factors such as sun exposure [1, 2]
We performed BrdU assays to investigate the effect of puerarin treatment on the proliferation rate in high-passage Normal human dermal fibroblasts (NHDFs) (Fig 1D and 1E)
BrdU-positive cells in microscopic fields were significantly increased in puerarin-treated NHDFs from 1.6% to 3.1% (25 μM puerarin) and 3.3% (50 μM puerarin), indicating that puerarin treatment enhanced cell proliferation
Summary
Skin aging is affected by diet and nutrition as well as other intrinsic factors such as chronological aging, and extrinsic factors such as sun exposure [1, 2]. Since excessive amounts of reactive oxygen species (ROS) generated by harmful stresses cause cellular senescence and aging phenotype, anti-oxidant-rich foods have been investigated as a preventive strategy to delay skin aging [2,3,4]. Recent evidence suggests that the targeting of aging-associated changes by natural products can prevent age-related phenotypes [5, 6]. Cellular senescence is a hallmark of normal aging, which is a state of irreversible growth arrest triggered by both endogenous and exogenous stresses [6,7,8]. Senescent cells secrete proinflammatory cytokines, growth factors, and matrix metalloproteases, that contribute to local and systemic dysfunction [9, 10]. Increasing evidence has demonstrated that the clearance of senescent cells prevents the age-associated decline of tissue function and extends
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