Oxytocin Alleviates Cellular Senescence through Oxytocin Receptor‐Mediated ERK/Nrf2 Signalling

Summary

Background

Oxytocin (OT) is a neuropeptide hormone that has many beneficial biological effects, including protection against age‐related disorders. However, less is known about its role in intrinsic skin ageing, which is accelerated by an increase in senescent cell fraction in skin tissue.

Objectives

Here, we investigated the novel function and the underlying mechanism of OT in preventing cellular senescence in normal human dermal fibroblasts (NHDFs) isolated from the skin of female donors of different ages.

Methods

NHDFs from young and old donors were exposed to conditioned medium (CM) from senescent or control NHDFs in the presence or absence of 10 nM OT for 3 days and continuously subcultured for 12 days. Subsequently, various age‐associated signs of senescence including decreased proliferation rate, elevated p16 and p21 level, and positivity for senescence‐associated β‐galactosidase (SA‐β‐Gal) expression were examined.

Results

We found that OT suppressed senescence‐associated secretory phenotype (SASP)‐induced senescence in NHDFs and its effect depended on the age of donor's NHDFs. The inhibitory effects of OT required the OT receptor‐mediated extracellular signal‐regulated kinase (ERK)/nuclear factor‐erythroid 2‐related factor 2 (Nrf2) signalling. Age‐dependent anti‐senescence effects of OT is closely related to the OT receptor (OTXR) gene hypermethylation.

Conclusions

Our findings bring to light OT role as a new clinical strategy for the prevention of skin ageing.

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