Jin Taewon, Kim Min Jeong, Heo Won Il, Park Kui Young, Choi Sun Young, Lee Mi-Kyung, Hong Seung-Phil, Kim Seong-Jin, Im Myung, Moon Nam Ju, Seo Seong Jun
Department of Dermatology, Chung-Ang University Hospital, Seoul, South Korea.
Department of Dermatology, Chung-Ang University Hospital, Seoul, South Korea.
Biochem Biophys Res Commun. 2016 Sep 2;477(4):678-684. doi: 10.1016/j.bbrc.2016.06.119. Epub 2016 Jun 25.
Stress-induced premature senescence or aging causes dysfunction in the human somatic system. Adiponectin (Acrp30) plays a role in functional recovery, especially with adenosine 3',5'-monophosphate (AMP)-activated protein kinase (AMPK) and silent mating type information regulation 2 homolog 1 (SIRT1). Acrp30 stimulation reduced the premature senescence positive ratio induced by hydrogen peroxide (H2O2) and restituted human β-defensin 2 (hBD-2) levels in senescent keratinocytes. Acrp30 recovered AMPK activity in senescent keratinocytes and increased SIRT1 deacetylation activity. As a result, FoxO1 and FoxO3 transcription activity was recovered. Additionally, Acrp30 stimulation suppresses NFκB p65, which induces abnormal expression of hBD-2 induced by H2O2. In the present study, we have shown that Acrp30 reduces premature senescence and recovers cellular function in keratinocytes. These results suggest a role for Acrp30 as an anti-aging agent to improve impaired skin immune barriers.
应激诱导的早衰或老化会导致人体体细胞系统功能障碍。脂联素（Acrp30）在功能恢复中发挥作用，尤其是通过3',5'-环磷酸腺苷（AMP）激活的蛋白激酶（AMPK）和沉默信息调节因子2同源物1（SIRT1）。Acrp30刺激降低了过氧化氢（H2O2）诱导的早衰阳性率，并恢复了衰老角质形成细胞中人β-防御素2（hBD-2）的水平。Acrp30恢复了衰老角质形成细胞中的AMPK活性，并增加了SIRT1去乙酰化活性。结果，FoxO1和FoxO3转录活性得以恢复。此外，Acrp30刺激抑制了NFκB p65，后者诱导H2O2诱导的hBD-2异常表达。在本研究中，我们表明Acrp30可减少角质形成细胞的早衰并恢复其细胞功能。这些结果表明Acrp30作为一种抗衰老剂，在改善受损皮肤免疫屏障方面发挥作用。
