<i>Dendranthema zawadskii</i> var. <i>lucidum</i> (Nakai) J.H. Park Extract Inhibits Cellular Senescence in Human Dermal Fibroblasts and Aging-Related Inflammation in Rats

• Main Authors: Jehun Choi, Gwi-Yeong Jang, Jeonghoon Lee, Hae-Young Chung, Hyung-Jun Noh, Geum-Soog Kim, Seung-Eun Lee
• Format: Article
• Language: English
• Published: MDPI AG 2021-05-01
• Series: Processes
• Subjects: senescence; aging; inflammation; <i>Dendranthema zawadskii</i> var. <i>lucidum</i>
• Online Access: https://www.mdpi.com/2227-9717/9/5/801

Senescence is the phenomenon by which physiological functions of organisms degenerate with time. Cellular senescence is marked by an inhibition of cell cycle progression. Beta-galactosidase accumulates in the lysosomes of aged cells. In this study, human dermal fibroblast cells (HDFs) were treated with 0.5 μM doxorubicin for 4 h to induce cellular senescence. Senescence-associated beta-galactosidase (SA-β-gal) activity was then measured 72 h after treatment with aerial parts of <i>Dendranthema zawadskii</i> var. <i>lucidum</i> (Nakai) J.H. Park (DZ) extract. Treatment with DZ extract significantly decreased SA-β-gal activity in a dose-dependent manner in HDFs. Additionally, DZ extract treatment reduced age-related oxidative stress and inflammation in the aortas of aged rats. The reactive oxygen species (ROS) levels in aortas of aged control rats were higher than those in young rats. However, DZ extract-fed aged rats showed significantly lower ROS levels than the aged control rats. When the aged rats were treated with DZ extract at either 0.2 or 1.0 mg∙kg⁻¹∙day⁻¹, NF-κB levels in aorta tissue decreased significantly compared to those in aorta tissue of the aged control rats without DZ treatment. In addition, DZ extract-fed aged rat aortas showed significant reductions in expression of iNOS and COX-2 induced by NF-κB translocation. Therefore, these results suggest that DZ effectively inhibited senescence-related NF-κB activation and inflammation. DZ extract may have a role in the prevention of the vascular inflammatory responses that occur during vascular aging.