Prunella vulgaris L. exerts a protective effect against extrinsic aging via NF-κB, MAPKs, AP-1, and TGF-β/Smad signaling pathways in UVB-aged normal human dermal fibroblasts

Rejuvenation Res. 2018 Jan 29. doi: 10.1089/rej.2017.1971. [Epub ahead of print] Zhang M1, Hwang E2, Lin P3, Gao W4, Ngo HTT5, Yi TH6. Author information 1 Yongin, Korea (the Republic of) ; zhangmy@khu.ac.kr. 2 Seoul, Korea (the Republic of) ; firsthes@khu.ac.kr. 3 Yongin, Korea (the Republic of) ; linpei@khu.ac.kr. 4 Yongin, Korea (the Republic of) ; weigao@khu.ac.kr. 5 Yongin, Korea (the Republic of) ; hienngo211@khu.ac.kr. 6 DeokyoungdaeroYongin, Korea (the Republic of) , 446-701 ; drhoo@khu.ac.kr. Abstract Prunella vulgaris L., a well-known traditional Chinese herbal medicine, has anti-inflammatory and antioxidant activities. In the present study, the underlying molecular mechanisms of the protective effect of P. vulgaris extract (PVE) were investigated in UVB-irradiated normal human dermal fibroblasts (NHDFs). The mRNA expression of matrix metalloproteinases (MMPs), procollagen type I and cytokines such as interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) was determined by RT-PCR. The expression of anti-photo aging-related signaling molecules in the NF-κB, MAPK/AP-1, and TGF/Smad pathways was assessed by Western blot. We observed that PVE blocked the up-regulated production of ROS induced in UVB-irradiated NHDFs in a dose-dependent manner. Treatment with PVE also significantly ameliorated the mRNA levels of MMPs, procollagen type I, TNF-α, and IL-6. In addition, the phosphorylation level of c-Jun and c-Fos was decreased through the attenuated expression levels of p-ERK and p-JNK after treatment with PVE. Furthermore, cells treated with PVE showed inhibited Smad 7 and increased Smad 2/3 expression in the TGF-β/Smad signaling pathway. Hence, synthesis of procollagen type I, a precursor of collagen I, was promoted. These findings indicate that treatment with PVE has a potential protective effect against UVB-induced photo aging and photo-inflammation. PMID: 29378470 DOI: 10.1089/rej.2017.1971