Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Jan 2;8(1):36-44.
doi: 10.1080/21655979.2016.1227572. Epub 2016 Sep 30.

Protective effect of Schizandrin B against damage of UVB irradiated skin cells depend on inhibition of inflammatory pathways

Chenguang Gao  1 , Hong Chen  1   2 , Cong Niu  1 , Jie Hu  1 , Bo Cao  1
Affiliations

Protective effect of Schizandrin B against damage of UVB irradiated skin cells depend on inhibition of inflammatory pathways

Chenguang Gao et al. Bioengineered. .

Abstract

Schizandrin B is extracted from Schisandra chinensis (Turcz.) Baill. This study evaluated the photoprotective effect of Schizandrin B on oxidative stress injury of the skin caused by UVB-irradiation and the molecular mechanism of the photoprotective effect of Schizandrin B, and we firstly found that Schizandrin B could block Cox-2, IL-6 and IL-18 signal pathway to protect damage of skin cells given by UVB-irradiation. In the research, we found that Schizandrin B can attenuate the UVB-induced toxicity on keratinocytes and dermal fibroblasts in human body, and can outstandingly eliminated intracellular ROS produced by UVB-irradiation. These results demonstrate that Schizandrin B can regulate the function of decreasing intracellular SOD's activity and increasing the expression level of MDA in HaCaT cells result from the guidance of UVB, and it markedly reduced the production of inflammatory factors such as Cox-2, IL-6 or IL-18, decreased the expression level of MMP-1, and interdicted degradation process of collagens in UVB-radiated cells. Therefore, skin keratinocytes can be effectively protected from UVB-radiated damage by Schizandrin B, and UVB-irradiation caused inflammatory responses can be inhibited by attenuating process of ROS generating.

Keywords: COX-2; ROS; Schizandrin B; UVB-irradiation; collagen; photoaging.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Schizandrin B protected from oxidative damage in UVB-induced HaCaT. Normal: Cells were treated with 0.1% DMSO. * p < 0.05, compared with control.
Figure 2.
Figure 2.
Morphological appearance of HaCaT cells treated with different doses of Schizandrin B by Confocal microscopy detection (×400): A HaCaT cells treated with 0.1% DMSO; B HaCaT cells treated with 0.1%DMSO + UVB; C HaCaT cells treated with 0.1 mol/L SchB + UVB; D HaCaT cells treated with 1 μmol/L SchB + UVB; E HaCaT cells treated with 10 μmol/L SchB + UVB.
Figure 3.
Figure 3.
Measurement of SOD on UVB-induced cellular fluid. Normal: Cells were treated with 0.1% DMSO. *p < 0.05, compared with 0μmol/L SchB group.
Figure 4.
Figure 4.
Measurement of MDA on UVB-induced cellular fluid. Normal: Cells were treated with 0.1% DMSO. *p< 0.05, compared with 0μmol/L SchB group.
Figure 5.
Figure 5.
Effect of Schizandrin B on Cox-2 expression in HaCaT Cells after UVB-irradiation. Normal: Cells were treated with 0.1% DMSO.
Figure 6.
Figure 6.
Effect of Schizandrin B on IL-18 expression in HaCaT Cells after UVB-irradiation. Normal: Cells were treated with 0.1% DMSO.
Figure 7.
Figure 7.
Effect of Schizandrin B on IL-18 expression in HaCaT Cells after UVB-irradiation. Normal: Cells were treated with 0.1% DMSO.
Figure 8.
Figure 8.
Effect of Schizandrin B on MMP-1 expression in FB Cells after UVB-irradiation. Normal: Cells were treated with 0.1% DMSO.
Figure 9.
Figure 9.
Effect of Schizandrin B on Type I pro-collage expression in FB Cells after UVB-irradiation. Normal: Cells were treated with 0.1% DMSO.
See this image and copyright information in PMC

References

    1. Kappes UP, Luo D, Potter M, Schulmeister K, Rünger TM. Runger.Short- and long-wave UV light (UVB and UVA) induce similar mutations in human skin cells. J Invest Dermatol 2006; 126(3):667-75; PMID:16374481; http://dx.doi.org/10.1038/sj.jid.5700093 - DOI - PubMed
    1. Ji C, Yang B, Yang Z, Tu Y, Yang YL, He L, Bi ZG. Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway. Biochem Biophys Res Commun 2012; 425(4):825-9; PMID:22892127; http://dx.doi.org/10.1016/j.bbrc.2012.07.160 - DOI - PubMed
    1. Van Laethem A, Claerhout S, Garmyn M, Agostinis P. The sunburn cell:regulation of death and survival of the keratinocyte. Int J Biochem Cell Biol 2005; 37(8):1547-53; PMID:15896663; http://dx.doi.org/10.1016/j.biocel.2005.02.015 - DOI - PubMed
    1. Ito T, Seo N, Yagita H, Tsujimura K, Takigawa M, Tokura Y. Alterations of immune functions in barrier disrupted skin by UVB irradiation. J Dermatol Sci 2003; 33(3):151-9; PMID:14643520; http://dx.doi.org/10.1016/S0923-1811(03)00177-4 - DOI - PubMed
    1. Fischer TW, Zbytek B, Sayre RM, Apostolov EO, Basnakian AG, Sweatman TW, Wortsman J, Elsner P, Slominski A. Melatonin increases survival of HaCaT keratinocytes by suppressing UV-induced apoptosis. J Pineal Res 2006; 40(1):18-26; PMID:16313494; http://dx.doi.org/10.1111/j.1600-079X.2005.00273.x - DOI - PubMed

MeSH terms

LinkOut - more resources