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. 2018 Feb 13;27(4):1157-1163.
doi: 10.1007/s10068-018-0331-3. eCollection 2018 Aug.

Preventive effect of Ephedra sinica extract on UVB-induced COX-2 and MMP-1 expression

Su Jeong Ha  1 , Chang Joo Lee  2 , Sung Keun Jung  1   3   4
Affiliations

Preventive effect of Ephedra sinica extract on UVB-induced COX-2 and MMP-1 expression

Su Jeong Ha et al. Food Sci Biotechnol. .

Abstract

Ultraviolet B (UVB)-induced cyclooxygenase (COX)-2 and matrix metalloproteinase (MMP)-1 are representative markers for skin inflammation and photoaging, respectively. To evaluate compounds that may counteract the effects of UVB-induced skin damage, we developed an immortalized human keratinocyte (HaCaT) cell line with an MMP-1 reporter construct. Among the 30 botanical extracts screened, we selected Ephedra sinica extract (ESE) as a promising candidate and confirmed that ESE significantly suppresses UVB-induced COX-2 and MMP-1 expression in HaCaT cells. Treatment with ESE also potently suppressed UVB-induced ERK1/2 phosphorylation, as well as UVB-induced MEK1/2 and Raf phosphorylation in HaCaT cells. These findings suggest that our MMP-1 reporter system can be used to evaluate compounds with anti-inflammatory and anti-photoaging effects. We also report that ESE has potent suppressive effects against COX-2 and MMP-1 expression, which occurs via downregulation of Raf/MEK1/2/ERK1/2 phosphorylation.

Keywords: Cyclooxygenase-2; Ephedra sinica extract; Matrix metalloproteinase-1; Mitogen-activated protein kinase.

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Conflict of interest statement

Compliance with ethical standardsThe authors declare no conflict of interest.

Figures

Fig. 1
Fig. 1
Development of MMP-1 promoter-expressing human keratinocyte HaCaT cells and measurement of ESE on UVB-induced MMP-1 promoter activity. (A) HaCaT cells were transfected with pGF1 vector containing the MMP-1 promoter and selected with puromycin treatment (1 μg/mL). Left figure: non-infected cell with puromycin; right figure: infected with MMP-1 promoter. (B) Optimization of MMP-1 promoter transactivity using varying UV dosages and incubation times. Asterisks (*) indicate a significant difference (p < 0.05) relative to the control group. Data are presented as mean ± SD of three independent experiments. (C) Effect of ESE on UVB-induced MMP-1 promoter activity in HaCaT cells. Promoter activity is presented as the mean ± SD of three independent experiments. Hash symbols (#) indicate a significant difference (p < 0.05) between the control group and the group exposed to UVB alone; asterisks [(*) and (**)] indicate significant differences [(p < 0.05) and (p < 0.01)] between groups irradiated with UVB and ESE and the group exposed to UVB alone. Data are presented as mean ± SD of three independent experiments. (D) ESE exhibits no detectable cell cytotoxicity up to 100 μg/mL in HaCaT cells. Cell viability was measured by MTS assay as described in “Materials and methods”
Fig. 2
Fig. 2
Effect of ESE on UVB-induced MMP-1 and COX-2 expression in HaCaT cells. (A) ESE inhibits UVB-induced MMP-1 expression in HaCaT cells. (B) ESE inhibits UVB-induced COX-2 expression in HaCaT cells. Expression levels of MMP-1, COX-2 and β-actin were determined by Western blot assay. Hash symbols (#) indicate a significant difference (p < 0.05) between the control group and the group exposed to UVB alone; asterisks [(*) and (**)] indicate significant differences [(p < 0.05) and (p < 0.01)] between groups irradiated with UVB and ESE and the group exposed to UVB alone. Data are presented as mean ± SD of three independent experiments
Fig. 3
Fig. 3
Effect of ESE on UVB-induced Raf/MEK/ERK1/2 phosphorylation and C-Fos nuclear translocation in HaCaT cells. (A) ESE inhibits UVB-induced ERK1/2 phosphorylation; and (B) Raf and MEK phosphorylation in HaCaT cells. Phosphorylation status and total expression were assessed by Western blot assay with specific antibodies. Data are presented as mean ± SD of three independent experiments. (C) ESE suppresses UVB-induced C-Fos nuclear translocation in HaCaT cells
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