Polysaccharide from Ophiopogon japonicus protects against ultraviolet B damage to the human dermal fibroblasts

doi:10.3969/j.issn.2095-4344.2017.32.017

Abstract

Abstract:

BACKGROUND: With the deterioration of environment, the atmospheric ozone layer is seriously destroyed; thereafter, ultraviolet B (UVB) radiation to the earth surface is increasing. Prevention and control of UVB-induced skin photoaging is of great significance.
OBJECTIVE: To study the protective effect of polysaccharide from Ophiopogon japonicus on the photoaged human dermal fibroblasts
METHODS: Human dermal fibroblasts were divided into five groups: control group received no UVB radiation, and cultured in the free-drug medium; other four groups were irradiated under 200 mJ/cm2 UVB to establish the photoaging model, and then cultured in the drug-free medium (model group), or in the medium of polysaccharide from Ophiopogon japonicus (10, 100, and 1 000 mg/L), respectively. The cell viability was detected by cell counting kit-8 assay after 48-hour culture; the levels of superoxide dismutase, glutathione peroxidase and malondialdehyde were detected by kit method; and the expression levels of matrix metalloproteinases-1 and -3 as well as c-Jun gene were detected by quantitative PCR.
RESULTS AND CONCLUSION: Compared with the control group, 200 mJ/cm2 UVB significantly reduced the viability of human dermal fibroblasts and levels of superoxide dismutase and glutathione peroxidase, as well as increased the malondialdehyde level, and expression levels of matrix metalloproteinase-1 and -3, and c-Jun gene (P < 0.05). In the meanwhile, 10, 100, and 1 000 mg/L polysaccharide from Ophiopogon japonicus significantly reversed all above phenomena (P < 0.05). To conclude, polysaccharide from Ophiopogon japonicas can reduce the damage of UVB to human dermal fibroblasts, maybe by alleviating UVB-induced oxidative stress, inhibiting the relative signaling pathways, and reducing the expression of c-Jun gene, further inhibiting the expression of matrix metalloproteinase-1 and -3, and reducing collagen degradation.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Ultraviolet Rays, Skin, Fibroblasts, Ophiopogon, Tissue Engineering

CLC Number:

R318

Chen Gao-min, Wang Lu, Du Pei, Li Zhong-ping, Shen Hong-yi. Polysaccharide from Ophiopogon japonicus protects against ultraviolet B damage to the human dermal fibroblasts[J]. Chinese Journal of Tissue Engineering Research, 2017, 21(32): 5183-5188.

Figures/Tables 2

References

[1] 殷花,林忠宁,朱伟. 皮肤光老化发生机制及预防[J]. 环境与职业医学,2014,31(7):565-569.

[2] 曹爽,付绍智,王永多, 等.麦冬多糖药理作用研究进展[J]. 安徽农业科学,2015,43(28):63-66.

[3] 杨金颖,孙芳芳. 麦冬多糖的药理作用研究[J]. 天津药学,2016, 28(2):52-55.

[4] Yu BC, Lee DS, Bae SM, et al. The effect of cilostazol on the expression of matrix metalloproteinase-1 and type I procollagen in ultraviolet-irradiated human dermal fibroblasts. Life Sci. 2013;92(4-5): 282-288.

[5] 李春雨,张丽宏,张宁,等. 紫外线诱导皮肤光老化的形成机制[J]. 中国美容医学, 2009,18(3): 416-419.

[6] Fisher GJ. The pathophysiology of photoaging of the skin. Cutis. 2005;75(2 Suppl): 5-8, 8-9.

[7] 马淑梅, 刘晓冬, 龚平生, 等. 中波紫外线对成纤维细胞的损伤作用[J]. 吉林大学学报,2005,31(3):365-367.

[8] 王玉贞,郭沈波,韩华, 等.中波紫外线诱导人真皮成纤维细胞凋亡的研究[J]. 青岛大学医学院学报,2002,38(4):287-288+306.

[9] 陈默,赵亚,孙懿. 杜仲预防UVB致人成纤维细胞光老化的作用及基因水平的机制探讨[J]. 日用化学工业,2016,46(1): 35-38+57.

[10] 郑雯,曾维惠,易清玲,等.白藜芦醇对UVB照射的人皮肤成纤维细胞MMP-1水平及细胞凋亡的影响[J]. 中国皮肤性病学杂志, 2012,26(4):296-299.

[11] 骆丹,明亚玲,徐晶, 等.UVB致成纤维细胞损伤及两种中药的保护作用研究[J]. 中国皮肤性病学杂志,2006,20(7):385-388.

[12] 吴迪,周炳荣,骆丹. 黄芩苷对UVB诱导人皮肤成纤维细胞光产物生成的干预作用[J]. 中国中西医结合皮肤性病学杂志,2011, 10(5):273-275.

[13] 王小勇,毕志刚,王云贵,等.人参皂苷和枸杞多糖对UVB诱导培养的成纤维细胞提早衰老的影响[J].中华皮肤科杂志.2010,43(3): 184-187.

[14] 李丹晖,宋坪,张文生.人参皂苷Rg1对UVB损伤PG12及成纤维细胞的保护作用[J]. 皮肤病与性病,2009,(4):6-9.

[15] 黄光辉,孙连娜. 麦冬多糖的研究进展[J]. 现代药物与临床, 2012,(5):523-529.

[16] 范俊,张旭. 麦冬多糖药理研究进展[J]. 中医药学刊,2006,(4): 626-627.

[17] Wolfle U, Seelinger G, Bauer G, et al. Reactive molecule species and antioxidative mechanisms in normal skin and skin aging. Skin Pharmacol Physiol. 2014;27(6): 316-332.

[18] Rinnerthaler M, Bischof J, Streubel MK, et al. Oxidative stress in aging human skin. Biomolecules. 2015;5(2): 545-589.

[19] Kammeyer A, Luiten RM. Oxidation events and skin aging. Ageing Res Rev. 2015;21: 16-29.

[20] Scharffetter-Kochanek K, Brenneisen P, Wenk J, et al. Photoaging of the skin from phenotype to mechanisms. Exp Gerontol. 2000;35(3): 307-316.

[21] Fisher GJ, Voorhees JJ. Molecular mechanisms of photoaging and its prevention by retinoic acid: ultraviolet irradiation induces MAP kinase signal transduction cascades that induce Ap-1-regulated matrix metalloproteinases that degrade human skin in vivo. J Investig Dermatol Symp Proc. 1998; 3(1): 61-68.

[22] Montagner S, Costa A. Molecular basis of photoaging. An Bras Dermatol. 2009;84(3): 263-269.

[23] Wlaschek M, Tantcheva-Poor I, Naderi L, et al. Solar UV irradiation and dermal photoaging. J Photochem and Photobiol B. 2001;63(1-3):41-51.

[24] Lopez-Camarillo C, Ocampo EA, Casamichana ML, et al. Protein kinases and transcription factors activation in response to UV-radiation of skin: implications for carcinogenesis. Int J Mol Sci. 2012;13(1):142-172.

[25] 刘平,杨荣丽,苏慧,等. 红外线影响人皮肤成纤维细胞中c-Jun、Ⅰ型和Ⅲ型胶原的表达[J]. 南方医科大学学报,2016,36(2): 163-169.

[26] Sardy M. Role of matrix metalloproteinases in skin ageing. Connect Tissue Res. 2009;50(2): 132-138.

[27] Quan T, Qin Z, Xia W, et al. Matrix-degrading metalloproteinases in photoaging. J Investig Dermatol Symp Proc. 2009;14(1): 20-24.

[28] Naylor EC, Watson RE, Sherratt MJ. Molecular aspects of skin ageing. Maturitas. 2011;69(3): 249-256.

[29] Quan T, Qin Z, Xia W, et al. Matrix-degrading metalloproteinases in photoaging. J Invest Dermatology Symposium Proceedings. 2009;14(1):20-24.

[30] 陆洪军,宋丽娜,付天佐,等. 麦冬多糖对亚急性衰老小鼠皮肤组织衰老程度的影响[J]. 中国老年学杂志,2015,35(8): 2160-2161.