| 引用本文: | 周凌,郭亮,王敏,周伟.甘草酸苷通过MAPK p38/NF-κB通路对炎症后色素沉着的抑制作用[J].中国现代应用药学,2019,36(8):930-934. |
| ZHOU Ling,GUO Liang,WANG Min,ZHOU Wei.Glycyrrhizic Acid Suppress Post-inflammatory Hyperpigmentation via MAPK p38/NF-κB Singalling Pathway[J].Chin J Mod Appl Pharm(中国现代应用药学),2019,36(8):930-934. |
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| 摘要: |
| 目的 探讨甘草酸苷对脂多糖（lipopolysaccharide，LPS）刺激后角质形成细胞分泌COX-2/PGE2和对共培养黑素细胞合成黑素的影响，并探讨其可能的作用机制。方法 以人表皮角质形成细胞为对象，分为对照组、LPS组、甘草酸苷组（2，5，10 μmol·L-1）。采用ELISA法检测PGE2的含量，Western blot检测细胞COX-2、NF-κB p-p65、p-IKKα/β和MAPKp-p38蛋白的表达，比色法检测共培养黑素细胞的黑素含量。结果 与对照组比较，LPS显著增加角质形成细胞COX-2、NF-κB p-p65、p-IKKα/β、MAPK p-p38蛋白表达（P<0.01）和PGE2的分泌（P<0.01），增加共培养黑素细胞黑素生成（P<0.01）。与LPS组比较，甘草酸苷呈剂量依赖性抑制COX-2、NF-κB p-p65、p-IKKα/β、MAPK p-p38蛋白表达（P<0.05）和PGE2的分泌（P<0.05），减少共培养黑素细胞黑素生成（P<0.05）。结论 甘草酸苷通过抑制角质形成细胞MAPK p38/NF-κB通路，从而降低COX-2/PGE2的表达，减少共培养黑素细胞合成黑素。 |
| 关键词: 甘草酸苷 角质形成细胞 炎症后色素沉着 COX-2 NF-κB 脂多糖 |
| DOI：10.13748/j.cnki.issn1007-7693.2019.08.007 |
| 分类号:R285.5 |
| 基金项目: |
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| Glycyrrhizic Acid Suppress Post-inflammatory Hyperpigmentation via MAPK p38/NF-κB Singalling Pathway |
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ZHOU Ling, GUO Liang, WANG Min, ZHOU Wei
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Plastic and Cosmetic Department of Zhongnan Hospital, Wuhan University, Wuhan 430071, China
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| Abstract: |
| OBJECTIVE To investigate the inhibitory effect of glycyrrhizic acid(GA) on LPS-induced expression of COX-2/PGE2 in keratinocytes and the melanin production in co-cultured melanocytes explore its possible mechanism. METHODS Human cutaneous keratinocytes were treated with GA of different concentration(0, 2, 5 and 10 μmol·L-1) and LPS. The level of cytokine PGE2 in the culture medium was determined using ELISA kit. The expression of COX-2, NF-κB p-p65, p-IKKα/β and MAPK p-p38 were studied by Western blotting. The melanin content in co-cultured melanocytes was measured by colorimetric method. RESULTS The expression of COX-2, NF-κB p-p65, p-IKKα/β and MAPK p-p38 in LPS-treated keratinocytes were significantly raised compared to that in control group. LPS also elevated PGE2 levels in the culture medium. The melanin content in co-cultured melanocytes increased after LPS stimulation. GA decreased COX-2, NF-κB p-p65, p-IKKα/β and MAPK p-p38 expression in LPS-treated keratinocytes in a dose-dependent manner(P<0.05). GA decreased PGE2 levels in the culture medium of keratinocytes dose-dependently (P<0.05). GA also decreased melanin production in co-cultured melanocytes dose-dependently(P<0.05). CONCLUSION GA decreases LPS-induced expression of COX-2/PGE2 in keratinocytes and melanin production in co-cultured melanocytes through suppressing MAPK p38/NF-κB signal pathway. |
| Key words: glycyrrhizic acid keratinocyte post-inflammatory hyperpigmentation COX-2 NF-κB lipopolysaccharide(LPS) |
