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作 者:鞠强[1] 尹兴平[1] 石继海[1] 辛燕[1] 康晓静[1] 陈沄[1] 崔盘根[1] 曹元华[1] 夏隆庆[1]
出 处:《中华皮肤科杂志》2005年第2期98-101,共4页Chinese Journal of Dermatology
摘 要:目的探讨丹参酮治疗痤疮的机制。方法用四甲基偶氮唑盐(MTT)法检测不同浓度的隐丹参酮、丹参酮ⅡΑ在作用24、48及72h对SZ95细胞增殖的影响;用流式细胞仪检测尼罗河红荧光染色的SZ95细胞中脂质含量的变化;用半定量逆转录PCR(RT-PCR)检测药物对SZ95细胞中AR mRNA表达的影响。结果隐丹参酮浓度在0.5~12.5μmol/L之间呈时间和剂量依赖性抑制SZ95细胞增殖,其半数抑制浓度为7.473μmol/L(48h)和2.146μmol/L(72h);丹参酮ⅡΑ浓度在1.25μmol/L~12.5μmol/L呈时间和剂量依赖性抑制SZ95细胞增殖,其半数抑制浓度为6.021μmol/L(48h)和2.250mol/L(72h)。0.125μmol/L丹参酮ⅡΑ作用SZ95细胞48h后,尼罗河红荧光染色的平均荧光强度较对照组明显下降(P<0.05);此外,1μmol/L和0.1μmol/L隐丹参酮以及1μmol/L丹参酮ⅡΑ对SZ95细胞AR mRNA的表达显示出抑制作用(P<0.01,P<0.05,P<0.01)。结论隐丹参酮、丹参酮ⅡΑ可能通过直接抑制皮脂腺细胞的增殖、脂质合成或间接下调皮脂腺细胞雄激素受体mRNA的表达而具有抗皮脂腺活性的作用,这可能是丹参酮治疗痤疮的机制之一。Objective To study the effects of tanshinone on the cultured immortalized human sebocytes and explore the mechanism of action of tanshinone in the treatment of acne. Methods MTT assay was applied to determine the effects of cryptotanshinone and tanshinone ⅡΑ at different concentrations on the proliferation of SZ95 sebocytes in 24 h, 48 h and 72 h after incubation. Lipid contents labeled with Nile red in SZ95 cells were analyzed by flow cytometry technique, and the expression of androgen receptor (AR) mRNA of SZ95 cells were detected by RT-PCR. Results Both cryptotanshinone and tanshinoneⅡΑ inhibited the proliferation of SZ95 cells in a dose- and time-dependent mode, with the 50% inhibition concentration (IC50) of 7.473 μmol/L (in 48 h) and 2.146μmol/L (in 72 h) for cryptotanshinone and 6.021 μmol/L (in 48 h) and 2.25 μmol/L (in 72 h) for tanshinone ⅡΑ. Additionally, as compared with the control group, the lipid content of SZ95 cells exposed to tanshinone ⅡΑ at 0.125μmol/L was decreased in 48h (P < 0.05), and cryptotanshinone at 1μmol/L and 0.1μmol/L and tanshinoneⅡΑ at 1μmol/L decreased AR mRNA expression in SZ95 cells in 24h (P < 0.01, P < 0.01, P < 0.05 respectively). Conclusions These results indicate that tanshinone can directly inhibit the proliferation and lipid synthesis of sebocytes and has indirect anti-androgen activity by down-regulating AR mRNA expression in sebocytes, which implicates its possible mechanism of action in treating acne.
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