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番泻叶种子中的活性化合物大黄酚通过抑制 JNK/p38 MAPK 信号通路抑制人皮脂腺的热诱导脂肪生成。

Active compound chrysophanol of Cassia tora seeds suppresses heat-induced lipogenesis via inactivation of JNK/p38 MAPK signaling in human sebocytes.

机构信息

Songpa R&D Center, Coreana Cosmetics Co., Ltd, 6, Samgok 2-gil, Seonggeo-eup, Seobuk-gu, Cheonan-si, Chungcheongnam-do, Republic of Korea.

出版信息

Lipids Health Dis. 2019 Jun 7;18(1):135. doi: 10.1186/s12944-019-1072-x.

DOI:10.1186/s12944-019-1072-x
PMID:31174532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6555928/
Abstract

BACKGROUND

Heat induced by infrared (IR) radiation from sun exposure increases skin temperature and can lead to thermal and photo-aging. However, little is known about the relationship between heat induced by IR radiation and lipid biosynthesis in human sebocytes. This study investigated the expression of factors involved in lipid biosynthesis in human sebocytes exposed to heat. The effect of Cassia tora extract and chrysophanol, which is widely used as anti-inflammatory agent, on the heat shock effect in sebocytes was then examined.

METHODS

For the treatment, cells were maintained in culture medium without FBS (i.e., serum starved) for 6 h and then moved for 30 min to incubators at 37 °C (control), 41 °C, or 44 °C (heat shock). Culture media were replaced with fresh media without FBS. To investigate expression of gene and signaling pathway, we performed western blotting. Lipid levels were assessed by Nile red staining. The cytokine levels were measured by cytokine array and ELISA kit.

RESULTS

We found that peroxisome proliferator-activated receptor (PPAR)γ and fatty acid synthase (FAS) were upregulated and the c-Jun N-terminal kinase (JNK)/p38 signaling pathways were activated in human sebocytes following heat exposure. Treatment with Cassia tora seed extract and chrysophanol suppressed this up-regulation of PPARγ and FAS and also suppressed the increase in IL-1β levels.

CONCLUSION

These findings provide evidence that IR radiation can stimulate sebum production; Cassia tora seed extract and chrysophanol can reverse lipid stimulated inflammatory mediation, and may therefore be useful for treating skin disorders such as acne vulgaris.

摘要

背景

太阳照射产生的红外线(IR)辐射引起的热量会升高皮肤温度,导致热老化和光老化。然而,人们对于 IR 辐射引起的热量与人类皮脂细胞中脂类生物合成之间的关系知之甚少。本研究调查了暴露于热环境中的人类皮脂细胞中参与脂类生物合成的因子的表达。然后,研究了广泛用作抗炎剂的槐树籽提取物和大黄素对皮脂细胞热休克效应的影响。

方法

在治疗中,将细胞在不含 FBS 的培养基中(即血清饥饿)中维持 6 小时,然后转移到 37°C(对照)、41°C 或 44°C(热休克)的培养箱中 30 分钟。将培养基更换为不含 FBS 的新鲜培养基。为了研究基因和信号通路的表达,我们进行了 Western blot 分析。通过尼罗红染色评估脂质水平。通过细胞因子阵列和 ELISA 试剂盒测量细胞因子水平。

结果

我们发现,在人类皮脂细胞暴露于热后,过氧化物酶体增殖物激活受体(PPAR)γ和脂肪酸合酶(FAS)上调,c-Jun N-末端激酶(JNK)/p38 信号通路被激活。槐树籽提取物和大黄素的处理抑制了 PPARγ 和 FAS 的这种上调,并抑制了 IL-1β水平的增加。

结论

这些发现提供了证据表明,IR 辐射可以刺激皮脂分泌;槐树籽提取物和大黄素可以逆转脂类刺激的炎症介导作用,因此可能对治疗寻常痤疮等皮肤疾病有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/f4eab8c11d69/12944_2019_1072_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/f5a7f05be795/12944_2019_1072_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/cde62479c887/12944_2019_1072_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/4860d5e61b4a/12944_2019_1072_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/5ea5008a5016/12944_2019_1072_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/f4eab8c11d69/12944_2019_1072_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/f5a7f05be795/12944_2019_1072_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/cde62479c887/12944_2019_1072_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/4860d5e61b4a/12944_2019_1072_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/5ea5008a5016/12944_2019_1072_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/6555928/f4eab8c11d69/12944_2019_1072_Fig5_HTML.jpg

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