Polyphyllin I Inhibits Propionibacterium acnes-Induced Inflammation In Vitro.
Polyphyllin I Inhibits Propionibacterium acnes-Induced Inflammation In Vitro.
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Polyphyllin I 可抑制痤疮丙酸杆菌引起的体外炎症。
DOI：
10.1007/s10753-018-0870-z
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发表时间：
2019-03
期刊：
影响因子：
5.1
通讯作者：
He L
中科院分区：
文献类型：
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作者：
Zhu T;Wu W;Yang S;Li D;Sun D;He L
痤疮丙酸杆菌（P. acnes）已涉及痤疮炎症的进展。由于目前的痤疮药物有各种副作用，有必要探索具有抗炎活性的替代药物。在体外实验中，我们研究了聚茶树素I （polyphyllin I， PPI）对痤疮链球菌诱导炎症的抑制作用。在这项研究中，我们检测了PPI对热杀死痤疮假单胞杆菌处理的HaCaT角化细胞产生炎症细胞因子的影响。这些处理过的HaCaT角质形成细胞显示toll样受体2 （TLR2）的表达增加和炎症细胞因子的产生。PPI显著抑制了P. acins处理细胞中炎症因子的分泌，包括白细胞介素(IL)-6、IL-8和肿瘤坏死因子(TNF)-α，以及TLR2的表达。此外，我们研究了PPI对P. acnes处理的角质形成细胞中核因子-κB （NF-κB）和丝裂原活化蛋白激酶（MAPK）信号通路的影响。PPI降低了NF-κB的活化。热杀痤疮p处理后磷酸化p38水平显著升高，PPI处理后磷酸化p38水平降低，而PPI对ERK磷酸化的影响不显著。热灭痘假单胞菌和PPI对JNK磷酸化无明显影响。此外，我们证实了NF-κB p65抑制剂（BAY11-7082）、p38 MAPK抑制剂（SB203580）和PPI阻断了热杀伤痤疮P.处理细胞中IL-8的表达。这些结果表明，PPI有潜力发展为痤疮炎症的治疗。
Propionibacterium acnes (P. acnes) has been implicated in the progression of acne inflammation. Because current acne medications have various side effects, it is necessary to explore alternative medications possessing anti-inflammatory activity against P. acnes. We investigated the inhibitory effects of polyphyllin I (PPI) on P. acnes-induced inflammation in vitro. In this study, we examined the effects of PPI on the production of inflammatory cytokines in HaCaT keratinocytes treated with heat-killed P. acnes. These treated HaCaT keratinocytes showed increased expression of Toll-like receptor 2 (TLR2) and production of inflammatory cytokines. PPI significantly suppressed the secretion of inflammatory cytokines, including interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, and the expression of TLR2 in P. acnes-treated cells. Moreover, we studied the influence of PPI on the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways in P. acnes-treated keratinocytes. PPI diminished the activation of NF-κB. Phosphorylated p38 levels were markedly increased after treatment with heat-killed P. acnes but were decreased after treatment with PPI, while the effect of PPI on ERK phosphorylation was not significant. Heat-killed P. acnes and PPI did not have any effect on JNK phosphorylation. Furthermore, we confirmed that NF-κB p65 inhibitor (BAY11-7082), p38 MAPK inhibitor (SB203580), and PPI blocked the expression of IL-8 in heat-killed P. acnes-treated cells. These results demonstrated that PPI has potential for development as a treatment for acne inflammation.
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影响因子：
--
作者：
Selway JL;Kurczab T;Kealey T;Langlands K
通讯作者：
Langlands K
影响因子：
6.1
作者：
Huang, Yu-Chun;Yang, Chao-Hsun;Hsu, Han-Chi
通讯作者：
Hsu, Han-Chi
影响因子：
6.5
作者：
Hay, Roderick J.;Johns, Nicole E.;Naghavi, Mohsen
通讯作者：
Naghavi, Mohsen
氯素E6介导的光动力疗法通过NFκB和MAPKS信号通路抑制了痤疮P.痤疮诱导的炎症反应。
影响因子：
3.7
作者：
Wang YY;Ryu AR;Jin S;Jeon YM;Lee MY
通讯作者：
Lee MY
影响因子：
6.5
作者：
Dispenza, Melanie C.;Wolpert, Ellen B.;Gilliland, Kathryn L.;Dai, Jenny P.;Cong, Zhaoyuan;Nelson, Amanda M.;Thiboutot, Diane M.
通讯作者：
Thiboutot, Diane M.