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权威发布 ‖ 不老莓原浆提取物有助于缓解各种炎症性皮肤病

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一起车尔西·举杯祝江山

 

不老莓原浆提取物

有助于缓解各种炎症性皮肤病

Aronia melanocarpa Concentrate Ameliorates Pro-Inflammatory Responses in HaCaT Keratinocytes and 12-O-Tetradecanoylphorbol-13-Acetate-Induced Ear Edema in Mice.








炎症的危害


炎症在人体中扮演重要角色,是不可缺少的功能。但应知道,虽然发炎能在受伤中保护我们,但如果失去控制,也会给健康带来危害。尤其是慢性炎症,是绝对应避免的事情,因为它不仅会诱发严重疾病,甚至还有致命风险。心脏病和癌症就是与炎症有关的疾病。心脏病会导致冠状动脉堵塞和心脏病发作,因此保健专家很早以前就开始告诫人们注意保持胆固醇水平,并防止在动脉积聚斑块。最新研究还发现,炎症在胆固醇增加和形成血栓方面扮演一个重要角色。

 


炎症还被视为癌症的诱因之一

已发现一些涉及发炎的细胞和化学物质会产生能最终导致癌症的DNA突变;因此,它还能使预癌细胞变成活性癌细胞。已知与炎症有关的癌症包括结肠癌,肺癌,胃癌,食道癌和乳腺癌等。

还有其它一些疾病也与炎症有关。如类风湿关节炎,骨质疏松症,狼疮,肺气肿和牙龈炎都是炎性疾病。实际上,滑囊炎,肌腱炎,关节炎,肝炎,结肠炎,扁桃体炎和皮炎等带“炎”字的病都是炎性疾病。

 


发炎的开始与过程

发炎是身体对有害刺激的反应。它的诱发源包括:

★ 细菌和病毒等病原体感染;

★ 身体损伤;

★ 碎片,灰尘和其它杂物进入身体;

★ 化学刺激;

★ 烧伤和冻伤;

★ 压力;

★ 源自空气或水的毒素。


谁都有过发炎经历,主要症状是红肿,发烧和疼痛。然而,仅持续几天到几周时间急性发炎占多数,并且大部分能在刺激物清除后自然消失。因此,多数情况下不是很严重。但另一方面,慢性炎症不能适当消除,会持续几个月,甚至几年。这种炎症对身体非常有害!





NCBI权威数据

【美国国家生物技术信息中心】




不老莓原浆提取物

可作为各种炎症性皮肤病的治疗剂


 AC-不老莓原浆提取物

因文中涉及很多专业术语,可能翻译存在误差,具体表述含义以英文为准!

 

炎性介质如细胞粘附分子和细胞因子的异常症状与各种炎症性皮肤疾病(包括特应性皮炎)有关。本研究采用体内外皮肤炎症模型,研究了不老莓原浆浓缩物(AC,下文AC特指不老莓原浆提取物)的抗炎活性及其作用机制。局部应用AC对小鼠耳显著抑制12-邻十四烷酰佛波醇-13-乙酸酯(TPA)诱导的耳水肿形成,如通过测量耳厚度和重量和组织学分析判断。局部给药可降低TPA刺激小鼠耳中TNF-α、IL-1β、IL-6等促炎性细胞因子的作用。

 

AC预处理抑制TNF-α诱导的角质形成细胞HaCaT细胞ICAM-I表达及随后的单核细胞粘附。此外,AC显著降低TNF-α刺激的HaCaT细胞的细胞内活性氧(ROS)生成以及丝裂原活化蛋白激酶(MAPK)活化。AC和其组成的矢车菊素3-葡萄糖苷还可减弱TNF-α诱导的HaCaT细胞IKK活化、IκB降解、p65磷酸化/核易位和p65 DNA结合活性。

 

总的来说,我们的结果表明,AC通过抑制ROS -MAPK-NF-κB信号通路在体外和体内抑制促炎介质的作用而发挥抗炎活性。因此,AC可有助于缓解各种炎症性皮肤病。

NCBI 数据中心英文原稿

Aronia melanocarpa Concentrate Ameliorates Pro-Inflammatory Responses in HaCaT Keratinocytes and 12-O-Tetradecanoylphorbol-13-Acetate-Induced Ear Edema in Mice.




Abnormal expression of pro-inflammatory mediators such as cell adhesion molecules and cytokines has been implicated in various inflammatory skin diseases, including atopic dermatitis. In this study, we investigated the anti-inflammatory activity of Aronia melanocarpa concentrate (AC) and its action mechanisms using in vivo and in vitro skin inflammation models. Topical application of AC on mouse ears significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema formation, as judged by measuring ear thickness and weight, and histological analysis. Topical administration of AC also reduced the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 in TPA-stimulated mouse ears. Pretreatment with AC suppressed TNF-α-induced ICAM-I expression and subsequent monocyte adhesiveness in human keratinocyte cell line HaCaT. In addition, AC significantly decreased intracellular reactive oxygen species (ROS) generation as well as mitogen-activated protein kinase (MAPK) activation in TNF-α-stimulated HaCaT cells. AC and its constituent cyanidin 3-glucoside also attenuated TNF-α-induced IKK activation, IκB degradation, p65 phosphorylation/nuclear translocation, and p65 DNA binding activity in HaCaT cells. Overall, our results indicate that AC exerts anti-inflammatory activities by inhibiting expression of pro-inflammatory mediators in vitro and in vivo possibly through suppression of ROS-MAPK-NF-κB signaling pathways. Therefore, AC may be developed as a therapeutic agent to treat various inflammatory skin diseases.







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