马齿苋提取物激活TRPV1调控痒信号通路治疗急性湿疹的分子机制研究

Acute eczema is a recurrent, inflammatory skin disease, often accompanied with severe itching syndrome, which seriously influence patient's quality of life. For a long time, we used to use corticosteroid and immunomodulators, but it will appear skin atrophy, pigmentation and other adverse reactions, so, they can not be used for long-term. We have found fresh Ma Chi Xian has obvious inhibitory effect on the vast majority of patients with acute eczema itching from rat experiment and clinical experiment in the earlier experiment. But its effective components, the key in the treatment process of regulator and important signal regulatory networks are still not clear. Recently, so many studies show TRPV1 plays a very important role in the pathogenesis of itching, therefore, on the basisi of "treatment of obstructive disease with dredge way", the experiment use different Ma Chi Xian extracting, confirmed the relationship between acute eczema itching and "Qi Stagnation and Blood Stasis" by TRPV1 pathway fromthe molecular biology, to confirm that effective components of Ma Chi Xian can acute eczema itch pathway blockade by regulation TRPV1, which achieve the purpose of treating acute eczema

急性湿疹是一种复发性、炎症性皮肤疾病，常伴有剧烈的瘙痒症状，严重影响了患者的生活质量。治疗该种疾病长期以来我们都使用了局部皮质类固醇激素制剂和免疫调节剂，但会出现皮肤萎缩、色素沉着等不良反应，不宜长期使用。前期我们通过大鼠实验以及临床实验，发现新鲜马齿苋溶液对绝大多数急性湿疹患者的瘙痒症状有明显抑制作用。但其具体有效成分以及其在治疗过程中关键调控因子和重要信号调控网络均尚未能明确。近年来研究表明，TRPV1在瘙痒发生机制中起着非常重要的作用。因此，结合中医“通因通用”学说，本实验提取马齿苋不同有效成分进行分组对比实验，从分子生物学的角度证实急性湿疹瘙痒症状与TRPV1痒信号通路导致局部“气血不畅”的关系，明确马齿苋活血消肿功能能够通过调控TRPV1阻断急性湿疹瘙痒通路，达到治疗疾病的目的。

急性湿疹是临床常见的皮肤病，发病率高，因其常伴有瘙痒症状，严重影响了患者的生活质量。最常用的就是皮质类固醇激素制剂等药物，副作用较明显，不宜长期使用。马齿苋提取液治疗急性湿疹效果好且副作用少。本项目主要通过对马齿苋成分的提取，比较各成分对对急性湿疹大鼠瘙痒的干预作用，探究其抑痒机制。主要结果：与正常组比，模型组大鼠湿疹面积及严重度指数（eczema area and severity index，EASL）显著增加（P<0.05）；大鼠皮肤H1R、PAR-2的含量及角质层细胞（Keratinocyte，KC）内Ca2+浓度均显著增加（P<0.05），TRPV1增加差异不明显（P>0.05）。与模型组比，黄柏组、马齿苋组大鼠EASL均有显著减小（P<0.05）；大鼠皮肤H1R、PAR-2的含量及KC细胞内Ca2+浓度显著减少（P<0.05），TRPV1减少差异不明显（P>0.05）。基于上述实验结果，我们可以得出以下结论：马齿苋可减少H1R、PAR-2含量及降低细胞内Ca2+浓度，发挥治疗急性湿疹瘙痒作用，其机制可能是通过降低上游分子H1R、PAR-2含量，使其下游分子TRPV1失活，减少Ca2+内流，达到抗瘙痒的作用。为临床医生的用药提供依据。

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