Oral administration of punicalagin attenuates imiquimod-induced psoriasis by reducing ROS generation and inflammation via MAPK/ERK and NF-κB signaling pathways.
Oral administration of punicalagin attenuates imiquimod-induced psoriasis by reducing ROS generation and inflammation via MAPK/ERK and NF-κB signaling pathways.
复制标题
DOI：
10.1002/ptr.8071
复制
发表时间：
2023-11
影响因子：
7.2
通讯作者：
Yuqian Wang;Dan Han;Yingjian Huang;Yilin Dai;Yan Wang;Meng Liu;Ning Wang;Tingyi Yin;Wenqian Du;Ke He;Yan Zheng
中科院分区：
文献类型：
--
作者：
Yuqian Wang;Dan Han;Yingjian Huang;Yilin Dai;Yan Wang;Meng Liu;Ning Wang;Tingyi Yin;Wenqian Du;Ke He;Yan Zheng
银屑病是一种免疫介导的慢性炎症性皮肤病，给患者带来巨大的心理和身体负担，严重影响患者的生活质量。石榴素(Pu)是石榴中含量最丰富的单宁，因其具有多种生物活性而成为研究热点。然而，它对牛皮癣的疗效尚不清楚。采用Western blotting、实时定量聚合酶链式反应(qRT-PCR)、苏木精伊红(H&E)染色、免疫组织化学和免疫荧光等方法，探讨PU对M5刺激的角质形成细胞株和咪喹莫特(Imquimod)诱导的BABL/c小鼠银屑病样皮肤炎症的影响及其分子机制。每天给药150和250 mg/kg的富含PU的石榴提取物显著减轻银屑病的严重程度，消除脾肿大，并减少ImQ诱导的异常表皮增殖、CD4+T细胞浸润和炎性因子表达。此外，在M5刺激的炎症细胞模型中，PU可通过抑制丝裂原活化蛋白激酶/细胞外调节蛋白激酶和核因子-κB信号通路抑制角质形成细胞的增殖，从而降低促炎症细胞因子IL-1α、IL-6、IL-8、肿瘤坏死因子-α、IL-17A、IL-22、IL-23A和ROS的表达水平。我们的结果表明，通过改善细胞氧化应激和炎症，PU可能成为银屑病的一种有前途的营养干预措施。
Psoriasis, an immune‐mediated chronic inflammatory skin disease, imposes a huge mental and physical burden on patients and severely affects their quality of life. Punicalagin (PU), the most abundant ellagitannin in pomegranates, has become a research hotspot owing to its diverse biological activities. However, its effects on psoriasis remain unclear. We explored the impact and molecular mechanism of PU on M5‐stimulated keratinocyte cell lines and imiquimod (IMQ)‐induced psoriasis‐like skin inflammation in BABL/c mice using western blotting, quantitative real‐time polymerase chain reaction (qRT‐PCR), hematoxylin and eosin (H&E) stain, immunohistochemistry, and immunofluorescent. Administration of PU‐enriched pomegranate extract at dosages of 150 and 250 mg/kg/day markedly attenuated psoriatic severity, abrogated splenomegaly, and reduced IMQ‐induced abnormal epidermal proliferation, CD4+ T‐cell infiltration, and inflammatory factor expression. Moreover, PU could decrease expression levels of pro‐inflammatory cytokines, such as IL‐1β, IL‐1α, IL‐6, IL‐8, TNF‐α, IL‐17A, IL‐22, IL‐23A, and reactive oxygen species (ROS), followed by keratinocyte proliferation inhibition in the M5‐stimulated cell line model of inflammation through inhibition of mitogen‐activated protein kinases/extracellular regulated protein kinases (MAPK/ERK) and nuclear factor kappaB (NF‐κB) signaling pathways. Our results indicate that PU may serve as a promising nutritional intervention for psoriasis by ameliorating cellular oxidative stress and inflammation.