Guo Jing, Peng Li, Zeng Jinhao, Zhang Meiheng, Xu Feng, Zhang Xiaotong, Wei Qin
Dermatological Department, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Geriatric Department, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Exp Ther Med. 2021 Jun;21(6):590. doi: 10.3892/etm.2021.10022. Epub 2021 Apr 8.
Paeoniflorin (PF) has been reported to be effective against several skin disorders, such as allergic contact dermatitis and psoriasis; however, it remains unclear whether PF can protect against urticarial lesions. Herein, the effects of PF on rats with urticarial lesions and the possible underlying mechanism were investigated. The effects of PF administration on a rat model of ovalbumin-induced urticarial-like lesions were evaluated via pathological analysis using hematoxylin-eosin staining. Toluidine blue staining was performed to detect mast cells and ELISA was performed to determine serum histamine levels. PF-induced regulatory effects on autophagic activity and the potential underlying mechanism of this were also investigated using transmission electron microscopy, immunohistochemistry and reverse transcription-quantitative PCR. It was demonstrated that PF suppressed allergic and inflammatory responses to improve urticarial lesions, as evidenced by the attenuation of pathological abnormalities, mast cell infiltration and histamine secretion. Mechanistically, PF treatment was found to markedly limit the production and release of inflammatory cytokine interleukin (IL)-23, while the levels of IL-17 remained unchanged. PF intervention led to an increased number of autophagosomes, along with higher levels of light chain 3B (LC3B) and Beclin-1, and lower levels of P62, indicating that PF could augment autophagic activity in urticarial lesions. PF treatment increased the expression of liver kinase B1 (LKB1) and AMP-activated protein kinase-α (AMPK-α), contributing to the PF-enhanced autophagic activity. In conclusion, PF could effectively improve urticarial lesions by inhibiting inflammatory cytokine IL-23 and increasing the autophagic activity via the LKB1/AMPK-α pathway.
据报道，芍药苷（PF）对多种皮肤疾病有效，如过敏性接触性皮炎和银屑病；然而，PF是否能预防荨麻疹病变仍不清楚。在此，研究了PF对荨麻疹病变大鼠的影响及其可能的潜在机制。通过苏木精-伊红染色进行病理分析，评估PF给药对卵清蛋白诱导的类荨麻疹病变大鼠模型的影响。进行甲苯胺蓝染色以检测肥大细胞，并进行酶联免疫吸附测定（ELISA）以测定血清组胺水平。还使用透射电子显微镜、免疫组织化学和逆转录定量聚合酶链反应研究了PF对自噬活性的调节作用及其潜在机制。结果表明，PF抑制过敏和炎症反应以改善荨麻疹病变，病理异常、肥大细胞浸润和组胺分泌的减轻证明了这一点。从机制上讲，发现PF治疗可显著限制炎性细胞因子白细胞介素（IL）-23的产生和释放，而IL-17水平保持不变。PF干预导致自噬体数量增加，同时轻链3B（LC3B）和Beclin-1水平升高，P62水平降低，表明PF可增强荨麻疹病变中的自噬活性。PF治疗增加了肝激酶B1（LKB1）和AMP激活的蛋白激酶-α（AMPK-α）的表达，有助于PF增强自噬活性。总之，PF可通过抑制炎性细胞因子IL-23并通过LKB1/AMPK-α途径增加自噬活性来有效改善荨麻疹病变。
