Liang Hua, Jin Xiaofei, He Tongtong, Zhou Xiaohong, Liu Zhenyi, Gao Weijuan
Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, No. 3 Xingyuan Road, Luquan District, Shijiazhuang 050200, China.
Pharmaceuticals (Basel). 2025 Apr 7;18(4):537. doi: 10.3390/ph18040537.
: Periostracum Cicadae (PC) is commonly used to treat chronic atrophic gastritis (CAG), but its underlying mechanisms are unclear. We investigated the therapeutic effects, active ingredients and molecular mechanisms of PC on CAG. : We analyzed the components in the serum extract of PC by UHPLC-Q-Orbitrap-MS/MS. Then, we used rat and cell models to assess the impact of PC on CAG and employed network pharmacology and bioinformatics to predict key targets and active ingredients. Finally, we confirmed hub targets through experiments and molecular docking. : A total of 22 components were identified in the PC extract-containing serum using UHPLC-Q-Orbitrap MS/MS. Network pharmacology combined with molecular docking revealed that the protective effect was primarily mediated by three compounds: (Z)-akuammidine, chicoric acid, and columbianadin. And we revealed that c-Fos/c-Jun signaling pathways were crucial in therapy. PC extract-containing serum inhibited the vitality, migration, invasion, and multiplication of MC cells (model cells for CAG), induced apoptosis, and caused G0/G1 phase cell cycle arrest. The expression level of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β) and gastrin 17 (G17) in the serum of CAG rats increased, while the expression level of pepsinogen I (PG I) and pepsinogen II (PG II) decreased. After 12 weeks of PC administration, these conditions were significantly improved. PC not only reduced the levels of antigen KI-67 (Ki67) and tumor protein p53 (P53) but also enhanced SRY-box Transcription Factor (SOX2). Simultaneously, PC down-regulated the expression of N-cadherin and Vimentin while up-regulating that of E-cadherin. : PC inhibited epithelial-mesenchymal transition (EMT) via the c-Fos/c-Jun signaling pathway, thereby providing therapeutic benefits for CAG. Our study elucidates the mechanisms and material basis of PC in treating CAG, providing experimental evidence to support its clinical application.
蝉蜕常用于治疗慢性萎缩性胃炎（CAG），但其潜在机制尚不清楚。我们研究了蝉蜕对CAG的治疗效果、活性成分及分子机制。我们采用超高效液相色谱-四极杆-轨道阱质谱联用技术（UHPLC-Q-Orbitrap-MS/MS）分析蝉蜕血清提取物中的成分。然后，我们使用大鼠和细胞模型评估蝉蜕对CAG的影响，并运用网络药理学和生物信息学预测关键靶点和活性成分。最后，我们通过实验和分子对接确认了核心靶点。使用UHPLC-Q-Orbitrap MS/MS在含蝉蜕提取物的血清中总共鉴定出22种成分。网络药理学结合分子对接显示，其保护作用主要由三种化合物介导：（Z）-阿枯米定、菊苣酸和哥伦比亚内酯。并且我们发现c-Fos/c-Jun信号通路在治疗中至关重要。含蝉蜕提取物的血清抑制了MC细胞（CAG模型细胞）的活力、迁移、侵袭和增殖，诱导细胞凋亡，并导致G0/G1期细胞周期阻滞。CAG大鼠血清中肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和胃泌素17（G17）的表达水平升高，而胃蛋白酶原I（PG I）和胃蛋白酶原II（PG II）的表达水平降低。给予蝉蜕12周后，这些情况得到显著改善。蝉蜕不仅降低了抗原KI-67（Ki67）和肿瘤蛋白p53（P53）的水平，还增强了性别决定区Y框转录因子（SOX2）。同时，蝉蜕下调了N-钙黏蛋白和波形蛋白的表达，而上调了E-钙黏蛋白的表达。蝉蜕通过c-Fos/c-Jun信号通路抑制上皮-间质转化（EMT），从而为CAG提供治疗益处。我们的研究阐明了蝉蜕治疗CAG的机制和物质基础，为其临床应用提供了实验证据。
