Haiyang Huang, Shumin Zhu, Shaowen Zhong, Ying Liu, Shaozhen Hou, Jie Gao, Jianzhao O U, Mingguo Dong, Weimin Ning
Institute of Traditional Chinese Medicine, Dongguan Hospital of Traditional Chinese Medicine, Dongguan 523000, China.
Department of Traditional Chinese Medicine, Guangdong Food and Drug Vocational College, Guangzhou 510520, China.
J Tradit Chin Med. 2025 Apr;45(2):272-280. doi: 10.19852/j.cnki.jtcm.2025.02.018.
To determine the effect of Traditional Chinese Medicine (TCM) Fuzheng Xuanfei Huashi prescription (, FZXF) on lipopolysaccharide (LPS)-induced pneumonia in mice and identify the mechanism of FZXF in the treatment of LPS-induced lung inflammation.
The pneumonia model was established by intraperitoneal injection of 5 mg/kg LPS in mice. Cytokines were detected by enzyme-linked immune-osorbent assay (ELISA), macrophages in lung tissue were determined by immunofluorescence, and pathway-related data were determined by quantitative real-time polymerase chain reaction (qPCR) and Western blot.
The liver, thymus, and spleen index values and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) obviously increased in LPS-treated mice. FZXF decreased the white blood cell count and reduced the increase in the lung wet weight/dry weight ratio caused by LPS. The hematoxylin-eosin staining result showed that FZXF could maintain the integrity of lung tissue structure, alleviate interstitial oedema and alveolar wall thickening, and reduce inflammatory cell infiltration. Moreover, FZXF markedly reduced the expression of proinflammatory cytokines. FZXF also significantly reduced LPS-induced malondialdehyde production and increased superoxide dismutase level in the lung. By immunofluorescence, we found that FZXF could reduce macrophage infiltration. The mRNA expression levels of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), toll-like receptor 4 (TLR4) and nuclear transcription factor κB (NF-κB) in the lung tissue of mice were decreased by treatment with FZXF. In addition, FZXF inhibited the protein expression of TLR4, p-p65 and COX-2. These results indicated that FZXF could inhibit the inflammatory response of LPS induced cytokine storm in mice through TLR4/NF-κB and COX-2/PGE2 signaling pathway.
These findings were suggested that FZXF prescription suppresses inflammation in LPS-induced pneumonia in mice TLR4/NF-κB and COX-2/ PGE2 pathway.
探讨中药扶正宣肺化湿方(FZXF)对脂多糖(LPS)诱导的小鼠肺炎的影响,并明确FZXF治疗LPS诱导的肺部炎症的机制。
通过给小鼠腹腔注射5 mg/kg LPS建立肺炎模型。采用酶联免疫吸附测定(ELISA)检测细胞因子,通过免疫荧光法测定肺组织中的巨噬细胞,并采用定量实时聚合酶链反应(qPCR)和蛋白质免疫印迹法检测通路相关数据。
LPS处理的小鼠肝脏、胸腺和脾脏指数值以及天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平明显升高。FZXF降低了白细胞计数,并减轻了LPS引起的肺湿重/干重比增加。苏木精-伊红染色结果显示,FZXF可维持肺组织结构的完整性,减轻间质水肿和肺泡壁增厚,并减少炎症细胞浸润。此外,FZXF显著降低促炎细胞因子的表达。FZXF还显著降低了LPS诱导的肺组织中丙二醛的产生,并提高了超氧化物歧化酶水平。通过免疫荧光法,我们发现FZXF可减少巨噬细胞浸润。FZXF处理可降低小鼠肺组织中环氧合酶-2(COX-2)、前列腺素E2(PGE2)、Toll样受体4(TLR4)和核转录因子κB(NF-κB)的mRNA表达水平。此外,FZXF抑制TLR4、p-p65和COX-2的蛋白表达。这些结果表明,FZXF可通过TLR4/NF-κB和COX-2/PGE2信号通路抑制LPS诱导的小鼠细胞因子风暴炎症反应。
这些研究结果提示,FZXF方剂通过TLR4/NF-κB和COX-2/PGE2途径抑制LPS诱导的小鼠肺炎炎症。