Guo Yan-Na, He Ke-Ren, Liang Shao-Shan, Mou Rui-Wei, Lu Meng-Han, He Yong-Ming, Tang Lu-Ping
School of Life Science and Engineering, Foshan University, Foshan, China.
Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Front Microbiol. 2024 Mar 8;15:1376819. doi: 10.3389/fmicb.2024.1376819. eCollection 2024.
This study aimed to develop a suitable dosage form of volatile oil from wampee leaves and to explore its antibacterial mechanism . The chemical composition of the volatile oil from wampee leaves was determined by gas chromatography-mass spectrometry (GC-MS). Different microemulsion ratios were tested and their stabilities were investigated to determine the optimal ratio. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of the wampee leaves volatile oil emulsion (WVOE) against () and () were determined using double-dilution and plate-counting methods, respectively. Morphological changes in these two bacteria were observed using scanning electron microscopy. Death, ultrastructural morphology, and biofilm formation were also assessed for . Finally, we established an -infected Lewis lung carcinoma (LLC) cell model to evaluate the protective effects of the volatile oil emulsion and the associated mechanisms. The volatile oil extracted from wampee leaves contained 37 compounds, of which 96.49% were aromatic hydrocarbons, terpenoids, and their oxygen-containing derivatives. The emulsion was most stable at 1:1 in the oil phase and 1:9 in the water phase. WVOE had poor antibacterial activity against , but the MIC and MBC against were 312.5 and 2,500 μg/mL, respectively. survival rates were 84.6%, 14.5%, and 12.8% in the 1/2, 1, and 4 × MIC groups, respectively, compared with 97.2% in the control group. survival was not affected by WVOE treatment. WVOE administration induced cavity formation and abnormal binary fission, and significantly inhibited biofilm formation in cells. The WVOE notably reduced the number of and inhibited , , , , , and gene expression in -infected LLC cells. The WVOE had a significant inhibitory effect on and altered its cell membrane permeability. Moreover, it alleviated inflammation by inhibiting the NF-κB-NLRP3 pathway in -infected LLC cells.
本研究旨在开发一种合适的黄皮叶挥发油剂型，并探索其抗菌机制。采用气相色谱 - 质谱联用（GC - MS）法测定黄皮叶挥发油的化学成分。测试不同微乳液比例并研究其稳定性以确定最佳比例。分别采用双倍稀释法和平板计数法测定黄皮叶挥发油乳液（WVOE）对（）和（）的最低抑菌浓度（MIC）和最低杀菌浓度（MBC）。使用扫描电子显微镜观察这两种细菌的形态变化。还评估了（）的死亡情况、超微结构形态和生物膜形成。最后，我们建立了一个感染（）的Lewis肺癌（LLC）细胞模型，以评估挥发油乳液的保护作用及其相关机制。从黄皮叶中提取的挥发油含有37种化合物，其中96.49%为芳烃、萜类及其含氧衍生物。该乳液在油相为1:1、水相为1:9时最稳定。WVOE对（）的抗菌活性较差，但对（）的MIC和MBC分别为312.5和2500μg/mL。与对照组的97.2%相比，在1/2、1和4×MIC组中，（）的存活率分别为84.6%、14.5%和12.8%。WVOE处理对（）的存活没有影响。WVOE给药诱导（）形成空洞和异常二分裂，并显著抑制其生物膜形成。WVOE显著减少了（）的数量，并抑制了感染（）的LLC细胞中（）、（）、（）、（）和（）基因的表达。WVOE对（）具有显著抑制作用并改变其细胞膜通透性。此外，它通过抑制感染（）的LLC细胞中的NF - κB - NLRP3途径减轻炎症。
