Shahina Zinnat, El-Ganiny Amira M, Minion Jessica, Whiteway Malcolm, Sultana Taranum, Dahms Tanya E S
1Department of Chemistry and Biochemistry, University of Regina, 3737 Wascana Parkway, Regina, SK Canada.
2Microbiology and Immunology Department, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt.
Fungal Biol Biotechnol. 2018 Feb 9;5:3. doi: 10.1186/s40694-018-0046-5. eCollection 2018.
Cinnamon ( bark extract exhibits potent inhibitory activity against but the antifungal mechanisms of this essential oil remain largely unexplored.
We analyzed the impact of cinnamon bark oil on RSY150, and clinical strains isolated from patients with candidemia and candidiasis. The viability of RSY150 was significantly compromised in a dose dependent manner when exposed to cinnamon bark oil, with extensive cell surface remodelling at sub inhibitory levels (62.5 μg/mL). Atomic force microscopy revealed cell surface exfoliation, altered ultrastructure and reduced cell wall integrity for both RSY150 and clinical isolates exposed to cinnamon bark oil. Cell wall damage induced by cinnamon bark oil was confirmed by exposure to stressors and the sensitivity of cell wall mutants involved in cell wall organization, biogenesis, and morphogenesis. The essential oil triggered cell cycle arrest by disrupting beta tubulin distribution, which led to mitotic spindle defects, ultimately compromising the cell membrane and allowing leakage of cellular components. The multiple targets of cinnamon bark oil can be attributed to its components, including cinnamaldehyde (74%), and minor components (< 6%) such as linalool (3.9%), cinamyl acetate (3.8%), α-caryophyllene (5.3%) and limonene (2%). Complete inhibition of the mitotic spindle assembly was observed in treated with cinnamaldehyde at MIC (112 μg/mL).
Since cinnamaldehyde disrupts both the cell wall and tubulin polymerization, it may serve as an effective antifungal, either by chemical modification to improve its specificity and efficacy or in combination with other antifungal drugs.
肉桂(树皮提取物)对[具体真菌名称未给出]表现出强大的抑制活性,但这种精油的抗真菌机制在很大程度上仍未被探索。
我们分析了肉桂树皮油对RSY150以及从念珠菌血症和念珠菌病患者中分离出的临床菌株的影响。当暴露于肉桂树皮油时,RSY150的活力以剂量依赖的方式显著受损,在亚抑制水平(62.5μg/mL)下细胞表面发生广泛重塑。原子力显微镜显示,暴露于肉桂树皮油的RSY150和临床分离株均出现细胞表面剥落、超微结构改变以及细胞壁完整性降低。通过暴露于应激源以及参与细胞壁组织、生物合成和形态发生的细胞壁突变体的敏感性,证实了肉桂树皮油诱导的细胞壁损伤。该精油通过破坏β微管蛋白分布引发细胞周期停滞,导致有丝分裂纺锤体缺陷,最终损害细胞膜并使细胞成分泄漏。肉桂树皮油的多个作用靶点可归因于其成分,包括肉桂醛(74%)以及少量成分(<6%),如芳樟醇(3.9%)、乙酸肉桂酯(3.8%)、α-石竹烯(5.3%)和柠檬烯(2%)。在用MIC(112μg/mL)的肉桂醛处理的[具体真菌名称未给出]中观察到有丝分裂纺锤体组装完全受到抑制。
由于肉桂醛破坏细胞壁和微管蛋白聚合,它可能作为一种有效的抗真菌剂,要么通过化学修饰来提高其特异性和疗效,要么与其他抗真菌药物联合使用。