基于酿酒酵母(Saccharomyces cerevisiae)及其细胞壁合成酶缺陷突变株组成的筛选模型对肉桂醛抗真菌的作用机制进行了研究。发现肉桂醛对细胞壁合成酶基因缺陷突变株及其野生型的抑制具有显著差异,对葡聚糖合酶缺陷突变株δfks1的最低抑制浓度MIC值为8μg/mL,比野生型低8倍,肉桂醛对几丁质合酶基因缺陷突变株CHS020和CHS003的MIC值也比野生型低4倍。肉桂醛对δfks1生长的抑制能被山梨醇等渗溶液部分挽救,经肉桂醛处理后,δfks1的β-葡聚糖和几丁质含量分别降低了23.48%和31.94%。研究结果表明,肉桂醛特异性抑制真菌细胞壁葡聚糖和几丁质的合成是其抑制真菌细胞生长的主要机制之一。

The antifungal mechanism of trans-cinnamaldehyde was studied using the research pattern consisting of wild-type Saccharomyces cerevisiae strain WHU2a and three cell wall synthase-deficient strains δfks1,CHS020 and CHS003 which were derivatives of WHU2a.The results showed trans-cinnamaldehyde had an obvious inhibition effect on glucan synthase-deficient strain δfks1,the minimum inhibitory concentration(MIC) of trans-cinnamaldehyde was 8 μg/mL,which was 8 folds lower than that against the wild-type strain.Besides,the MIC against chitin synthase-deficient strains CHS020 and CHS003 were 4 folds lower as well.By growth rescue assay,it was proved that the growth inhibition effect of trans-cinnamaldehyde on δfks1 could partly be rescued by sorbitol,which confirmed the susceptibility of trans-cinnamaldehyde on cell wall.Furthermore,the contents of β-glucan and chitin on δfks1 cell wall were proved decreasing by 23.48% and 31.94%,respectively,after treated by trans-cinnamaldehyde.Based on the data presented,it is reasonable to conclude that the main antifungal mechanism of trans-cinnamaldehyde is to specifically inhibit the synthesis of β-glucan and chitin on fungal cell wall.