Department of Dermatology and Venereology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China.
Translational Medicine Center, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China.
BMC Complement Med Ther. 2022 Jan 31;22(1):32. doi: 10.1186/s12906-021-03468-y.
The incidence rate of invasive candidiasis is high, its treatment is difficult, and the prognosis is poor. In this study, an immunosuppressive mouse model of invasive Candida albicans (C. albicans) infection was constructed to observe the effects of cinnamaldehyde (CA) on the C. albicans cell wall structure and cell wall (1,3)-β-D-glucan contents. This study provides a theoretical basis for CA treatment to target invasive C. albicans infection.
Immunosuppressed mice with invasive C. albicans infection were given an oral dosage of CA (240 mg.kg.d) for 14 days. Then, mouse lung tissue samples were collected for detection of the levels of (1,3)-β-D-glucan and transmission electron microscopy observations, using fluconazole as a positive control and 2% Tween 80 saline as a negative control.
The immunosuppressive mouse model of invasive C. albicans infection was successfully established. The levels of (1,3)-β-D-glucan in the CA treatment group, fluconazole positive control group, invasive C. albicans infection immunosuppressive mouse model group, and 2% Tween 80 normal saline control group were 86.55 ± 126.73 pg/ml, 1985.13 ± 203.56 pg/ml, 5930.57 ± 398.67 pg/ml and 83.36 ± 26.35 pg/ml, respectively. Statistically, the CA treatment group, fluconazole positive control group and invasive C. albicans infection immunosuppressive mouse model group were compared with each other (P < 0.01) and compared with the 2% Tween 80 saline group (P < 0.01), showing that the differences were very significant. Comparison of the CA treatment group with the fluconazole positive control group (P < 0.05) displayed a difference as well. Electron microscopy showed that CA destroyed the cell wall of C. albicans, where the outer layer of the cell wall fell off and became thinner and the nuclei and organelles dissolved, but the cell membrane remained clear and intact.
CA destroys the cell wall structure of C. albicans by interfering with the synthesis of (1,3)-β-D-glucan to kill C. albicans. However, CA does not affect the cell membrane. This study provides a theoretical basis for CA treatment to target invasive C. albicans infection.
侵袭性念珠菌病的发病率较高，治疗困难，预后较差。本研究构建了免疫抑制小鼠侵袭性白念珠菌（C. albicans）感染模型，观察了肉桂醛（CA）对念珠菌细胞壁结构和细胞壁（1,3）-β-D-葡聚糖含量的影响。为 CA 靶向治疗侵袭性白念珠菌感染提供了理论依据。
免疫抑制小鼠感染侵袭性白念珠菌后，给予 CA（240mg.kg.d）口服 14 天。然后，采集小鼠肺组织样本，检测（1,3）-β-D-葡聚糖含量，并用氟康唑作为阳性对照，2%吐温 80 生理盐水作为阴性对照，进行透射电镜观察。
成功建立了免疫抑制小鼠侵袭性白念珠菌感染模型。CA 治疗组、氟康唑阳性对照组、侵袭性白念珠菌感染免疫抑制小鼠模型组和 2%吐温 80 生理盐水对照组（1,3）-β-D-葡聚糖水平分别为 86.55±126.73pg/ml、1985.13±203.56pg/ml、5930.57±398.67pg/ml 和 83.36±26.35pg/ml。统计学分析显示，CA 治疗组、氟康唑阳性对照组、侵袭性白念珠菌感染免疫抑制小鼠模型组与对照组比较（P<0.01），与 2%吐温 80 生理盐水组比较（P<0.01），差异均非常显著；CA 治疗组与氟康唑阳性对照组比较（P<0.05），差异亦有统计学意义。电镜显示 CA 破坏了白念珠菌的细胞壁，使细胞壁外层脱落变薄，核和细胞器溶解，但细胞膜仍清晰完整。
CA 通过干扰（1,3）-β-D-葡聚糖的合成破坏白念珠菌细胞壁结构，从而杀死白念珠菌，但不影响细胞膜。本研究为 CA 靶向治疗侵袭性白念珠菌感染提供了理论依据。
