The physiological and iTRAQ-based proteomic analyses were used to reveal the inhibitory roles of pinocembrin on mitochondria of P. italicum and its cell death mechanism. The results show that pinocembrin damages both mitochondrial structure and function. 167 and 807 differentially expressed proteins (DEPs) were detected in P. italicum mycelia after treatment with pinocembrin for 8 h and 24 h respectively, and the DEPs were significantly enriched in the oxidative phosphorylation (OXPHOS) pathway, especially for mitochondrial respiratory chain (MRC) complexes I and V. Furthermore, the expression levels of proteins related to programmed cell death (PCD) were significantly up-regulated in mycelia with Pinocembrin incubation for 24 h. Combined with the results of physio-chemical analysis, the data revealed that pinocembrin targeted MRC complexes I and V, to induce ATP depletion, enhance ROS accumulation, stimulate mitochondrial permeability transition pore (MPTP) opening, accelerate the loss of mitochondrial membrane potential (MMP) and promote cytochrome c release from mitochondria to the cytoplasm, which, as a result, effectively triggered three classical types of PCD pathways in mycelia of P. italicum.

中文翻译：

---

基于生理学和 iTRAQ 的蛋白质组学分析揭示松木素通过靶向线粒体对抗青霉菌的机制

生理学和基于 iTRAQ 的蛋白质组学分析用于揭示松柏素对 P. italicum 线粒体的抑制作用及其细胞死亡机制。结果表明pinocembrin损害线粒体结构和功能。分别用 pinocembrin 处理 8 h 和 24 h 后，在 P. italicum 菌丝体中检测到 167 和 807 个差异表达蛋白 (DEPs)，并且 DEPs 在氧化磷酸化 (OXPHOS) 途径中显着富集，尤其是线粒体呼吸链 (MRC) ) 复合物 I 和 V。此外，与程序性细胞死亡 (PCD) 相关的蛋白质的表达水平在菌丝体中与 Pinocembrin 孵育 24 小时显着上调。结合理化分析结果，