Physiological and iTRAQ-based proteomic analyses reveal the mechanism of pinocembrin against Penicillium italicum through targeting mitochondria

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.