Sweet potato (Ipomoea batatas L.) leaf is a natural source of phenolic compounds with strong antioxidant activity and potential utility as an antioxidant. The aim of this study was to evaluate the polyphenol composition and antioxidant activities of ethanol extracts and their various solvent-partitioned fractions (petroleum ether, ethyl acetate, and aqueous fraction) from sweet potato leaves and petioles. Seven caffeoylquinic acid (CQA) derivatives and four flavonoids were detected in sweet potato leaves by HPLC-ESI-MS. The total phenolic content (TPC) and total flavonoid content (TFC) in leaf (112.98 ± 4.14 mg gallic acid equivalent (GAE)/g of dried extract, 56.87 ± 5.69 mg rutin equivalent (RE)/g of dried extract) was more than ten times higher than in petiole (9.22 ± 2.67 mg GAE/g of dried extract, 3.81 ± 0.52 mg RE/g of dried extract). The antioxidant contents of ethyl acetate fractions increased dramatically relative to those of crude extracts for both leaves and petioles. Purification using solvent partition with ethyl acetate increased TPC and TFC of crude extracts, especially the CQA derivatives including 3,4-dicaffeoylquinic acid, 3,5-dicaffeoylquinic acid, 4,5-dicaffeoylquinic acid, and 3,4,5-tricaffeoylquinic acid. Meanwhile, the ethyl acetate fractions with the highest CQA content were associated with the highest scavenging activities towards 2,2-diphenyl-1-picrylhydrazyl (DPPH) and higher ferric ion reducing antioxidant power (FRAP)-reducing power.

This study explored how plantaricin Q7 acts against Pseudomonas fluorescens at cellular and protein expression levels. Plantaricin Q7 exhibited a minimum inhibitory concentration (MIC) of 144 AU/mL against P. fluorescens. The scanning electron microscopy and transmission electron microscopy revealed morphological changes in P. fluorescens upon exposure to 1 MIC of plantaricin Q7, disrupting cell membrane permeability and integrity, forming pores, and causing intracellular material leakage. The confocal laser scanning microscopy and leakage tests confirmed these observations. The attenuated total reflectance-Fourier transform infrared spectroscopy indicated alterations in cell proteins and carbohydrates due to plantaricin Q7. Proteomics analysis of bacterial protein content showed significant differences between untreated and plantaricin Q7-treated P. fluorescens, as confirmed by principal component analysis. Downregulation of MlaC, MlaF, FadA, FadB, PyrB, IlvC, GlnA, L29, L31, and L32 at protein and transcriptional levels post-treatment with plantaricin Q7 suggested inhibition of the maintenance of lipid asymmetry system primarily responsible for membrane damage. Furthermore, plantaricin Q7 inhibited fatty acid degradation, disrupted amino acid metabolism, and potentially suppressed ribosomal protein expression, revealing a new target for its anti-P. fluorescens activity. This study provides important insights into plantaricin Q7’s mechanism against P. fluorescens.