Lipopeptides from Bacillus velezensis induced apoptosis-like cell death in the pathogenic fungus Fusarium concentricum.

AIMS: Stem rot caused by Fusarium concentricum is a new disease of Paris polyphylla reported by our research group. The present study investigates the growth inhibitory and apoptotic effects of Bacillus velezensis FJAT-54560 lipopeptide against F. concentricum. METHODS AND RESULTS: HPLC preparation and LC-MS analysis results show that the crude lipopeptides secreted by Bacillus velezensis FJAT-54560 isolated from Jasminum sambac consist of C14-17 iturin A, C14 fengycin B, C16 fengycin A/A2, C18 fengycin A, C20 fengycin B2, C21 fengycin A2, C22-23 fengycin A, C12-16 surfactin A, and C15 surfactin A derivatives. The mass ratios (g/g) of iturin, fengycin, and surfactin in lipopeptides are 2.40, 67.51, and 30.08%, respectively. Through inhibition zone and inhibition rate experiments, we found that crude lipopeptides and purified fengycin exhibit strong antifungal activity against F. concentricum, including accumulation of reactive oxygen species, loss of mitochondrial membrane potential, DNA fragmentation, Ca2+ accumulation, chromatin condensation, and phosphatidylserine externalization. Transcriptomic analysis indicates that crude lipopeptide-induced apoptosis in F. concentricum cells may be mediated by apoptosis-inducing factors and apoptosis mediators and can serve as a metacaspase-independent model. CONCLUSION: Lipopeptides from Bacillus velezensis FJAT-54560 can control the pathogenic fungus F. concentricum by inducing apoptosis.

Structural Characteristic, Strong Antioxidant, and Anti-Gastric Cancer Investigations on an Oleoresin from Ginger (Zingiber officinale var. roscoe).

It is known that ginger oleoresin contains various active components and possesses bioactivities. In this study, ginger oleoresin from Chinese ginger (Zingiber officinale var. roscoe) was extracted using a CO2 supercritical fluid extraction method with a 0.52% yield (g/g), based on dry weights. Zingiberene with a content of 51.6 mg/g was the main volatile in the ginger oleoresin. In total, 17 phenolic compounds were identified, and their contents were calculated as 587.54 mg/g. Among them, a new gingertriol was detected in the Z. officinale. Antioxidant activity tests showed that the ginger oleoresin and six gingerols exhibited strong scavenging free radical activities, and the zingerone exhibited the strongest antioxidant activity, with IC50 values of 11.3 µg/mL for the 2, 2'-diphenyl-1-picrylhydrazyl radical and 19.0 µg/mL for the 2, 2'-amino-di (2-ethyl-benzothiazoline sulphonic acid-6) ammonium salt radical cation, comparable to vitamin C. Ginger oleoresin inhibits HGC-27 human gastric cancer cell proliferation at a rate of 4.05~41.69% and induces cell apoptosis at a rate of 10.4~20.9%. The Western blot result demonstrated that the AKT signaling pathway has the potential mechanism of ginger oleoresin acting on HGC-27 cells. The anticancer potential of the gingerol standards on HGC-27 cells followed the order of 8-gingerol > 6-gingerol > 10-gingerol > zingerone. The different antioxidant and anticancer potentials of the ginger phenolic compounds could be attributed to the presence of hydroxyl groups in the unbranched 1-alkyl chain and the length of carbon side chain. Consequently, ginger oleoresin shows substantial antioxidant and anticancer therapeutic potential and can be used for novel food-drug development.

Lipopeptide C17 Fengycin B Exhibits a Novel Antifungal Mechanism by Triggering Metacaspase-Dependent Apoptosis in Fusarium oxysporum.

Fusarium wilt is a worldwide soil-borne fungal disease caused by Fusarium oxysporum that causes serious damage to agricultural products. Therefore, preventing and treating fusarium wilt is of great significance. In this study, we purified ten single lipopeptide fengycin components from Bacillus subtilis FAJT-4 and found that C17 fengycin B inhibited the growth of F. oxysporum FJAT-31362. We observed early apoptosis hallmarks, including reactive oxygen species accumulation, mitochondrial dysfunction, and phosphatidylserine externalization in C17 fengycin B-treated F. oxysporum cells. Further data showed that C17 fengycin B induces cell apoptosis in a metacaspase-dependent manner. Importantly, we found that the expression of autophagy-related genes in the TOR signaling pathway was significantly upregulated; simultaneously, the accumulation of acidic autophagy vacuoles in F. oxysporum cell indicated that the autophagy pathway was activated during apoptosis induced by C17 fengycin B. Therefore, this study provides new insights into the antifungal mechanism of fengycin.