Inhibitory effects and mechanisms of cinnamaldehyde against Fusarium oxysporum, a serious pathogen in potatoes.

BACKGROUND: Potatoes, a major economic crop, are significantly impacted by Fusarium dry rot, a prevalent postharvest disease. Despite the broad-spectrum antimicrobial properties of cinnamaldehyde, a naturally-derived plant substance, its efficacy against the causal pathogen of potato dry rot (Fusarium oxysporum) and the underlying mechanisms have not been extensively studied. RESULTS: Our study demonstrates that cinnamaldehyde effectively inhibits the growth of Fusarium oxysporum, the pathogen responsible for potato dry rot, and increases its sensitivity to environmental stress factors such as extreme temperatures and high salt stress. Treatment with cinnamaldehyde results in altered fungal mycelium morphology, compromised cell wall stability, and disrupted cell membrane integrity, thereby reducing spore viability. Specifically, it interferes with the cell membrane and cell wall structures of the fungus, potentially disrupting fungal growth by modulating signaling pathways involved in cell wall maintenance, chitin metabolism, and GPI-anchored protein function. Notably, we show that cinnamaldehyde induces a form of regulated cell death in F. oxysporum, which is characterized not as typical apoptosis, as evidenced by Annexin V negative staining. However, the specific cell death type and underlying mechanism still needed to be further explored. CONCLUSION: Cinnamaldehyde, an environmentally friendly plant-based active compound, exhibits strong inhibitory effects on F. oxysporum, indicating its potential use in the prevention and control strategies for potato dry rot. This research contributes to the understanding of novel antifungal mechanisms and offers promising insights into eco-friendly alternatives for managing this economically significant postharvest disease. © 2024 Society of Chemical Industry.

Anti-Oomycete Effect and Mechanism of Salicylic Acid on Phytophthora infestans.

Pathogenic oomycetes infect a wide variety of organisms, including plants, animals, and humans, and cause massive economic losses in global agriculture, aquaculture, and human health. Salicylic acid (SA), an endogenous phytohormone, is regarded as an inducer of plant immunity. Here, the potato late blight pathogen Phytophthora infestans was used as a model system to uncover the inhibitory mechanisms of SA on pathogenic oomycetes. In this research, SA significantly inhibited the mycelial growth, sporulation, sporangium germination, and virulence of P. infestans. Inhibition was closely related to enhanced autophagy, suppression of translation initiation, and ribosomal biogenesis in P. infestans, as shown by multiomics analysis (transcriptomics, proteomics, and phosphorylated proteomics). Monodansylcadaverine (MDC) staining and Western blotting analysis showed that SA promoted autophagy in P. infestans by probably targeting the TOR signaling pathway. These observations suggest that SA has the potential to control late blight caused by P. infestans.

Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced Cardiomyocytes Injury.

Objective: The aim of this study was to investigate the effects of sodium hydrosulfide (NaHS) on Lipopolysaccharide (LPS)-induced cardiomyocyte injury in H9c2 cells. Methods: H9c2 cardiomyocytes cultivated with medium containing 10 µg/mL LPS were used to recapitulate the phenotypes of those in sepsis. Two sequential experiments were performed. The first contained a control group, a LPS group, and a LPS + NaHS group, with the aim to assure the protective effects of NaHS on LPS-treated cardiomyocytes. The second experiment added a fourth group, the LPS + NaHS + miR-133a-3p inhibition group, with the aim to preliminarily explore whether miR-133-3p exerts a protective function downstream of NaHS. The adenosine triphosphate (ATP) kit was used to detect ATP content; real-time quantitative polynucleotide chain reaction (qPCR) was used to measure the levels of mammalian targets of rapamycin (mTOR), AMP-dependent protein kinase (AMPK), and miR-133a-3p, and Western blot (WB) was used to detect protein levels of mTOR, AMPK, myosin-like Bcl2 interacting protein (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3I/II), and P62 (sequestosome-1, sqstm-1/P62). Results: Compared with the control group, the expressions of miR-133a-3p (P < 0.001), P62 (P < 0.001), and the content of ATP (P < 0.001) decreased, while the expressions of Beclin-1 (P = 0.023) and LC3I/II (P = 0.048) increased in the LPS group. Compared with the LPS group, the expressions of miR-133a-3p (P < 0.001), P62 (P < 0.001), and the content of ATP (P < 0.001) in the NaHS + LPS group increased, while the expressions of Beclin-1 (P = 0.023) and LC3I/II (P = 0.022) decreased. Compared with the NaHS + LPS group, the expression levels of miR-133a-3p (P < 0.001), P62 (P = 0.001), and the content of ATP (P < 0.001) in the LPS + NaHS + miR-133a-3p inhibition group were downregulated, and the expression levels of Beclin-1 (P = 0.012) and LC3I/II (P = 0.010) were upregulated. The difference was statistically significant. There was no significant difference in the expression of AMPK and mTOR between groups. Conclusion: Our research demonstrated that NaHS relieved LPS-induced myocardial injury in H9c2 by promoting the expression of miR-133a-3p, inhibiting autophagy in cardiomyocytes, and restoring cellular ATP levels.