Integrative physiological, critical plant endogenous hormones, and transcriptomic analyses reveal the difenoconazole stress response mechanism in wheat (Triticum aestivum L.).

Difenoconazole (DFN) is widely utilized as a fungicide in wheat production. However, its accumulation in plant tissues has a profound impact on the physiological functions of wheat plants, thus severely threatening wheat growth and even jeopardizing human health. This study aims to comprehensively analyze the dynamic dissipation patterns of DFN, along with an investigation into the physiological, hormonal, and transcriptomic responses of wheat seedlings exposed to DFN. The results demonstrated that exposure of wheat roots to DFN (10 mg/kg in soil) led to a significant accumulation of DFN in wheat plants, with the DFN content in roots being notably higher than that in leaves. Accumulating DFN triggered an increase in reactive oxygen species content, malonaldehyde content, and antioxidant enzyme activities, while concurrently inhibiting photosynthesis. Transcriptome analysis further revealed that the number of differentially expressed genes was greater in roots compared with leaves under DFN stress. Key genes in roots and leaves that exhibited a positive response to DFN-induced stress were identified through weighted gene co-expression network analysis. Metabolic pathway analysis indicated that these key genes mainly encode proteins involved in glutathione metabolism, plant hormone signaling, amino acid metabolism, and detoxification/defense pathways. Further results indicated that abscisic acid and salicylic acid play vital roles in the detoxification of leaf and root DFN, respectively. In brief, the abovementioned findings contribute to a deeper understanding of the detrimental effects of DFN on wheat seedlings, while shedding light on the molecular mechanisms underlying the responses of wheat root and leaves to DFN exposure.

Physcion and chitosan-Oligosaccharide (COS) synergistically improve the yield by enhancing photosynthetic efficiency and resilience in wheat (Triticum aestivum L.).

As progressively increasing food safety concerns, diversified plant diseases and abiotic stresses, environmental-friendly bio-pesticides and bio-stimulants combinations may are likely to serve as a vital means of safeguarding green and sustainable food production. Accordingly, in this study, pot and field trials were performed to examine the application potential of the combination of physcion and chitosan-Oligosaccharide (COS) in wheat production. Wheat seeds were coated with physcion and COS and the effects exerted by them on morphology, physiology and yield of the wheat were investigated. As indicated by the results, the combination of physcion and COS not only did not inhibit the growth of wheat seedlings, but also synergistically increased root vigor and photosynthetic pigment content. Simultaneously, the lignin content in the roots and leaves was increased significantly. Moreover, the result confirmed that the combination of both substances reduced the MDA content, which was correlated with the up-regulation of the transcript expression level of antioxidant enzyme genes and the resulting increased enzyme activity. Furthermore, this combination synergistically increased the net photosynthetic rate (Pn) of the flag leaves and ultimately contributed to the increase in yield. Notably, the above-mentioned desirable cooperative effect was not limited by cultivars and cultivation methods. The conclusion of this study suggested that the combination of physcion and COS synergistically improved the photosynthetic rate and resilience in wheat, such that high wheat yields can be more significantly maintained, and future food security can be more effectively ensured.

Polygoni multiflori radix exacerbates idiosyncratic inflammatory liver injury through the FXR-SHP pathway and altered pharmacokinetic behavior.

Polygoni multiflori radix (PM) is a well-known tonic herb. It has been reported that PM could cause idiosyncratic inflammatory liver injury in some individuals. In this study, we investigated the mechanism of PM-induced idiosyncratic inflammatory liver injury in zebrafish and rat models based on pharmacodynamics and pharmacokinetics. The zebrafish were administered with polygoni multiflori radix extract (PME), emodin (EMO), and 2,3,5,4'-tetrahydroxystilbene-2-Ο-ß-D-glucoside (TSG) after lipopolysaccharide (LPS) treatment, to establish an idiosyncratic inflammation model. In zebrafish with idiosyncratic inflammation, PME, EMO, and TSG decreased liver area and brightness and increased the number of immune cells around the colliculi. PME+LPS produced hepatocyte damage, aggravated mitochondrial and endoplasmic reticulum damage, and increased AST and ALT activity. RT-PCR showed that PME and EMO up-regulated the expression of IL-6, IL-1ß, and INF-γ, and PME down-regulated expression of FXR and SHP. In rats with idiosyncratic inflammation, AST and ALT activities increased significantly, and liver tissues showed pathological damage. An efficient and sensitive LC-MS/MS method was established for the pharmacokinetic study of EMO and TSG in rats with idiosyncratic inflammation. The AUC0-t was higher for EMO and TSG in the model group compared with the normal group. The MRT0-t was significantly prolonged in EMO, while CLz/F was significantly reduced. The present results suggested that the absorption of potentially toxic components of PM increased and metabolism slowed down under inflammatory stress, and PM induced idiosyncratic liver injury via the FXR-SHP axis.