Fusarium head blight, caused primarily by Fusarium graminearum, is a destructive disease of wheat throughout the world. However, the mechanisms of host resistance to FHB are still largely unclear. Deoxynivalenol (DON) produced by F. graminearum which enhances the pathogen to spread could be converted into inactive form D3G by UDP-glycosyltransferases (UGTs). A DON responsive UGT gene, designated as TaUGT4, was first cloned from wheat in this study. The putative open reading frame (ORF) of TaUGT4 was 1386 bp, encoding 461 amino acids protein. TaUGT4 was placed on chromosome 2D using a set of nulli-tetrasomic lines of wheat cultivar Chinese Spring (CS). When fused with eGFP at C terminal, TaUGT4 was shown to localize in cytoplasm of the transformed tobacco cells. The transcriptional analysis revealed that TaUGT4 was strongly induced by F. graminearum or DON in both of FHB-resistant cultivar Sumai 3 and susceptible cultivar Kenong 199, especially in Sumai 3 under DON treatment. Similar increase of TaUGT4 expression was observed in Sumai 3 and Kenong 199 in response to salicylic acid (SA) treatment. But interestingly, the transcripts level of TaUGT4 in Sumai 3 showed significantly higher than that in Kenong 199 after treated with methyl jasmonate (MeJA). According to the expression patterns, TaUGT4 might lead to different effects between FHB-resistant genotype and susceptible genotype in the process against F. graminearum inoculation. It had also been discussed in this paper that JA signaling pathway might play a significant role in the resistance against F. graminearum compared to SA signaling pathway.

BackgroundAcute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. In this study, we investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats.ResultsGLA treatment at dose of 30 mg/kg decreased LPS-induced lung W/D ratio and alleviated evident lung histopathological changes. Expressions of TNF-α and IL-18 were suppressed by GLA in plasma. The levels of SPA, MDA and NO in lung were down-regulated significantly in groups administrated with GLA. While the SOD level increased after GLA administration. Additionally, the attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPS-induced ARDS rats.Materials and MethodsSixty-four Wistar rats were randomly assigned into control group, Glabridin (GLA) alone group, LPS groups (6 h, 12 h, 24 h), GLA with LPS groups (6 h, 12 h, 24 h). ARDS was induced in rats by intraperitoneal administration of LPS (10 mg/kg). The degree of lung edema was evaluated by calculating the wet/dry weight ratio. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin-18 (IL-18) were assayed by enzyme-linked immunosorbent assay (ELISA). Surfactant protein A (SPA), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were analyzed. Pathological changes of lung tissues were observed by H&E staining. The protein expression of p38MAPK and ERK was detected using immunohistochemical techniques. Lung phosphorylated p38MAPK (p-p38MAPK) and pERK protein expression changes were detected by Western blotting.ConclusionsGlabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation.

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