Phytophthora root rot (PRR) caused by Phytophthora sojae is a major soybean disease that causes severe economic losses worldwide. Using soybean cultivars carrying a Rps resistance gene is the most effective strategy for controlling this disease. We previously detected a novel Phytophthora resistance gene, RpsZS18, on chromosome 2 of the soybean cultivar Zaoshu18. The aim of the present study was to identify and finely map RpsZS18. We used 232 F2:3 families generated from a cross between Zaoshu18 (resistant) and Williams (susceptible) as the mapping population. Simple sequence repeat (SSR) markers distributed on chromosome 2 were used to map RpsZS18. First, 12 SSR markers linked with RpsZS18 were identified by linkage analyses, including two newly developed SSR markers, ZCSSR33 and ZCSSR46, that flanked the gene at distances of 0.9 and 0.5 cM, respectively. Second, PCR-based InDel markers were developed based on sequence differences between the two parents and used to further narrow down the mapping region of RpsZS18 to 71.3 kb. Third, haplotype analyses were carried out in the RpsZS18 region using 14 soybean genotypes with whole-genome resequencing. We detected six genes with unique haplotype sequences in Zaoshu18. Finally, quantitative real-time PCR assays of the six genes revealed an EF-hand calcium-binding domain containing protein encoding gene (Glyma.02g245700), a pfkB carbohydrate kinase encoding gene (Glyma.02g245800), and a gene with no functional annotation (Glyma.02g246300), are putative candidate PRR resistance genes. This study provides useful information for breeding P. sojae-resistant soybean cultivars.
Ficus hirta, a widely consumed food by Hakka people, has been reported to show potent antifungal activity against phytopathogen Penicillium italicum. However, there is no report of chemical constituents responsible for the antifungal activity. In the current study, nine monosubstituted benzene derivatives, including three new derivatives (1-3), were isolated from the fruits of F. hirta. The structures of these isolates were elucidated on the basis of the analysis of spectroscopic data (mass spectrometry and nuclear magnetic resonance). All of the isolates were evaluated for antifungal activities against P. italicum. At an equivalent concentration, compound 1 exhibited stronger antifungal activity than that of the ethanol extract of F. hirta fruits.
In schistosomiasis, egg deposition in the liver contributes to the formation of hepatic granuloma and fibrosis, which are the most serious clinical pathological features. It has been proposed that activation of the nuclear factor kappa B (NF-κB) signaling pathways is closely associated with the development of hepatic granuloma and fibrosis. Genistein has been shown to inhibit the activity of NF-κB signaling pathways, which might be a potential agent to protect against Schistosoma japonicum egg-induced liver granuloma and fibrosis. In this study, liver granuloma and fibrosis were induced by infecting BALB/c mice with 18 ± 3 cercariae of S. japonicum. At the beginning of egg granuloma formation (early phase genistein treatment from 4 to 6 weeks after infection) or after the formation of liver fibrosis (late phase genistein treatment from 6 to 10 weeks after infection), the infected mice were injected with genistein (25, 50 mg/kg). The results revealed that genistein treatment significantly decreased the extent of hepatic granuloma and fibrosis in infected mice. The activity of NF-κB signaling declined sharply after the treatment with genistein, as evidenced by the inhibition of NF-κB-p65, phospho-NF-κB-p65, and phospo-IκB-α expressions, as well as the expression of IκB-α and the messenger RNA (mRNA) expression of inflammatory cytokines (MCP1, TNFα, IL1β, IL4, IL10) mediated by NF-κB signaling pathways in the early phase of the infection. Moreover, western blot and immunohistochemistry assays demonstrated that the contents of α-smooth muscle actin (α-SMA) and transforming growth factor-β were dramatically reduced in liver tissue under the treatment of genistein in the late phase of the infection. At the same time, the mRNA expression of MCP1, TNFα, and IL10 was inhibited markedly. These results provided evidence that genistein reduces S. japonicum egg-induced liver granuloma and fibrosis, at least partly due to decreased NF-κB signaling, and subsequently decreased MCP1, TNFα, and IL10 expressions. This implies that genistein can be a potential natural agent against schistosomiasis.
To examine the effects of formononetin (FMN) on Acetaminophen (APAP)-induced liver injury in vitro and in vivo. Human non-tumor hepatic cells LO2 were pretreated with either vehicle or FMN (20, 40 μM), for 6 h, followed by incubation with or without APAP (10 mM) for 24 h. In an in vivo assay, male BALB/c mice were randomly divided into four groups: (1) control group; (2) APAP group; (3) APAP + FMN (50 mg/Kg); (4) APAP + FMN (100 mg/Kg). The mice in the control and APAP groups were pre-treated with vehicle; the other two groups were pretreated daily with FMN (50, 100 mg/Kg) orally for 7 consecutive days. After the final treatment, acute liver injury was induced in all groups, except the control group, by intraperitoneal (i.p.) injection of 300 mg/Kg APAP. In LO2 cells, APAP exposure decreased the cell viability and glutathione (GSH) content, which were both greatly restored by FMN pretreatment. Overdose of APAP increased hepatic malondialdehyde (MDA) content, serum alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activity in experimental mice. Supplementation with 100 mg/Kg FMN significantly reduced APAP-induced elevated levels of MDA (1.97 ± 0.27 vs 0.55 ± 0.14 nmol/mg protein, p < 0.001), ALT (955.80 ± 209.40 vs 46.90 ± 20.40 IU/L, p < 0.001) and AST (1533.80 ± 244.80 vs 56.70 ± 28.80 IU/L, p < 0.001), and hepatic GSH level (5.54 ± 0.93 vs 8.91 ± 1.11 μmol/mg protein, p < 0.001) was significantly increased. These results were further validated by histopathology and TdT-mediated biotin-dUTP nick-endlabeling (TUNEL) staining, pretreatment with 100 mg/Kg FMN significant decreased APAP-induced hepatocellular damage and cell apoptosis (36.55 ± 3.82 vs 2.58 ± 1.80%, p < 0.001). Concomitantly, FMN stimulated the expression of Nrf2 and antioxidant gene expression in the presence of APAP. These data provide an experimental basis for the use of FMN in the treatment of patients with APAP-induced hepatotoxicity.
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