Our study aimed to identify the novel acaricidal compound in Xenorhabdus szentirmaii and X. nematophila using the easyPACId approach (easy Promoter Activated Compound Identification). We determined the (1) effects of cell-free supernatant (CFS) obtained from mutant strains against T. urticae females, (2) CFS of the acaricidal bioactive strain of X. nematophila (pCEP_kan_XNC1_1711) against different biological stages of T. urticae, and females of predatory mites, Phytoseiulus persimilis and Neoseiulus californicus, (3) effects of the extracted acaricidal compound on different biological stages of T. urticae, and (4) cytotoxicity of the active substance. The results showed that xenocoumacin produced by X. nematophila was the bioactive acaricidal compound, whereas the acaricidal compound in X. szentirmaii was not determined. The CFS of X. nematophila (pCEP_kan_XNC1_1711) caused 100, 100, 97.3, and 98.1% mortality on larvae, protonymph, deutonymph and adult female of T. urticae at 7 dpa in petri dish experiments; and significantly reduced T. urticae population in pot experiments. However, the same CFS caused less than 36% mortality on the predatory mites at 7dpa. The mortality rates of extracted acaricidal compound (xenocoumacin) on the larva, protonymph, deutonymph and adult female of T. urticae were 100, 100, 97, 96% at 7 dpa. Cytotoxicity assay showed that IC50 value of xenocoumacin extract was 17.71 μg/ml after 48 h. The data of this study showed that xenocoumacin could potentially be used as bio-acaricide in the control of T. urticae; however, its efficacy in field experiments and its phytotoxicity need to be assessed in future.
ObjectiveHistone acetylation and deacetylation may play a role in the pathogenesis of inflammatory lung diseases. We evaluated the preventive effect of valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, on neonatal hyperoxic lung injury.MethodsForty newborn rat pups were randomized in normoxia, normoxia+VPA, hyperoxia and hyperoxia+VPA groups. Pups in the normoxia and normoxia+VPA groups were kept in room air and received daily saline and VPA (30 mg/kg) injections, respectively, while those in hyperoxia and hyperoxia+VPA groups were exposed to 95% O2 and received daily saline and VPA (30 mg/kg) injections for 10 days, respectively. Growth, histopathological, biochemical and molecular biological indicators of lung injury, apoptosis, inflammation, fibrosis and histone acetylation were evaluated.ResultsVPA treatment during hyperoxia significantly improved weight gain, histopathologic grade, radial alveolar count and lamellar body membrane protein expression, while it decreased number of TUNEL(+) cells and active Caspase-3 expression. Expressions of TGFβ3 and phospho-SMAD2 proteins and levels of tissue proinflammatory cytokines as well as lipid peroxidation biomarkers were reduced, while anti-oxidative enzyme activities were enhanced by VPA treatment. VPA administration also reduced HDAC activity while increasing acetylated H3 and H4 protein expressions.ConclusionsThe present study shows for the first time that VPA treatment ameliorates lung damage in a neonatal rat model of hyperoxic lung injury. The preventive effect of VPA involves HDAC inhibition.
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