Relative potency of a novel acaricidal compound from Xenorhabdus, a bacterial genus mutualistically associated with entomopathogenic nematodes.

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.

The effect of baicalein on Wnt/ß-catenin pathway and miR-25 expression in Saos-2 osteosarcoma cell line

Background/aim: Osteosarcoma is the most common primary bone malignancy that occurs frequently in children and adolescents. Baicalein, a flavonoid that has attracted great attention in recent years with its strong antitumor activity, shows a wide range of biological and pharmaceutical effects.MicroRNAs have been found to be involved in many critical processes in cancers. This study aimed to investigate the effect of baicalein and miR-25 on Wnt/ß-catenin signaling pathway of osteosarcoma cell line Saos-2. Materials and methods: Cell viability was assessed, and qRT-PCR and Western blot were performed to study the effects of baicalein on expression of Wnt/ß-catenin signaling pathway-realted genes (ß-catenin, GSK-3ß, and Axin2) of Saos-2 cells. Results: Our results indicated that baicalein can inhibit the proliferation (IC50 value 35 µM), regulate Wnt/ß-catenin pathway and also increase miR-25 expression of Saos-2. Baicalein and also miR-25 decreased the expression of ß-catenin and Axin2, while increasing the expression of GSK-3ß. Down regulation of miR-25 decreased the expression of GSK-3ß, while ß-catenin and Axin2 expression increased. Conclusion: These findings demonstrate that baicalein may target genes related to the Wnt/ß-catenin pathway by regulating miR-25 expression and may be a potential Wnt/ß-catenin pathway inhibitor for osteosarcoma therapy.

In vivo protective effect of Uridine, a pyrimidine nucleoside, on genotoxicity induced by Levodopa/Carbidopa in mice.

Parkinson's disease (PD) is a common neurodegenerative disorder that affects millions of people all over the world. Motor symptoms of PD are most commonly controlled by L-3,4-dihydroxyphenylalanine (Levodopa, L-DOPA), a precursor of dopamine, plus a peripherally-acting aromatic-L-amino-acid decarboxylase (dopa decarboxylase) inhibitor, such as carbidopa. However, chronic treatment with a combination of Levodopa plus carbidopa has been demonstrated to cause a major complication, namely abnormal involuntary movements. On the other hand, the effect of this treatment on bone marrow cells is unknown. Therefore, in this study, we aimed to investigate possible genotoxic effects of Levodopa and Carbidopa using male Balb/C mice. Our results showed that Levodopa alone or in combination with carbidopa caused genotoxicity in in vivo micronucleus test (mouse bone marrow) and Comet assay (blood cells). Furthermore, we showed that simultaneous administration of uridine, a pyrimidine nucleoside, reversed the genotoxic effect of Levodopa and Carbidopa in both assays. Our data show for the first time that Levodopa plus carbidopa combination causes genotoxicity which is reversed by uridine treatment. These findings might enhance our understanding for the complications of a common Parkinson's treatment and confer benefit in terms of reducing a possible genotoxic effect of this treatment.