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Pentachlorophenol (PCP) is a persistent organic pollutant usually present in the form of sodium salts (PCP-Na) that has been banned for many years, but it can still be detected in animal food. The present study established a method of detecting PCP-Na and its metabolites—tetrachlorocatechol (TCC), pentachlorophenol acetate (PCP-acetate), and pentachloroanisole (PCA)—in swine samples (pork, fat, liver, heart, lungs and kidney), simultaneously using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and gas chromatography-tandem mass spectrometry (GC-MS/MS) based on the modified QuEChERS pre-treatment method. The validation results exhibited a good sensitivity with limits of quantitation (LOQs) of 1 μg/kg–2 μg/kg. The recoveries of spiked samples were in the range of 60.5–119.9%, with a relative standard deviation (RSD) between replicates (n = 5) of between 0.70% and 12.06%. [ABSTRACT FROM AUTHOR]

Praziquantel (PZQ) is a pyrazino-isoquinoline compound with broad spectrum of activity against parasitic trematodes and cestodes, and a key veterinary drug in the parasitic disease control field. However, PZQ residues caused by non-conforming or excessive use in food-producing animals may pose a serious threat to human health. Herein, a simple, sensitive and reproducible LC-MS/MS method was developed for the simultaneous determination of praziquantel and trans- and cis-4-hydroxypraziquantel in black goat tissues to guide the reasonable use of PZQ. The mean recoveries for three target analytes were 71.2 ∼ 117.6%, and the limits of quantification were 1.0 μg/kg. Twenty-five healthy black goats were administered a single dose of praziquantel tablets at a dose of 35 mg/kg of body weight for residue elimination study, The results revealed that praziquantel and 4-hydroxypraziquantel were rapidly depleted in goat tissues and the elimination half-lives did not exceed 1 day in all tissues except for muscle and lung. It provides guidance for the establishment of maximum residue limit of praziquantel in goat. [ABSTRACT FROM AUTHOR]

Pulmonary fibrosis is a severe condition with limited therapeutic options and characterized by increased fibroblast activation and progressive accumulation of extracellular matrix. Ghrelin, a gastrointestinal hormone, has been reported to possess protective roles in lung diseases including pulmonary fibrosis. However, the precise mechanisms underlying the protective effects of ghrelin remain unknown. The present study was designed to investigate the effects of ghrelin on transforming growth factor-β1 (TGF-β1)-induced pulmonary fibrosis in vitro and in vivo and the possible mechanism of action. It was found that ghrelin significantly attenuated TGF-β1-induced fibrotic responses in human lung fibroblast (IMR-90) cells and bleomycin (BLM)-induced fibrotic lung tissues. Meanwhile, ghrelin decreased the expressions of miR-125a-5p and phosphorylated smad2/3 and increased protein expressions of Kruppel-like factor 13 (KLF13) in vivo and in vitro. Ghrelin–induced anti-fibrotic effects and smad2/3 downregulation in TGF-β1-stimulated IMR-90 cells were markedly reversed by miR-125a-5p mimics and KLF13 siRNA. Furthermore, miR-125a-5p directly targeted KLF13 in IMR-90 cells. Our findings suggest that ghrelin attenuates TGF-β1-induced pulmonary fibrosis via the miR-125a-5p/KLF13 axis, which supports ghrelin as a new therapeutic agent against pulmonary fibrosis by antagonizing the TGF-β1 signaling pathway. [Display omitted] • Ghrelin attenuates TGF-β1-induced pulmonary fibrosis via the miR-125a-5p/KLF13 axis. • Targeting the miR-125a-5p/KLF13 axis reversed ghrelin-induced smad2/3 downregulation. • TGF-β1 regulated the miR-125a-5p/KLF13 axis in a smad-independent non-canonical manner. [ABSTRACT FROM AUTHOR]

Background: Immunosuppression has been described as a consequence of brain injury and infection by different mechanisms. Angiostrongylus cantonensis can cause injury to the central nervous system and eosinophilic meningitis to human. Both T cell and B cell immunity play an essential role in the resistance of the infection. However, whether brain injury caused by A. cantonensis infection can lead to immunosuppression is not clear. Therefore, the present study sought to observe the alteration of immune responses in mice infected with A. cantonensis.Methods: Mice were infected with 20 third-stage A. cantonensis larvae. The messenger RNA (mRNA) expression of inflammatory mediators in brain tissues was observed by qRT-PCR. Cell surface markers including CD3, CD4, CD8, CD19, B220, 7-AAD, annexin-V, IgM, AA4.1, and CD23 were evaluated by using flow cytometry. The immune functions of T and B lymphocytes were detected upon stimulation by ConA and antibody responses to a nonself antigen OVA, respectively. Activation of the hypothalamic-pituitary-adrenal axis was evaluated by analyzing the concentration of plasma corticosterone and levels of mRNA for corticotropin-releasing hormone, tyrosine hydroxylase, and c-fos.Results: A. cantonensis infection results in obvious immunosuppression evidenced as progressive spleen and thymus atrophy and significant decrease in the number of lymphocyte subsets including B cells, CD3+ T cells, CD4+ T cells, and CD8+ T cells, as well as reduced T cell proliferation at 21 days post-infection and antibody reaction to exogenous protein after infection. However, the sharp decrease of splenic and thymic cells was not due to cell apoptosis but to B cell genesis cessation and impairing thymocyte development. In addition, helminthicide treatment with albendazole on infected mice at 7 days post-infection could prevent immunosuppressive symptoms. Importantly, infected mice displayed hypothalamic-pituitary-adrenal axis activation, with peak responses occurring at 16 days post-infection, and glucocorticoid receptor antagonist could partially restore the infection-induced cessation of B cell genesis.Conclusions: Brain injury caused by A. cantonensis infection, like that of brain stroke and trauma, enhanced endogenous corticosteroid activity, resulting in peripheral immunosuppression. [ABSTRACT FROM AUTHOR]