Search

Background: Canine distemper virus (CDV) is a pathogen with the capability of cross-species transmission. It has crossed the species barrier to infect many other species, and its host range is expanding. The reverse genetic platform, a useful tool for scientific research, allows the generation of recombinant viruses from genomic cDNA clones in vitro. Methods: To improve the reverse genetic system of CDV, a plasmid containing three independent expression cassettes was constructed for co-expression of the N, P, and L genes and then transfected with a full-length cDNA clone of CDV into Vero cells. Results: The results indicated that the established rescue system has the advantages of being more convenient, easy to control the transfection ratio, and high rescue efficiency compared with the conventional reverse genetics system. Conclusion: This method not only reduces the number of transfection plasmids, but also improves the rescue efficiency of CDV, which could provide a reference for the recovery of other morbilliviruses. [ABSTRACT FROM AUTHOR]

Abstract Dexmedetomidine (DEX) protects against liver damage caused by sepsis. The purpose of this study was to confirm the regulatory effects of DEX on glycogen synthase kinase 3 beta (GSK-3β) via the α2 adrenergic receptor (α2AR) and evaluate the role of GSK-3β in lipopolysaccharide (LPS)-induced liver injury. Sprague-Dawley (SD) rats were administered an intraperitoneal injection of DEX (30 μg/kg) 30 min before an intraperitoneal injection of LPS (10 mg/kg). HE staining and serum biochemical test results indicated that DEX significantly improved liver histopathological damage and liver function indices. Furthermore, DEX increased super oxide dismutase (SOD) activity and L-glutathione (GSH) levels, and inhibited malondialdehyde (MDA) production. Western blot (WB) analysis demonstrated that treatment with the GSK-3β inhibitor SB216763 increased antioxidant-related protein mitogen-activated protein kinase phosphatase 1 (MKP-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expression. In addition, anti-apoptosis-related proteins were up-regulated and pro-apoptosis-related proteins were down-regulated by SB21676 administration. WB analysis also showed that DEX increased anti-apoptosis-related protein levels and decreased pro-apoptotic protein levels in LPS-induced liver injury. Nrf2, p53, and activated caspase-3 levels were further evaluated using immunohistochemistry (IHC), producing results consistent with WB results. The α2AR antagonist atipamezole (AT) significantly reversed the protective effects of DEX, as shown by WB analysis. Our data suggested that α2AR plays an important role in reversing the effects of liver oxidative stress and apoptosis via DEX, and that DEX exerts antioxidant and anti-apoptosis effects through regulation of the GSK-3β/MKP-1/Nrf2 pathway. Highlights • DEX can regulate GSK-3β via α2 adrenergic receptor. • GSK-3β can regulate the MKP-1 /Nrf2 pathway in LPS model. • DEX can inhibit LPS-induced oxidative stress and apoptosis by regulating GSK-3β. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "An improved system to generate recombinant canine distemper virus" published in BMC Veterinary Research. The correction addresses a typesetting error that resulted in the omission of the co-corresponding author's name, Jingqiang Ren, and their email address. The original article has been corrected to include this information. Springer Nature, the publisher, maintains a neutral stance on jurisdictional claims and institutional affiliations. The authors of the article are Huai Cheng, Hewei Zhang, Huayun Zhang, Huanchang Cai, Min Liu, Mingen Yu, Meihua Xiang, Shubo Wen, and Jingqiang Ren. [Extracted from the article]

Acute lung injury (ALI) is a serious complication of sepsis and an important cause of death in intensive care. Studies have shown that DEX can inhibit inflammation. However, the anti-inflammatory effect and protective mechanism of DEX in lipopolysaccharide (LPS) induced ALI are still unclear. ALI model was established by intraperitoneal injection of LPS (10 mg/kg) in Sprague-Dawley (SD) male rats. Firstly, at 4, 6, 8, 12 and 24 h after LPS treatment, lung injury including pathologic histology, lung edema, and inflammation were detected. The optimal time point for lung injury was determined to be 12 h, at which time DEX was added to further test. Furthermore, STAT3 inhibitor (NSC74859) and GSK-3β inhibitor (SB216763) were added to verify the role of STAT3, GSK-3β and NF-κB in ameliorated ALI. Our results show that DEX pretreatment significantly decreased lung Wet-to-Dry weight (W/D) ratio and MPO activity and ameliorated LPS induced lung histopathological alterations. In addition, we confirmed that DEX can increased the phosphorylation of STAT3 and GSK-3β, and inhibit the phosphorylation of nuclear factor-κB (NF-κB) p65 in the inflammatory response induced by LPS. What's more, NSC74859 inhibited the phosphorylation of STAT3 and reversed the protect effect of DEX on LPS. SB216763 inhibited the phosphorylation of NF-κB and reversed the damage effect of LPS and plays the same anti-inflammatory effect as DEX. In summary, our data demonstrated that DEX can ameliorate ALI induced by LPS through GSK-3β/STAT3-NF-κB pathway. Unlabelled Image • Lung injury was most significant by intraperitoneal injection of LPS 12 h in rats. • DEX can inhibit LPS-induced inflammatory reaction. • NSC74859 (STAT3 inhibitor) reversed the protective effect of DEX on lung by inhibiting the activity of STAT3. • SB216763 (GSK-3β inhibitor) has the same protective effect as DEX by inhibiting the activity of GSK-3β. [ABSTRACT FROM AUTHOR]

Acute stress is a frequent and unpredictable disease for many animals. Stress is widely considered to affect liver function. However, the underlying mechanism by which dexmedetomidine (DEX) attenuates acute stress‐induced liver injury in rats remains unclear. In this study, we used forced swimming for 15 min and acute 3‐hr restraint stress model. Behavioral tests and changes in norepinephrine levels confirmed the successful establishment of the acute stress model. Acute stress‐induced liver injury, evidenced by hematoxylin and eosin‐stained pathological sections and increased serum aminotransferase and aspartate aminotransferase levels, was reduced in DEX‐treated livers. Reactive oxygen species and oxidative stress levels were dramatically decreased with DEX treatment compared with acute stress‐induced liver injury. DEX significantly reduced acute stress‐induced liver inflammation and apoptosis, as assessed by terminal deoxynucleotidyl transferase dUTP nick‐end labeling staining and inflammation and apoptosis‐related protein levels. DEX treatment also effectively inhibited acute stress‐induced c‐Jun N‐terminal kinase (JNK), P38, and BAD signaling pathway activation, and significantly induced MKP‐1 activation. Thus, DEX has a protective effect on acute‐stress‐induced liver injury by reducing inflammation and apoptosis, which suggests a potential clinical application for DEX in stress syndrome. [ABSTRACT FROM AUTHOR]

Abstract: A selective and sensitive LC–MS/MS method was developed and validated for the simultaneous determination of five constituents (cimicifugoside H-2, cimicifugoside H-1, 23-epi-26-deoxyactein, cimigenol xyloside and 25-O-acetylcimigenoside) of Cimicifuga foetida L. in beagle dog plasma. The quantitation was performed on a LC–MS/MS with negative electrospray ionization in selected reaction monitoring (SRM) mode. A gradient mobile phase composed of methanol and water was used at a flow rate of 0.4ml/min. All the analytes and internal standard (20 (S)-ginsenoside Rg3) were isolated from plasma samples by a liquid–liquid extraction method. The average extraction recoveries were 73–74% for cimicifugoside H-2, 89–94% for cimicifugoside H-1, 73–80% for 23-epi-26-deoxyactein, 89–91% for cimigenol xyloside, 87–96% for 25-O-acetylcimigenoside, respectively. The method showed good linearity and no endogenous material interfered with all the five compounds and I.S. peaks. The lower limit of quantification (LLOQ) of all analytes was 0.5ng/ml. The intra- and inter-day precision of analysis was less than 15% for each analyte at concentrations of 2.0, 50, 500ng/ml, and the accuracy ranged from 85.8% to 107%. This method was successfully applied to reveal the pharmacokinetic properties of cimicifugoside H-2, cimicifugoside H-1, 23-epi-26-deoxyactein, cimigenol xyloside and 25-O-acetylcimigenoside after oral administration. [Copyright &y& Elsevier]