Erratum to: Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling.

Erratum to: J Zhejiang Univ-Sci B (Biomed & Biotechnol) 2019 2019 20(10):816-827. https://doi.org/10.1631/jzus.B1900071. The original version of this article unfortunately contained a mistake. In p.823, Figs. 8c and 8d were in-correct, and the obvious pathological changes were mistakenly placed in the picture. The correct versions should be as follows.

Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling.

Catalpol is the main active ingredient of an extract from Radix rehmanniae, which in a previous study showed a protective effect against various types of tissue injury. However, a protective effect of catalpol on uterine inflammation has not been reported. In this study, to investigate the protective mechanism of catalpol on lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and mouse endometritis, in vitro and in vivo inflammation models were established. The Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway and its downstream inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), western blot (WB), and immunofluorescence techniques. The results from ELISA and qRT-PCR showed that catalpol dose-dependently reduced the expression of pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-1ß, and IL-6, and chemokines such as C-X-C motif chemokine ligand 8 (CXCL8) and CXCL5, both in bEECs and in uterine tissue. From the experimental results of WB, qRT-PCR, and immunofluorescence, the expression of TLR4 and the phosphorylation of NF-κB p65 were markedly inhibited by catalpol compared with the LPS group. The inflammatory damage to the mouse uterus caused by LPS was greatly reduced and was accompanied by a decline in myeloperoxidase (MPO) activity. The results of this study suggest that catalpol can exert an anti-inflammatory impact on LPS-induced bEECs and mouse endometritis by inhibiting inflammation and activation of the TLR4/NF-κB signaling pathway.

Decomposition Kinetics of Omethoate in Blood / 法医学杂志

Objective To study the decomposition kinetics of omethoate in blood.Methods The acetonitrile precipitated protein was added into the blood, with the chromatographic column of a Waters BEH C18column (2.1 mm×50 mm, 1.7μm), the mobile phase of 5 mmol/L ammonium acetate aqueous solution-methanol, and the gradient elution with a flow rate of 0.3 mL/min and injection volume of 2μL.With electrospray ionization (ESI) source and positive ion detection, qualitative and quantitative analyses were taken using multi-reaction monitoring mode.Omethoate standard was added into blank human blood to the mass concentrations of 0.78, 1.40, 2.30, 4.50, and 7.20μg/mL, and each mass concentration was preserved at 3 temperatures of-20℃, 4℃, and 20℃, respectively.The content of omethoate was detected at different time points (0, 1, 3, 4, 7, 11, 15, 24, 32, 40, 48, 64, 80, 96, and 120 d).Results Different concentrations of omethoate all showed a descended trend in human blood under different temperature conditions.The decomposition in storage environment of-20℃, 4℃, and 20℃was fit to a one-compartment open model with a first-order kinetic process, which could be expressed as Ct=Coe-αt, with the calculated theoretical values of omethoate concentration close to the measured values.Conclusion All concentrations of omethoate are decomposed in the blood, which vary a lot in different preservation conditions.It is suggested that blood samples should be frozen and detected timely in suspected omethoate poisoning cases.