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The article titled "Two Coordination Polymers: Protective Activity on Nerve Injury by Increasing miR-219 and Reducing Inflammatory Response" has been retracted by the Editor-in-Chief and the Publisher of the Journal of Cluster Science. The retraction was prompted by an investigation that revealed evidence of systematic manipulation of the publication process, including citations that do not support claims made in the text, non-standard phrasing, anomalies in the figures, and discrepancies in ethics approval statements. The Editor-in-Chief no longer has confidence in the results and conclusions of the article. Some of the authors have agreed to the retraction, while others have not responded to correspondence from the Editor-in-Chief/Publisher. Springer Nature, the publisher, remains neutral regarding jurisdictional claims and institutional affiliations. [Extracted from the article]

Two novel transition metal coordination polymers (CPs) of {Cu(tdc)(Hdmea)2 (1, Hdmea = N,N-dimethylethanolamine, tdc = 2,5-thiopenedicarboxylate) and [Co3(H2O)3(tdc)3(dioxane)]·2(dioxane) (2) were prepared via the reaction of Co(NO3)2·6H2O or Cu(NO3)2·3H2O and H2tdc with or without the template reagent Hdmea. The following experiments were carried out to determine the treatment activity for compounds against nerve injury. Firstly, the real time RT-PCR was carried out to determine the miR-219 relative expression in the nerve cells. Then the activation level of the AMPK signaling pathway in the nerve cells was measured with western blot. In addition to this, the ELISA detection was also used in this research, for the inflammatory cytokines' evaluation. Finally, the inhibition of the compound 1 and compound 2 on the death of the nerve cells was determined with MTT assay. [ABSTRACT FROM AUTHOR]

Baicalin, a flavonoid monomer derived from Scutellaria baicalensis called Huangqin in mandarin, is the main active ingredient contributing to S. baicalensis' efficacy. It is known in China that baicalin has potential therapeutic effects on inflammatory diseases. However, its anti-inflammatory mechanism has still not been fully interpreted. We aim to investigate the anti-inflammatory effect of baicalin on lipopolysaccharide (LPS)-induced inflammation in HBE16 airway epithelial cells and also to explore the underlying signaling mechanisms. The anti-inflammatory action of baicalin was evaluated in human airway epithelial cells HBE16 treated with LPS. Airway epithelial cells HBE16 were pretreated with a range of concentrations of baicalin for 30 min and then stimulated with 10 μg/ml LPS. The secretions of interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) in cell culture supernatants were quantified by enzyme-linked immunosorbent assay (ELISA). The messenger RNA (mRNA) expressions of IL-6, IL-8, and TNF-α were tested by quantitative real-time polymerase chain reaction (real-time RT-PCR). Furthermore, Western blotting was used to determine whether the signaling pathway NF-κB was involved in the anti-inflammatory action of baicalin. The inflammatory cell model was successfully built with 10 μg/ml LPS for 24 h in our in vitro experiments. Both the secretions and the mRNA expressions of IL-6, IL-8, and TNF-α were significantly inhibited by baicalin. Moreover, the expression levels of phospho-IKKα/β and phospho-NF-κB p65 were downregulated, and the phospho-IκB-α level was upregulated by baicalin. These findings suggest that the anti-inflammatory properties of baicalin may be resulted from the inhibition of IL-6, IL-8, and TNF-α expression via preventing signaling NF-κB pathway in HBE16 airway epithelial cells. In addition, this study provides evidence to understand the therapeutic effects of baicalin on inflammatory diseases in clinical practice. [ABSTRACT FROM AUTHOR]