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Fresh Co(II) concluding coordination polymer based on {[Co(μ-ppda)(μ-pbmeix)]∙0.5pbmeix·H 2 O} n (1) was formed smoothly through the reaction of Co(II) salt with p -phenylenediacetic acid (H 2 ppda) under the conditions of N-donor co-ligand semirigid 1,4-bis(2-methylimidazol-1-ylmethyl)benzene (pbmeix) for cervical cancer therapy. In our biological research, we explored the pathogenesis of cervical cancer and provided new targets for cervical cancer treatment. In patients with cervical cancer and the cervical cancer rat model, the expression of Breast Cancer Susceptibility Protein-1 (BRCA1) was aberrantly upregulated. This phenomenon may play a role in the occurrence and development of cervical cancer. Then, bioinformatics prediction was conducted, and miR-9-5p was speculated as the up-regulator of BRCA1 in cervical cancer cells. The influence of miR-9-5p on the vascular endothelial growth factor and pigment epithelium-derived factor contents of cervical cancer lesions was determined via enzyme‐linked immunosorbent (ELISA) assay. Then, the proliferation of cervical cancer cells was determined via CCK-8 assay after miR-9-5p transfection. Finally, we proved that complex 1 is an excellent candidate for cervical cancer therapy through miR-9-5p-regulated BRCA1-OCT1-GADD45 pathways. [ABSTRACT FROM AUTHOR]

Objective: Microcystin-leucine-arginine (MC-LR) exposure induces lipid metabolism disorders in the liver. Secreted frizzled-related protein 5 (SFRP5) is a natural antagonist of winglesstype MMTV integration site family, member 5A (Wnt5a) and an anti-inflammatory adipocytokine. In this study, we aimed to investigate whether MC-LR can induce lipid metabolism disorders in hepatocytes and whether SFRP5, which has anti-inflammatory effects, can alleviate the effects of hepatic lipid metabolism by inhibiting the Wnt5a/Jun N-terminal kinase (JNK) pathway., Methods: We exposed mice to MC-LR in vivo to induce liver lipid metabolism disorders. Subsequently, mouse hepatocytes that overexpressed SFRP5 or did not express SFRP5 were exposed to MC-LR, and the effects of SFRP5 overexpression on inflammation and Wnt5a/JNK activation by MC-LR were observed., Results: MC-LR exposure induced liver lipid metabolism disorders in mice and significantly decreased SFRP5 mRNA and protein levels in a concentration-dependent manner. SFRP5 overexpression in AML12 cells suppressed MC-LR-induced inflammation. Overexpression of SFRP5 also inhibited Wnt5a and phosphorylation of JNK., Conclusion: MC-LR can induce lipid metabolism disorders in mice, and SFRP5 can attenuate lipid metabolism disorders in the mouse liver by inhibiting Wnt5a/JNK signaling., (Copyright © 2024 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.)

Glial cell is an ideal vehicle for gene therapy of brain diseases. However, there are many limits in using primary glial cells. Therefore, an immortalized rat glial cell line (RGLT) was established by SV40 large T-antigen (LTag) gene from the primary rat fetal glial cells. The RGLT cell was shown to be non-tumorigenic after transplantation to nude mice (up to 4 weeks) and rat striatum (up to 18 months). Rat tyrosine hydroxylase (TH) gene was transfected into RGLT cell to obtain RGLT-TH cell. The TH immunohistochemical staining and HPLC-ECD analysis demonstrated the TH expression and dopamine (DA) production in RGLT-TH cells in vitro. When implanting RGLT-TH cells into the striatum of 6-hydroxydopamine (6-OHDA) lesioned hemiparkinsonism model rats, TH immunohistochemical staining showed the TH presence in striatum and HPLC-ECD analysis held at 6 months after cell implantation showed an increase of DA content in striatum. The asymmetric rotation of rats receiving RGLT-TH cells was reduced by 50%-60% and this reduction persisted stably at least for 18 months. These results suggest that the immortalized glial cell line could serve as an ideal vehicle for therapeutic gene delivery system to achieve a long-term gene therapy of neurodegenerative diseases.