This study investigated the effect of transplantation of bone marrow mesenchymal stem cells (BM-MSCs) on functional deterioration and neuroinflammatory response in aged C57BL/6J mice. Mice were divided into 3 groups: normal aged group, saline control group, and BM-MSCs treatment group. Saline and BM-MSCs were administrated by intraventricular injection into the right ventricle. Spatial Y-maze (SYM) test, novel objective recognition (NOR) test, and locomotor activity test were used to evaluate cognitive and locomotor ability at 7 and 42 days after transplantation. Microglia and astrocyte expression in the hippocampus CA1 region and dentate gyrus (DG) were evaluated by immunohistochemical method. Furthermore, the content of TNF-α, IL-1α, and IL-1β in the hippocampus and cortex were detected with ELISA. We found that BM-MSCs transplantation increased time in novel arm and percentage of alteration in SYM test, discrimination ratio and discrimination index in the NOR test, and traveled total distance and mean velocity in the locomotor activity test. It also inhibited microglia and astrocyte expression, and reduced the content of IL-1α and IL-1β in the hippocampus. Our results suggested that BM-MSCs transplantation could delay cognitive and locomotor function deterioration through inhibiting neuroinflammation response, which would provide a rationale for exploring the viability of using BM-MSCs transplantation in cognitive deficit diseases.
Purpose: To investigate the potential influence of long non-coding RNA (lncRNA) TUG1 on the development of endometrial cancer (EC).Methods: A total of 24 paired EC species and paracancerous species were collected, and the differential expressions of TUG1 in them were determined. The regulatory effects of TUG1 on proliferative and migratory potential in Ishikawa and HEC-1A cells were assessed using cell counting kit-8 (CCK-8) and Transwell assay, respectively. Potential protein binding TUG1 was predicted by bioinformatics analysis and subsequently verified using RIP (RNA-Binding Protein Immunoprecipitation) assay. Rescue experiments were conducted to uncover the mechanism of TUG1 in regulating the development of EC.Results: TUG1 was highly expressed in EC species and cell lines. Higher levels of TUG1 was observed in EC patients with metastases than those without metastatic cancer (p < 0.05). Overexpression of TUG1 markedly facilitated proliferative and migratory potential in EC cells. Taurine-upregulated gene 1 (TUG1) directly bound Fragile X-related protein 1 (FXR1) and positively regulated its level (p < 0.05). Through interaction with FXR1, TUG1 stimulated the malignant development of EC.Conclusion: LncRNA TUG1 is upregulated in EC species, which facilitates proliferative and migratory potentials in EC cells by interacting with FXR1.
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