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Item Minocycline protects neurons against glial cells-mediated bilirubin neurotoxicity(Elsevier, 2020-01-01) Zhou, Changwei; Sun, Rong; Sun, Chongyi; Gu, Minghao; Guo, Chuan; Zhang, Jiyan; Du, Yansheng; Gu, Huiying; Liu, Qingpeng; Neurology, School of MedicineUnconjugated bilirubin, the end product of heme catabolism and antioxidant, induced brain damage in human neonates is a well-recognized clinical syndrome. However, the cellular and molecular mechanisms underlying bilirubin neurotoxicity remain unclear. To characterize the sequence of events leading to bilirubin-induced neurotoxicity, we investigated whether bilirubin-induced glial activation was involved in bilirubin neurotoxicity by exposing co-cultured rat glial cells and cerebellar granule neurons (CGN) to bilirubin. We found that bilirubin could markedly induce the expression of TNF-α and iNOS in glial cells, and even at low concentrations, the co-culture of glial cells with neurons significantly enhances neurotoxicity of bilirubin. Pretreatment of the co-cultured cells with minocycline protected CGN from glia-mediated bilirubin neurotoxicity and inhibited overexpression of TNF-α and iNOS in glia. Furthermore, we found that high doses of bilirubin were able to induce glial injury, and minocycline attenuated bilirubin-induced glial cell death. Our data suggest that glial cells play an important role in brain damage caused by bilirubin, and minocycline blocks bilirubin-induced encephalopathy possibly by directly and indirectly inhibiting neuronal death pathways.Item Minocycline reduces alveolar bone loss and bone damage in Wistar rats with experimental periodontitis(Public Library of Science, 2024-10-04) Frazão, Deborah Ribeiro; Matos-Souza, José Mario; dos Santos, Vinicius Ruan Neves; Farias Nazario, Rayssa Maite; dos Santos Chemelo, Victoria; Bittencourt, Leonardo Oliveira; de Souza Balbinot, Gabriela; Collares, Fabrício Mezzomo; Gomes-Leal, Walace; Ferreira, Railson Oliveira; Kuchenbecker Rösing, Cassiano; Movila, Alexandru; Rodrigues Lima, Rafael; Biomedical and Applied Sciences, School of DentistryThis study aimed to investigate the impact of minocycline on the alveolar bone in experimental periodontitis in rats. Thirty Wistar rats were randomly assigned to three groups: control without periodontitis; experimental periodontitis induced by ligature; experimental periodontitis + intraperitoneal administration minocycline for seven days. Ligatures remained in place in both periodontitis groups for 14 days. At the end of the experiment, the animals were euthanized and one hemimandible underwent micro-computed tomography (micro-CT) analysis to assess vertical bone loss and alveolar bone quality. Histopathological analysis was performed on the other hemimandible. Statistical analysis was performed using ANOVA with Tukey's post-test (p<0.05). The results showed a significant reduction in vertical bone loss in the animals treated with minocycline compared with untreated animals. Minocycline also preserved the alveolar bone thickness, number, spacing, and bone volume to tissue volume ratio. Histopathological analysis indicated that minocycline reduced bone resorption, decreased inflammatory response, and maintained the bone collagen fibers. This study demonstrated the effectiveness of minocycline in reducing vertical bone loss and preserved bone quality in rats with experimental periodontitis. The results of this study indicate that minocycline has the potential to serve as an additional treatment option for periodontitis. However, further research is warranted to assess the efficacy and safety of minocycline use in patients with periodontitis.