动物双歧杆菌
牙周炎
医学
脂肪因子
益生菌
内科学
内分泌学
长双歧杆菌
乳酸乳球菌
胰岛素抵抗
双歧杆菌
生物
胰岛素
乳酸菌
生物化学
遗传学
发酵
细菌
乳酸
作者
André L. Moreira,Giselle A. Silva,Pedro Henrique Félix Silva,Sérgio Luiz de Souza Salvador,Raphael M. Vicente,Graziele C. Ferreira,José E. Tanus‐Santos,Márcia Pinto Alves Mayer,K. Ishikawa,Sérgio Luı́s Scombatti de Souza,Flávia Aparecida Chaves Furlaneto,Michel Reis Messora
摘要
Abstract Objective To determine whether Bifidobacterium animalis subspecies lactis HN019 ( B. lactis HN019) can reduce the sequelae of experimental periodontitis (EP) in rats modulating systemic parameters. Background This study evaluated the effects of probiotic therapy (PROB) in the prevention of local and systemic damage resulting from EP. Methods Forty‐eight rats were allocated into four groups: C (control), PROB, EP, and EP‐PROB. PROB (1 × 10 10 CFU/mL) administration lasted 8 weeks and PE was induced on the 7th week by placing ligature on the animals' lower first molars. All animals were euthanized in the 9th week of the experiment. Biomolecular analyses, RT‐PCR, and histomorphometric analyses were performed. The data obtained were analyzed statistically (ANOVA, Tukey, p < .05). Results The EP group had higher dyslipidemia when compared to the C group, as well as higher levels of insulin resistance, proteinuria levels, percentages of systolic blood pressure, percentage of fatty hepatocytes in the liver, and expression of adipokines was up‐regulated (LEPR, NAMPT, and FABP4). All these parameters (except insulin resistance, systolic blood pressure, LEPR and FABP4 gene expression) were reduced in the EP‐PROB group when compared to the EP group. The EP group had lower villus height and crypt depth, as well as a greater reduction in Bacteroidetes and a greater increase in Firmicutes when compared to the EP‐PROB group. Greater alveolar bone loss was observed in the EP group when compared to the EP‐PROB group. Conclusion Bifidobacterium lactis HN019 can reduce the sequelae of EP in rats modulating intestinal parameters, attenuating expression of lipogenic genes and hepatic steatosis.
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