Leda Marília Fonseca Lucinda

Radiographic evidence of mandibular osteoporosis improvement in Wistar rats treated with Ginkgo biloba

Objective: Evaluate the effects of the extract of Ginkgo biloba (EGb) on the rat mandibular glucocorticoid‐induced‐osteoporosis. Method: 36 female rats were divided into six groups (n=6): control, osteoporosis, positive control and EGb1 (14mg/kg/day), EGb2 (28mg/kg/day), and EGb3 (56mg/kg/day) treatment. Treatments were conducted for 30 days after osteoporosis induction. The animals were euthanized and their left mandibles were removed and radiographed to evaluate the cortical and the periodontal bone support. The control group was compared with the osteoporosis group (Students t‐test). The other groups were analyzed by ANOVA test followed by Tukey post‐hoc test (p < 0.05). Results: There was a significant reduction in periodontal bone support in the osteoporosis group. The positive control group showed a significant increase in the mesial periodontal bone support, as well as the EGb group treated with 28 and 56 mg/Kg, which showed a significant increase in the mesial and distal periodontal bone support. The mandibular cortical was not affected by osteoporosis; however, the group treated with EGb using 56 mg/Kg showed a significant increase in the thickness of the mandibular cortical. Conclusions: The EGb recovered the periodontal bone support and increased the mandibular cortical thickness. The EGb may be effective in the treatment of osteoporosis. Copyright

Efeito do extrato de Ginkgo biloba L., Ginkgoaceae, na osteoporose induzida em ratas Wistar

The objective of this study was to investigate the effect of a 20 day treatment with extract of Ginkgo biloba (EGb) in glucocorticoid-induced-osteoporosis. 36 rats were divided into six groups (n=6): control, osteoporosis, positive control, EGb1 (14 mg EGb/kg/day), EGb2 (28 mg EGb/kg/day) and EGb3 (56 mg EGb/kg/day). Treatments were conducted for twenty days, after osteoporosis was induced. Following euthanasia the femur and mandible of all animals were removed. The left mandible was radiographed to evaluate the cortical and the periodontal bone support (PBS). The histomorphometric analysis was performed on the right mandible and the right femur. The control group was compared with the osteoporosis group (Students t-test). The other groups were analyzed through ANOVA test followed by Dunnett post-hoc test. There was a significantly reduction in the mesial PBS, in the percentage of the alveolar bone (PAB) of the mandible and percentage of the trabecular bone (PTB) of the femur in the osteoporosis group. There was an increase in the mesial PBS in the positive control group, EGb2 and EGb3. The PAB of the mandible and the PTB of the femur increased in the EGb2 and EGb3 groups. The EGb in the 28 mg/kg and 56 mg/kg doses were effective to increase the mesial PBS, the PAB of the mandible and the PTB of the femur.

Factors Associated With Functional Capacity in Hemodialysis Patients

Hemodialysis patients have a marked decrease in functional capacity when compared to healthy individuals. We evaluated the factors associated with functional capacity in hemodialysis patients. A total of 102 hemodialysis patients were evaluated. The patients were submitted to a 6-min walk test, peripheral muscle strength tests, and an evaluation of quality of life, anxiety, and depression. The laboratory data were measured. The 6-min walk test distance correlated significantly with age, educational level, hemoglobin, creatinine, number of comorbidities, peripheral muscle strength, and some domains of SF-36 quality of life questionnaire and depression (P < 0.05). Multiple linear regression showed that educational level, hemoglobin, peripheral muscle strength, and depression significantly affected the 6-min walk test distance (P < 0.05). The multiple correlation coefficient was 0.74, and the squared multiple correlation coefficient adjusted was 0.52. In conclusion, functional capacity was significantly associated with educational level, hemoglobin, peripheral muscle strength, and depression in hemodialysis patients.

Emphysema induced by elastase enhances acute inflammatory pulmonary response to intraperitoneal LPS in rats.

Abnormalities in lungs caused by emphysema might alter their response to sepsis and the occurrence of acute lung injury (ALI). This study compared the extension of ALI in response to intraperitoneal lipopolysaccharide (LPS) injection in Wistar rats with and without emphysema induced by elastase. Adult male Wistar rats were randomized into four groups: control, emphysema without sepsis, normal lung with sepsis and emphysema with sepsis. Sepsis was induced, and 24 h later the rats were euthanised. The following analysis was performed: blood gas measurements, bronchoalveolar lavage (BAL), lung permeability and histology. Animals that received LPS showed significant increase in a lung injury scoring system, inflammatory cells in bronchoalveolar lavage (BAL) and IL‐6, TNF‐α and CXCL2 mRNA expression in lung tissue. Animals with emphysema and sepsis showed increased alveolocapillary membrane permeability, demonstrated by higher BAL/serum albumin ratio. In conclusion, the presence of emphysema induced by elastase increases the inflammatory response in the lungs to a systemic stimulus, represented in this model by the intraperitoneal injection of LPS.

Emphysema induced by elastase alters the mRNA relative levels from DNA repair genes in acute lung injury in response to sepsis induced by lipopolysaccharide administration in Wistar rats

ABSTRACT Purpose/Aim of the study: Patients suffering from chronic obstructive pulmonary disease (COPD) in association with acute respiratory distress syndrome (ARDS) present oxidative stress in lung cells, with production of free radicals and DNA lesions in pulmonary and adjacent cells. Once the DNA molecule is damaged, a set of enzymatic mechanisms are trigged to preserve genetic code integrity and cellular homeostasis. These enzymatic mechanisms include the base and the nucleotide excision repair pathways, as well as telomere regulation. Thus, the aim of this work was to evaluate the mRNA levels from APEX1, ERCC2, TP53, and TRF2 genes in lung tissue from Wistar rats affected by acute lung injury in response to sepsis and emphysema. Materials and Methods: Adult male Wistar rats were randomized into 4 groups (n = 6, for each group): control, emphysema, sepsis, and emphysema with sepsis. Pulmonary emphysema was induced by intratracheal instillation of elastase (12 IU/animal) and sepsis induced by intraperitoneal Escherichia coli lipopolysaccharide (LPS) injection (10 mg/kg). Lungs were removed, and samples were withdrawn for histological analysis and total RNA extraction, cDNA synthesis, and mRNA level evaluation by real time quantitative polymerase chain reaction. Results: Data show acute lung injury by LPS and emphysema by elastase and that APEX1, ERCC2, TP53, and TRF2 mRNA levels are increased significantly (p < 0.01) in emphysema with sepsis group. Conclusion: Our results suggest that alteration in mRNA levels from DNA repair and genomic stability could be part of cell response to acute lung injury in response to emphysema and sepsis.

Pre-treatment with dexamethasone attenuates experimental ventilator-induced lung injury

ABSTRACT Objective: To evaluate the effects that administering dexamethasone before the induction of ventilator-induced lung injury (VILI) has on the temporal evolution of that injury. Methods: Wistar rats were allocated to one of three groups: pre-VILI administration of dexamethasone (dexamethasone group); pre-VILI administration of saline (control group); or ventilation only (sham group). The VILI was induced by ventilation at a high tidal volume. Animals in the dexamethasone and control groups were euthanized at 0, 4, 24, and 168 h after VILI induction. We analyzed arterial blood gases, lung edema, cell counts (total and differential) in the BAL fluid, and lung histology. Results: At 0, 4, and 24 h after VILI induction, acute lung injury (ALI) scores were higher in the control group than in the sham group (p < 0.05). Administration of dexamethasone prior to VILI induction decreased the severity of the lung injury. At 4 h and 24 h after induction, the ALI score in the dexamethasone group was not significantly different from that observed for the sham group and was lower than that observed for the control group (p < 0.05). Neutrophil counts in BAL fluid were increased in the control and dexamethasone groups, peaking at 4 h after VILI induction (p < 0.05). However, the neutrophil counts were lower in the dexamethasone group than in the control group at 4 h and 24 h after induction (p < 0.05). Pre-treatment with dexamethasone also prevented the post-induction oxygenation impairment seen in the control group. Conclusions: Administration of dexamethasone prior to VILI induction attenuates the effects of the injury in Wistar rats. The molecular mechanisms of such injury and the possible clinical role of corticosteroids in VILI have yet to be elucidated.