Background: After injuries, infections, or tumor removal, endogenous healing depends on bone repair. Disorders of bone healing are difficult to treat in clinical settings. There are numerous induced methods for correcting bone abnormalities, such as the induced membrane technique, allogenic bone grafting, synthetic bone grafting, artificial joint replacement, and autologous bone grafting. However, the delivery of the bone graft and bone filling materials necessitates surgical implantation at the fracture site, which could cause edema, infection, and the development of heterotopic bone locally. Therefore, systemically administered osteogenic drugs will provide an excellent method for bone lesion healing. Aim of the study: to evaluate the systemic effect of metformin on bone healing after surgical induction of bony defect and to determine the amount of newly formed bone using histological, histomorphometric analysis, and the surface area measurement of newly formed bone. Also to study the safety of metformin administration at the administered dose for this purpose. Materials and methods: Twenty mature male New Zealand rabbits were separated into two groups, each including ten rabbits for the study. The same surgical procedure was performed on all rabbits. Two holes were made at the femur (3 mm in diameter and 3 mm in depth) and left empty. Metformin tablets were ground into a fine powder and the resultant powder was dissolved in 10ml of water to prepare a liquid dosage containing 50 mg /1ml of metformin. Metformin is administered orally to the rabbits through a feeding tube at a dose of 50 mg/kg body weight. Animals were euthanized at two-time intervals, 14 and 28 days. The femur was separated, sectioned preserved, and sent for histological analysis and histomor-phometry. Results: The results revealed that there is an increase in new bone formation and bone-forming cells in the metformin-treated group. Conclusion: Metformin increases bone healing by increasing the number of bone-forming cells and the surface area of newly formed bone tissues and causes less inflammatory response at the site of a bone lesion. So it possesses an osteogenic effect.
Background: Overconsumption of fructose may cause metabolic syndrome (MetS). MetS pathogenesis is caused by oxidative stress, cellular malfunction, and systemic inflammation caused by hereditary and environmental factors. N-acetylcysteine (NAC) has become associated with the phrase "antioxidant." Most researchers use and test NAC with the goal of preventing or reducing oxidative stress.Aim: To determine the positive effects of NAC on blood glucose, lipid profile, and body weight in fructose-induced metabolic syndrome in albino rats.Materials and Methods: Forty male albino rats, 10-12 weeks old, were haphazardly divided into five groups of identical size. Group I (negative control) received tap water for 12 weeks. Group II (positive control) received a 60% w/w fructose solution (60% FS) instead of tap water for 12 weeks. Group III (NAC) received tap water and an intra-peritoneal (IP) injection of NAC (150 mg/kg/day) for 12 weeks. Group IV (protection) co-administered 60% FS orally and NAC IP injection (150 mg/kg/day) for 12 weeks. Group V (treatment) received 60% FS for 8 weeks followed by 4 weeks of drinking tap water with NAC IP injection (150 mg/kg/day). Blood samples were taken at weeks 0, 8, and 12 and were tested for serum glucose and lipid profile. All animals of each group were weighted at weeks 0, 8 and 12 of the study.Results: Concerning serum glucose, group II showed increased glycaemia at week 8 and further elevation during week 12. Group III displayed normal glycaemia at weeks 8 and 12. In group IV, glycaemia showed elevation at week 8 followed by almost complete restoration at week 12. In group V, there was an increased glycaemia at week 8 followed by a partial restoration at week 12. Regarding lipid profile parameters, group II demonstrated a deterioration during week 8 and more worsening during week 12. There were no significant changes in group III's parameters during weeks 8 and 12. Group IV displayed a worsening in lipid profile during week 8 followed by a nearly complete improvement during week 12. During week 8, group V deteriorated, followed by a partial recovery during week 12. Concerning body weight, group II showed a weight gain at week 8 and further elevation during week 12. Group III displayed normal glycaemia at weeks 8 and 12. In group IV, glycaemia showed elevation at week 8 followed by almost complete restoration at week 12. In group V, there was an increased glycaemia at week 8 followed by a partial restoration at week 12. At week 8, there was a significant elevation in body weights in groups II and V compared to group I. Moreover, a significant reduction in body weight was recorded in group IV compared to group II during week 8. At week 12, a significant elevation in body weight was noticed in groups II and V compared to group I. Moreover, there was a significant reduction in body weight in group III compared to group I. On the other hand, there was a significant fall in body weight in groups IV and V compared to group II during week 12.Conclusion: MetS was caused by a high-fructose diet, which has been shown to have a negative impact on serum glucose, lipid profiles, and body weight. Moreover, NAC has been shown to enhance these parameters in a time-dependent manner.
- MeSH
- acetylcystein * aplikace a dávkování farmakologie MeSH
- fruktosa aplikace a dávkování škodlivé účinky MeSH
- krevní glukóza účinky léků MeSH
- krysa rodu rattus MeSH
- metabolický syndrom * chemicky indukované farmakoterapie krev MeSH
- modely nemocí na zvířatech MeSH
- tělesná hmotnost účinky léků MeSH
- výsledek terapie MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
Background and objectives: hyperlipidemia is the hallmark of cardiovascular diseases, namely hypertension, ischemic heart diseases, and strokes. Treatment should be satisfactory to tackle the lipid disorder and maintain the circulatory normal lipid profile. Many factors/cofactors coordinate to maintain lipid levels within normal to avoid subsequent hazards associated with hyperlipidemia. Coenzyme Q10 is a ubiquitous endogenous biomolecule that plays an important biological role in the lipid catabolic pathway. The goal of the study is to define the role of Coenzyme Q10 in hyperlipidemic mice model induced manually.Methods: to do so, a diet based hyperlipidemia state was induced in mice and they were distributed into different groups to conform with our study objectives. A Coenzyme Q10 treated group was compared to the negative control group and the positive control group was used as well.Results: The biochemical and histological outcomes declared that Coenzyme Q10 has important lipid-reducing effects which are parallel or even superior to lipid reducing drugs (e.g. Rosuvastatin). Conclusion of the present study addressed the lipid-lowering properties of Coenzyme Q10 in a newly induced hyperlipidemia mouse model bestowing the use of Coenzyme Q10 as add-on adjuvant therapy in a high-risk group or as a monotherapy in a prophylactic group.
