BackgroundDiabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats.MethodsThe study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method.ResultsTreatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups.ConclusionOur findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.
Objective:To evaluate effects of titanium dioxide /gelatin nanocomposite on wound healing in mice as a model study. Methods:Fifty male rats were randomized into five groups of ten animals each. In group I, 0.1 mL sterile saline 0.9% solution was added to the wounds with no infection. In group II, the wounds were infected with MRSA and only treated with 0.1 mL the sterile saline 0.9% solution. In group III, infected wounds were treated with gelatin. In group IV, animals with infected wounds were treated with 0.1 mL titanium dioxide nanoparticles. In group V, animals with infected wounds were treated with titanium dioxide /gelatin nanocomposite. Wound size was measured on 2, 6, 10, 14, 18 and 20 days after surgery. Results:Reduction in wound area indicated that there was significant difference between group IV and other groups (p<0.05). Quantitative histological and morphometric studies and mean rank of the qualitative studies demonstrated that there was significant difference between group IV and other groups (P<0.05). Conclusion:Titatnium dioxide nanoparticles/gelatin composite offered potential advantages in wound healing acceleration and fibroblast proliferation on early days of healing phases. Acceleration in wound repair could be associated with earlier wound contraction and stability of damaged area by rearrangement of granulation tissue and collagen fibers.
A b s t r a c tBackground: Ischaemic heart disease is the main cause of mortality in the world. After myocardial infarction (MI) cardiomyocytes apoptosis and ventricular remodelling have occurred. Apelin is a peptide that has been shown to exert cardioprotective effects.
Aim:The aim of this study was to investigate the anti-apoptotic and anti-remodelling effects of [Pyr 1 ]apelin-13 in the rat model of post-MI.Methods: Thirty-six male Wistar rats were randomly divided into three groups: (1) ]apelin-13 has anti-hypertrophic, anti-remodelling, and anti-apoptotic effects via overexpression of Apel, Apelr, and Bcl-2 and reduces gene expression of Bax and Casp-3 in the infarcted myocardium, which can in turn lead to repair myocardium.
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