The present study was designed to determine the effect of a new (25)Mg(2+)-carrying nanoparticle ((25)MgPMC16) on energy depletion, oxidative stress, and electrocardiographic (ECG) parameters on heart tissue of the rats poisoned by aluminum phosphide (AlP). (25)MgPMC16 at doses of 0.025, 0.05, and 0.1 median lethal dose (LD50 = 896 mg/kg) was administered intravenously (iv) 30 min after a single intragastric administration of AlP (0.25 LD50). Sodium bicarbonate (Bicarb; 2 mEq/kg, iv) was used as the standard therapy. After anesthesia, the animals were rapidly connected to an electronic cardiovascular monitoring device for monitoring of ECG, blood pressure (BP), and heart rate (HR). Later lipid peroxidation, antioxidant power, ATP/ADP ratio, and Mg concentration in the heart were evaluated. Results indicated that after AlP administration, BP and HR decreased while R-R duration increased. (25)MgPMC16 significantly increased the BP and HR at all doses used. We found a considerable increase in antioxidant power, Mg level in the plasma and the heart and a reduction in lipid peroxidation and ADP/ATP ratio at various doses of (25)MgPMC16, but (25)MgPMC16-0.025 + Bicarb was the most effective combination therapy. The results of this study support that (25)MgPMC16 can increase heart energy by active transport of Mg inside the cardiac cells.(25)MgPMC16 seems ameliorating AlP-induced toxicity and cardiac failure necessitating further studies.
Background: Alzheimer's disease (AD) is a progressive cognitive disorder that is generally age-related. Although there has been great research focusing on this disease, there is still a lack of reliable therapeutic methods. Amyloid-β (Aβ) peptide has a critical function in neuropathology of AD. Stem cell therapy provides treatment by improving the neuronal system in neurodegenerative disorders. Human adipose-derived stem cells (hADSCs) are the most appropriate sources of stem cells due to their safety, high proliferative potential, and easy isolation. Objectives: The present study was designed to evaluate the histological and behavioral alterations after intravenous administration of hADSCs in the AD rat model. Methods: In this study, 32 male rats were used in four groups, as follows: control, sham, AD rat model, and hADSCs-treated group. We used Morris Water Maze (MWM) for evaluating behavioral changes and Nissl staining for determining the histological studies. Results: In this study, the AD model was confirmed by behavioral and histological analysis. Behavioral results showed that the spatial memory improved after hADSCs injection in the AD rat model while the time spent in the target quadrant was significantly higher in the hADSCs-treated group than in the AD rat model group. On the other hand, the number of dead cells significantly decreased in the hADSCs-treated group as analyzed by Nissl staining. Conclusions: Our findings revealed that hADSCs could transfer into the brain and improve memory and neuronal damage in the AD rat model.
Background: Alzheimer's disease (AD) is a progressive neuropsychiatric disorder that gradually impairs memory and behavioral functions. Amyloid beta (Aβ) is considered as the most toxic substance in the brain of AD patients. Objectives: The present study was designed to evaluate Aβ deposits by Immuno-and Thioflavin S-costaining in the hippocampus of a rat model of AD after intravenous injection of human adipose-derived stem cells (hADSCs). Methods: Thirty-two male rats were included in the four groups of control, sham, AD and hADSCs. The hADSCs characterization was confirmed by the flow cytometry technique. Immuno-and Thioflavin S-costaining was utilized for detecting Aβ plaques in the hippocampus of a rat model of AD following injection of hADSCs. Results: Statistical analysis revealed that Aβ plaques increased significantly in the AD group compared to the control and sham groups. The administration of hADSCs significantly decreased immunoreactivity and Thio-S-positive plaques in the AD group. We also found that the plaques detected by anti-Aβ antibody (immunohistochemical staining) were significantly more than those distinguished by Thioflavin-S in all the groups. Conclusions: Results showed that hADSCs played an effective role in decreasing amyloids aggregation following migration to the hippocampus of the rat model of AD.
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