Journal of Microscopy and Ultrastructure最新文献

Introduction: This study was done to assess the injurious effects of omeprazole by an in vivo experimental study on rat kidneys.

Materials and methods: Forty-two adult male albino rats were divided into four groups: Control group (I) in which rats were not administrated any treatment. In Groups IIa, IIb, and IIc rats received daily oral omeprazole in dose of 0.75 mg per kg for 2, 4, and 6 weeks, respectively. At the end of the experiment, blood samples were collected for serum creatinine and blood urea nitrogen measurement. Then, animals were sacrificed, and kidney specimens were processed for paraffin blocks, sectioned and stained with H and E, Mallory trichrome and Periodic acid-Schiff, then examined by the light microscope. Stained sections and image analysis were used to count vacuolated cells, pyknotic nuclei, tubular casts, and area percent of collagen fiber deposition, and then, data were subjected to the statistical analysis.

Results: Examination of omeprazole-treated groups showed injury of renal corpuscles, renal tubules, and vascular congestion with inflammatory cell infiltrate in renal interstitium. Thickening of basement membrane with deposition of collagen fibers was also detected. Statistically significant increase in the number of vacuolated cells, pyknotic nuclei, hyaline casts, and area percentage of collagen fiber deposition as compared with the control group was noticed, with deterioration of renal function tests.

Conclusion: It was concluded that the long-term use of omeprazole resulted in structural damage of rat renal tissue associated with deterioration of renal function in a time-dependent manner.

Context: Alzheimer's disease (AD) is a challenging neurodegenerative disease, and Vitamin D was proved to have neuroprotective effects.

Aim: This study was conducted to evaluate the potential neuroprotective effects of Vitamin D3 supplementation on AlCl₃-induced AD rat model in different hippocampal subregions (CA1, CA2, and CA3). It also aimed to compare the protective effects of protective versus therapeutic effects of Vitamin D3 regiments on the number of degenerated neurons and the neuronal layer thickness.

Materials and methods: Twenty-four adult male Albino Wister rats were sorted into GI: control; GII: AlCl₃-AD model (100 mg/kg) orally for 42 days; GIII: Rats were co-treated with AlCl₃ (as GII) and Vitamin D₃ (400 IU/kg/day) orally for 42 days; GIV: Rats were treated with AlCl₃ for 42 days then with Vitamin D₃ for further 2 weeks. Sagittal sections (5 μ) from paraffin-processed brains previously fixed in 10% neutral-buffered formalin were stained with hematoxylin and eosin to evaluate the thickness and number of degenerated neurons in the hippocampal CA1, CA2, and CA3 subregions.

Statistical analysis: The results of this study were expressed as mean ± standard deviation and analyzed by using IBM SPSS Statistics for Windows, version 23 (IBM SPSS, IBM Corp., Armonk, N.Y., USA). P < 0.05 was considered statistically significant.

Results: Vitamin D₃ supplementations modulated the degenerative changes observed in the hippocampus of AD rat model. In all hippocampal subregions, the thickness was higher in rats treated with Vitamin D₃ after the AD induction than rats treated with Vitamin D₃ during AD induction. However, this increase was only significant in CA2. Comparison of the number of degenerated neurons between both groups treated with Vitamin D₃ revealed that in CA1, the number of degenerated neurons did not statistically differ between the two groups. However, it was insignificantly lower in CA2 in rats treated with Vitamin D₃ after the AD induction, and in CA3, it was insignificantly lower in rats treated with Vitamin D₃ during the AD induction.

Conclusions: Vitamin D₃ was found to be effective in ameliorating histological and morphometric alterations in AlCl₃-induced AD in rat model and could be proposed as both preventive and therapeutic supplements in high-risk AD patients.