Differential expression of epithelial and smooth muscle lineage-specific markers of metanephros in one-humped camel foetuses.

The development of the metanephros in one-humped camels involves a complex series of interactions between epithelial and mesenchymal cells. As a result, there is a synchronized differentiation process of stromal, vascular and epithelial cell types during glomerulogenesis, angiogenesis and tubulogenesis. In the current work, the metanephros of camel foetuses were divided into four stages where kidneys from each stage were processed and immunoassayed, followed by quantitative analysis to determine target protein intensities throughout metanephrogenesis in the camel. This study demonstrated robust expression of α-smooth muscle actin (α-SMA) in the glomerular mesangium, as well as in interlobular and glomerular arterioles during the earlier stages of development. However, in the late stages, α-SMA expression became more localized around the blood capillaries in both the cortex and medulla. Strong expression of CD34 was observed in the immature glomerular and peritubular endothelial cells within the subcapsular zone, as well as in the glomerular, proximal tubular and distal tubular epithelium of stage one foetuses, although its expression gradually diminished with foetal maturation. The expression pattern of osteopontin was prominently observed in the distal convoluted tubules throughout all stages, however, no expression was detected in the proximal tubules, glomeruli and arterioles. E-cadherin was detected in the developing renal tubular epithelial cells but not in the glomeruli. In conclusion, this study reveals the spatiotemporal distribution of key proteins, including α-SMA, CD34, Osteopontin and E-cadherin, which play a crucial role in metanephrogenesis in camel foetuses.

Cefepime and diclofenac sodium combined treatment-potentiated multiple organ injury: Role of oxidative damage and disrupted lipid metabolism.

Concurrent exposure to antimicrobial and nonsteroidal anti-inflammatory drugs (NSAIDs) is usually inevitable in most infections and postsurgery. Consequently, the present study was designed to assess the intertwining impact of coadministration of cefepime (CP, a wide spectrum antibiotic) and diclofenac sodium (DF, an NSAID) on rat's liver, kidney, and testes. Rats received saline, CP (180 mg/kg/day, IM), DF (10 mg/kg/day, IM), or a combination of CP and DF. After 14 days, CP or DF induced tissue damage expressed by marked biochemical alterations in hepatic and renal function tests. Besides this, disrupted lipid metabolism and testosterone levels along with significant histological changes in hepatic, renal, and testicular tissues were noticed. A significant increase in malondialdehyde and decreases in superoxide dismutase and catalase activities alongside significant upregulated caspase 3 expression in tissues following CP or DF treatment suggested a bearable influence of oxidative stress, lipid peroxidation, and cell death. Accordingly, the simultaneous therapy of CP and DF evoked more obvious tissue damage than their individual treatment. Overall, data concluded that concurrent use of CP and DF in medical practice is a worrisome matter, so it should be done cautiously to avoid synergistic deleterious outcomes.

Exploring the possible neuroprotective and antioxidant potency of lycopene against acrylamide-induced neurotoxicity in rats' brain.

Acrylamide (Ac) is a carbonyl compound extracted from hydrated acrylonitrile with a significantly high chemical activity. It is widely existed and used in food processing, industrial manufacturing and laboratory personnel work. However, lycopene (Ly) is a most potent natural antioxidant among various common carotenoids extracted from red plants. Nevertheless, little is known about the relationship of Ac-induced neurotoxicity and the ameliorative role of Ly in the regulation of oxidative and antioxidant capacity during Ac exposure. Therefore, this work sought to investigate the neurotoxicity induced by Ac exposure and the potential modulatory role of Ly by reversing the brain dysfunctions during Ac exposure. For this purpose, forty male albino rats were assigned into four equal groups. Control group received distilled water, Ly group was given with a daily dose of 10 mg/kg bw, Ac group was given with a daily dose of 25 mg/kg bw, and Ac-Ly group was gavaged Ac plus Ly at the same doses as the former groups. All treatments were given orally for 21 consecutive days. The concentrations of antioxidants (reduced glutathione and glutathione peroxidase) and oxidative stress (malondialdehyde, nitric oxide and protein carbonyl) biomarkers, as well as neurotransmitters (serotonin and dopamine) and acetylcholinesterase (AChE) were measured in the brain homogenates. An immunohistochemical staining was applied with anti-GFPA antibody to determine the severity of astrocytosis. The in vivo study with rat model demonstrated that Ac exposure significantly decline the hematological parameters, brain neurotransmitters concentrations and AChE activity, as well as levels of antioxidant biomarkers but markedly elevate the levels of oxidative stress biomarkers. Moreover, marked histological alterations and astrocytosis were observed through the increased number of GFAP immunopositively cells in cerebral, cerebellar and hippocampal tissues compared with the other groups. Interestingly, almost all of the previously mentioned parameters were retrieved in Ac-Ly group compared to Ac group. These findings conclusively indicate that Ly oral administration provides adequate protection against the neurotoxic effects of Ac on rat brain tissue function and structure through modulations of oxidative and antioxidant activities.