Pancreatic histological changes in adult female albino rats treated with Orlistat and the possible protective role of B- carotene.

2020 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Amira Ali ◽  
Magda Mansour ◽  
Somaia Ali ◽  
Dalia Noya
2014 ◽  
Vol 27 (4) ◽  
pp. 793 ◽  
Author(s):  
MonaAbd El Mawla Mohammed Soliman ◽  
AhmedAbozaid Ali ◽  
GhadaHassan El-Seify ◽  
HalaMohammed El Haroun

2014 ◽  
Vol 37 (3) ◽  
pp. 453-463
Author(s):  
Eman A. El-Kordy ◽  
Heba A. El-Din Mubarak ◽  
Madiha M. Makhlouf ◽  
Asmaa F. Abdel Mola

2014 ◽  
Vol 38 (3) ◽  
pp. 774-782 ◽  
Author(s):  
Merve Bacanlı ◽  
Sevtap Aydın ◽  
Gökçe Taner ◽  
Hatice Gül Göktaş ◽  
Tolga Şahin ◽  
...  

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.


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