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Title: | Effect of camel milk against renal toxicity in experimental rats |
Authors: | Al-Asmari, Abdulrahman Abbasmanthiri, Rajamohamed Al-Elawi, Abdulrahman M Horaib, Ghaleb Al Sadoon, Khalid Al Al-Asmari, Bayan |
Keywords: | Gentamicin camel milk kidney rats toxicity |
Issue Date: | Mar-2017 |
Publisher: | Faculty of Pharmacy & Pharmaceutical Sciences |
Citation: | Al-Asmari, A. K., Abbasmanthiri, R., Al-Elawi, A. M., Al-Horaib, G., Al-Sadoon, K., & Al-Asmari, B. A. (2017). Effect of camel milk against renal toxicity in experimental rats. Pakistan Journal of Pharmaceutical Sciences, 30. |
Abstract: | Most of the antibiotics are associated with considerable side effects. Gentamicin (GM) is one of the most commonly used antibiotics, but has significant nephrotoxic side effects. Hence, the current study is investigating the beneficial role of camel milk (CM) that ameliorate GM unwanted renal defects and dysfunctions in some experimental animals. Sprague-Dawely rats weighing (200-220g) were divided into groups (four) of six. Group 1 (Control) received normal saline (only). Group 2 was given oral administration of CM at the dose of 5ml/rat/day for fifteen days. Group 3 was injected with GM (80mg/kg b.wt., i.p.) for 10 days. Group 4 was first given oral administration of CM at the dose of 5ml/rat/day alone, for five days, and then followed with the administration GM for next 10 days, accordingly. The results show that administration of GM significantly enhanced the kidney weight and levels of renal toxicity markers like urea and creatinine, in addition to decreased levels of blood glucose. Treatment with CM ameliorated and reversed these drastic changes in levels of creatinine, urea and improved renal weight. Glucose levels were also reversed and increased significantly. Furthermore, GM induced renal histological anomalies like degeneration of glomeruli and tubules were suppressed by CM and showed better progress. The present study confirm that pretreatment with CM attenuates GM unwanted, induced renal dysfunction and cellular damage. |
URI: | http://142.54.178.187:9060/xmlui/handle/123456789/13911 |
ISSN: | 1011-601X |
Appears in Collections: | No.2(Supplementary),March 2017 |
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2-SUP-662.htm | 146 B | HTML | View/Open |
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