The Experimental Effects of Lipopolysaccharide-Induced Renal Injury in Mice Model | ||||
| Archives of Pharmaceutical Sciences Ain Shams University | ||||
| Article 4, Volume 5, Issue 1, June 2021, Page 46-51 PDF (925.55 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/aps.2021.30593.1049 | ||||
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| Authors | ||||
Mina Nessem   1; Ahmed Esmat 2; Samar Azab2; Ebtehal El-Demerdash2
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| 1Egyptian Drug Authority (EDA), Giza, 22311, Egypt | ||||
| 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo 11566, Egypt | ||||
| Abstract | ||||
| Acute renal injury (AKI) is a serious case with high mortality rate especially among hospitalized patients. It could be induced by sepsis, hypovolemia, atherosclerosis, and ischemia. Sepsis is caused mainly by Lipopolysaccharides (LPS) of gram-negative bacteria. The aim of current work was to assess the potential ability of LPS to induce AKI in mice as well as the probable mechanism. Experimentally, three different doses of LPS (2.5, 5 and 7.5 mL/kg) were evaluated. Results showed that LPS single dose (2.5 mg/kg, i.p.) was optimum to induce AKI in mice. Moreover, LPS induced severe pathological injuries in kidney tissues. It significantly increased the levels of blood urea nitrogen and serum creatinine in LPS-exposed mice, demonstrating deteriorated kidney function. Notably, LPS increased tumor necrosis factor (TNF)-α in renal tissue homogenate, indicating its ability to initiate severe inflammatory cascade. In summary, LPS (2.5 mg/kg, ip, single dose) has a potential capability to induce AKI with inflammatory insult. | ||||
| Keywords | ||||
| acute kidney injury; lipopolysaccharides; TNF-α; inflammation; BUN | ||||
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