کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4256174 | 1284511 | 2013 | 7 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: The Role of Protein Kinase CK2 in Cyclosporine-Induced Nephropathy in Rats The Role of Protein Kinase CK2 in Cyclosporine-Induced Nephropathy in Rats](/preview/png/4256174.png)
ObjectivesProtein kinase casein kinase II (PKCK2) has multiple, overlapping roles in induction of apoptosis. Apoptosis can be a common pathway of renal injury caused by a nephrotoxic drug or an injury. We evaluated the role of PKCK2 in cyclosporine (CsA)-induced nephropathy in rats by inhibiting PKCK2 with emodin.MethodsMale Sprague-Dawley rats fed a low-sodium diet were divided into four treatment groups: control (0.9% saline injection), CsA (15 mg/kg/d subcutaneously), CsA + emodin (CsA plus emodin 20 mg/kg/d subcutaneously), and emodin only. The expression levels of apoptosis-associated factors and of PKCK2 were examined by Western blot analysis.ResultsOverexpression of PKCK2 noted with CsA treatment was prevented by emodin, a low-molecular-weight PKCK2 inhibitor, which dampend drug-induced up-regulation phosphorylated p53 and activation of caspases 3, 7, and 8. In addition, emodin prevented increased Bax/Bcl-2 ratio induced by CsA. Emodin prevented up-regulation of PKCK2 by CsA treatment, suggesting that its apoptotic-preventing activity was mediated via PKCK2.ConclusionsOur findings indicated that PKCK2 may play a role in apoptotic injury associated with CsA-induced nephropathy in rats.
Journal: Transplantation Proceedings - Volume 45, Issue 2, March 2013, Pages 756–762