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10.1155/2015/859383 http://scihub22266oqcxt.onion/10.1155/2015/859383 C4455533!4455533!26089605     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mediators+Inflamm 2015 ; 2015 (ä): ä Nephropedia Template TP {{tp|p=26089605|t=2015. Mechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Induced Toxicity in Rats |pdf=|usr=}}{{26089605}} gab.com Text Mechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Induced Toxicity in Rats JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26089605 #FOAvip To investigate mechanisms by which thymoquinone (TQ) can prevent methotrexate- (MTX-) induced hepatorenal toxicity, TQ (10?mg/kg) was administered orally for 10 days. In independent rat groups, MTX hepatorenal toxicity was induced via 20?mg/kg?i.p. at the end of day 3 of experiment, with or without TQ. MTX caused deterioration in kidney and liver function, namely, blood urea nitrogen, creatinine, alanine aminotransferase, and aspartate aminotransferase. MTX also caused distortion in renal and hepatic histology, with significant oxidative stress, manifested by decrease in reduced glutathione and catalase, as well as increase in malondialdehyde levels. In addition, MTX caused nitrosative stress manifested by increased nitric oxide, with upregulation of inducible nitric oxide synthase. Furthermore, MTX caused hepatorenal inflammatory effects as shown by increased tumor necrosis factor-?, besides upregulation of necrosis factor-?B and cyclooxygenase-2 expressions. MTX also caused apoptotic effect, as it upregulated caspase 3 in liver and kidney. Using TQ concurrently with MTX restored kidney and liver functions, as well as their normal histology. TQ also reversed oxidative and nitrosative stress, as well as inflammatory and apoptotic signs caused by MTX alone. Thus, TQ may be beneficial adjuvant that confers hepatorenal protection to MTX toxicity via antioxidant, antinitrosative, anti-inflammatory, and antiapoptotic mechanisms. Twit Text FOAVip Mechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Induced Toxicity in Rats ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26089605 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26089605 #FOAvip English Wikipedia <ref>{{Cite pmid|26089605}}</ref> Mechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Induced Toxicity in Rats #MMPMID26089605 El-Sheikh AAK; Morsy MA; Abdalla AM; Hamouda AH; Alhaider IA Mediators Inflamm 2015[]; 2015 (ä): ä PMID26089605show ga To investigate mechanisms by which thymoquinone (TQ) can prevent methotrexate- (MTX-) induced hepatorenal toxicity, TQ (10?mg/kg) was administered orally for 10 days. In independent rat groups, MTX hepatorenal toxicity was induced via 20?mg/kg?i.p. at the end of day 3 of experiment, with or without TQ. MTX caused deterioration in kidney and liver function, namely, blood urea nitrogen, creatinine, alanine aminotransferase, and aspartate aminotransferase. MTX also caused distortion in renal and hepatic histology, with significant oxidative stress, manifested by decrease in reduced glutathione and catalase, as well as increase in malondialdehyde levels. In addition, MTX caused nitrosative stress manifested by increased nitric oxide, with upregulation of inducible nitric oxide synthase. Furthermore, MTX caused hepatorenal inflammatory effects as shown by increased tumor necrosis factor-?, besides upregulation of necrosis factor-?B and cyclooxygenase-2 expressions. MTX also caused apoptotic effect, as it upregulated caspase 3 in liver and kidney. Using TQ concurrently with MTX restored kidney and liver functions, as well as their normal histology. TQ also reversed oxidative and nitrosative stress, as well as inflammatory and apoptotic signs caused by MTX alone. Thus, TQ may be beneficial adjuvant that confers hepatorenal protection to MTX toxicity via antioxidant, antinitrosative, anti-inflammatory, and antiapoptotic mechanisms. äMechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Indu(epmc).pdf DeepDyve Pubget Overpricing