Glutamine attenuates tubular cell apoptosis in acute kidney injury via inhibition of the c-Jun N-terminal kinase phosphorylation of 14-3-3*

• DOI: 10.1097/ccm.0b013e3181a005ba
• Publication Date: 2009-05-21T16:44:44Z
• Authors: Yoon Sook Kim; Myeong Hee Jung; Mee Young Choi; Young Hee Kim; Vadim Sheverdin; Jin Hyun Kim; Hye Jeong Ha; Dong Jun Park; Sang Soo Kang; Gyeong Jae Cho; Wan Sung Choi; Se-Ho Chang
• Keywords: c-jun

Tubular cell apoptosis is linked to the development of acute kidney injury (AKI), which a frequent complication traumatic rhabdomyolysis. The 14-3-3 protein, multifunctional regulatory binds variety apoptotic proteins and target c-Jun N-terminal kinase (JNK) in death signaling pathway. Therefore, we examined whether JNK phosphorylates downstream mitochondrial pathway mediates myoglobinuric determine these events are regulated by glutamine, known induce heat shock protein 70 (Hsp70), or involved synthesis glutathione (GSH).A prospective, randomized, controlled animal trial.University research laboratory.Male Sprague-Dawley rats.We utilized rat model AKI. Glutamine saline was administered intraperitoneally before after glycerol injection. Apoptotic determined via transferase-mediated deoxyuridine triphosphate nick-end labeling staining, Hsp70, JNK, phospho-JNK, 14-3-3, phospho-14-3-3, many other were Western blot. Relative interactions between tested coimmunoprecipitation analyses. Also, GSH levels further test glutamine affects AKI.Glutamine treatment elevated Hsp70 reduced attenuated tubular tissues rats with Further, physically associated thereby limiting its activation. In addition, evidently interacted leading phosphorylation, Bad Bax dissociation from subsequent translocation caspase activation renal failure. very modestly lowered serum creatinine AKI rats.A link may partly act as an early that promotes AKI, at least partially prevent enhancing levels.