ArticleInternational urology and nephrology2014
Roles of MAPKAPK-2 and HSP27 in the reduction of renal ischemia-reperfusion injury by ischemic postconditioning in rats.
Article in International urology and nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Pooled it
- Effects of transforming growth factor beta-activated kinase 1 (TAK1) on apoptosis of HK-2 cells in the high glucose environment.Bioengineered · 2022Article
- Multiplex enzyme activity imaging by MALDI-IMS of substrate library conversions.Scientific reports · 2020Article
- Protective effect of renal ischemic postconditioning in renal ischemic-reperfusion injury.Translational andrology and urology · 2020Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIschemic postconditioning is a procedure during which intermittent reperfusions are performed in the early phase of reperfusion to protect organs from ischemia/reperfusion injury. And in this study, we mainly investigated the injury-alleviative role of mitogen-activated protein kinase-activating protein kinase-2 (MAPKAPK-2) and heat shock protein 27 (HSP27) in renal ischemic reperfusion injury during the procedure of ischemic postconditioning.
methodsSprague-Dawley rats were randomly divided into four groups. The injury models were prepared by clipping the left renal pedicle of rats after ligating the right renal pedicle for 60 min. In the ischemic postconditioning group, sequential reperfusions were done for 10 s and another ischemia for 10 s for six cycles after kidney ischemia for 60 min. In addition, the specific inhibitor SB203580 was injected through caudal vein before ischemia. Serum creatinine, blood urea nitrogen and the expression of HSP27 and MAPKAPK-2 were detected 1, 3, 6 and 24 h later after reperfusion. Furthermore, phosphorylation of HSP27 and MAPKAPK-2 protein contents, histological changes and apoptosis were compared 24 h later after reperfusion.
resultsOur data showed that ischemic postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of MAPKAPK-2 and HSP27. The results indicated that ischemic postconditioning decreased apoptosis and improved renal function.
conclusionsTaken together, it is suggested that the renal protective effect may be related to the levels of HSP27 and MAPKAPK-2 activation.
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