期刊
MOLECULAR MEDICINE REPORTS
卷 10, 期 2, 页码 719-724出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2234
关键词
necroptosis; renal ischemia injury; ATP depletion; human proximal tubule cells; necrostatin-1
资金
- National Natural Science Foundation [81170683]
- National Key Technology RAMP
- D Program, National Clinical Key Specialty Construction Preparatory Projects [2011BAI10B08]
Acute kidney injury (AKI) induced by renal ischemia is a common clinical problem associated with a high morbidity and mortality. The present study investigated whether necroptosis was present in an in vitro renal ischemia model and whether the addition of necrostatin-1 (Nec-1) has a protective effect. In addition, whether autophagy was inhibited following the use of Nec-1 was also examined. When apoptosis was inhibited by z-VAD-fmk and energy was depleted with antimycin A for 1 h, the morphological abnormalities of human proximal tubular epithelial (HK-2) cells were markedly attenuated, and the cell viability was significantly improved following incubation with Nec-1. LC3-II/I ratios and LC3-II/GAPDH ratios demonstrated a statistically significant decrease in the Nec-1 + tumor necrosis factor (TNF)-alpha + z-VAD-fmk + antimycin A (1 h) group compared with the control group. In conclusion, the present study suggested that necroptosis was present in HK-2 cells subjected to TNF-alpha stimulation and energy depletion. Nec-1 inhibits a caspase-independent necroptotic pathway involving autophagy and may have therapeutic potential to prevent and treat renal ischemic injury.
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