科研之友
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摘要
Background: Inflammation plays a crucial role in kidney damage after crush syndrome (CS). Several researchers report that high mobility group box-1 protein (HMGB1) may be the vital trigger in kidney damage, and tumor necrosis factor-a (TNF-alpha) and c-Jun N-terminal kinase (JNK) are involve in this pathophysiological process, but their biological roles are unclear. This study aimed to explore the relationship between HMGB1, JNK, and TNF-alpha in kidney damage. Methods: The crush injury model was established using weight compression. The reliability of the crush injury model was determined by hematoxylin-eosin (HE) staining. Western blot was used to detect the expression of HMGB1, JNK, and TNF-alpha, and TUNEL was used to mark apoptotic cells in the renal cortex. Results: The results showed that the highest expression of HMGB1 in muscle was 12 h after CS. JNK and TNF-alpha increased and peaked at 1 day after CS in kidneys. Western blot analysis revealed that anti-HMGB1 antibody could downregulate the expression of JNK and TNF-alpha. Anti-TNF-alpha could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-alpha in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-alpha antibody, and SP600125 could reduce cellular apoptosis in the renal cortex. Conclusions: It is possible that JNK and TNF-alpha commonly contribute to kidney damage by assembling a positive feedback cycle after CS, leading to increased apoptosis in the renal cortex. HMGB1 from the muscle may be the trigger.
- 出版日期2017-7-12
- 单位西安交通大学
