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10.1186/s13018-017-0614-z http://scihub22266oqcxt.onion/10.1186/s13018-017-0614-z C5508710!5508710 !28701229     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28701229 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       J+Orthop+Surg+Res 2017 ; 12 (1 ): 110 Nephropedia Template TP {{tp|p=28701229 |t=2017. Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-? and c-Jun N-terminal kinase pathway |pdf=|usr=}}{{28701229 }} gab.com Text Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor- and c-Jun N-terminal kinase pathway JO: J Orthop Surg Res http://www.kidney.de/pget.php?&tw=1&pmid=28701229 #FOAvip 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-? (TNF-?) 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-? 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-?, 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-? 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-?. Anti-TNF-? could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-? in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-? antibody, and SP600125 could reduce cellular apoptosis in the renal cortex. CONCLUSIONS: It is possible that JNK and TNF-? 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. Twit Text FOAVip Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor- and c-Jun N-terminal kinase pathway ????J Orthop Surg Res http://www.kidney.de/pget.php?&tw=1&pmid=28701229 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28701229 #FOAvip English Wikipedia <ref>{{Cite pmid|28701229 }}</ref> Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-? and c-Jun N-terminal kinase pathway #MMPMID28701229 Zhang BF ; Wang PF ; Cong YX ; Lei JL ; Wang H ; Huang H ; Han S ; Zhuang Y J Orthop Surg Res 2017[Jul]; 12 (1 ): 110 PMID28701229 show ga 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-? (TNF-?) 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-? 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-?, 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-? 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-?. Anti-TNF-? could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-? in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-? antibody, and SP600125 could reduce cellular apoptosis in the renal cortex. CONCLUSIONS: It is possible that JNK and TNF-? 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. |*MAP Kinase Signaling System [MESH] |Animals [MESH] |Anthracenes [MESH] |Crush Syndrome/*metabolism/mortality/pathology [MESH] |HMGB1 Protein/antagonists & inhibitors/*metabolism [MESH] |In Situ Nick-End Labeling [MESH] |Kidney/metabolism/*pathology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Muscle, Skeletal/metabolism/pathology [MESH]Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney dama(epmc).pdf DeepDyve Pubget Overpricing