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10.12659/msm.902806 http://scihub22266oqcxt.onion/10.12659/msm.902806 C5580518!5580518 !28831032     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28831032 &cmd=llinks): Failed to open stream: HTTP request failed! 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Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidative Stress via Upregulating Heme Oxygenase-1 (HO-1) Expression |pdf=|usr=}}{{28831032 }} gab.com Text Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidative Stress via Upregulating Heme Oxygenase-1 (HO-1) Expression JO: Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=28831032 #FOAvip BACKGROUND Hyperglycemia is one of the most dangerous factors causing diabetic nephropathy. Salidroside is considered to have the effects of reducing oxidative stress damage and improving cell viability. This study was performed to investigate whether and how salidroside reduces high-glucose (HG)-induced apoptosis in mouse podocytes. MATERIAL AND METHODS We examined whether salidroside could decrease HG-induced podocyte oxidative stress and podocyte apoptosis in vitro. The potential signaling pathways were also investigated. Podocytes (immortalized mouse epithelial cells) were treated with normal glucose (5.5 mM) as control or HG (30 mM), and then exposed to salidroside treatment. RESULTS HG enhanced the generation of intracellular reactive oxygen species (ROS) and apoptosis in podocytes. Salidroside reduced HG-induced apoptosis-related consequences via promoting HO-1 expression. Salidroside increased the expression level of phosphorylated Akt (p-Akt) and phosphorylated ILK (p-ILK), p-JNK, and p-ERK and localization of Nrf-2. JNK inhibitor and ILK inhibitor decreased HO-1 expression to different degrees. Moreover, specific siRNAs of ILK, Nrf-2, and HO-1, and inhibitors of HO-1 and ILK significantly increased ROS generation and Caspase9/3 expression in the presence of salidroside and HG. CONCLUSIONS The results suggest that salidroside reduces HG-induced ROS generation and apoptosis and improves podocytes viability by upregulating HO-1 expression. ILK/Akt, JNK, ERK1/2, p38 MAPK, and Nrf-2 are involved in salidroside-decreased podocyte apoptosis in HG condition. Twit Text FOAVip Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidative Stress via Upregulating Heme Oxygenase-1 (HO-1) Expression ????Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=28831032 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28831032 #FOAvip English Wikipedia <ref>{{Cite pmid|28831032 }}</ref> Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidative Stress via Upregulating Heme Oxygenase-1 (HO-1) Expression #MMPMID28831032 Lu H ; Li Y ; Zhang T ; Liu M ; Chi Y ; Liu S ; Shi Y Med Sci Monit 2017[Aug]; 23 (ä): 4067-4076 PMID28831032 show ga BACKGROUND Hyperglycemia is one of the most dangerous factors causing diabetic nephropathy. Salidroside is considered to have the effects of reducing oxidative stress damage and improving cell viability. This study was performed to investigate whether and how salidroside reduces high-glucose (HG)-induced apoptosis in mouse podocytes. MATERIAL AND METHODS We examined whether salidroside could decrease HG-induced podocyte oxidative stress and podocyte apoptosis in vitro. The potential signaling pathways were also investigated. Podocytes (immortalized mouse epithelial cells) were treated with normal glucose (5.5 mM) as control or HG (30 mM), and then exposed to salidroside treatment. RESULTS HG enhanced the generation of intracellular reactive oxygen species (ROS) and apoptosis in podocytes. Salidroside reduced HG-induced apoptosis-related consequences via promoting HO-1 expression. Salidroside increased the expression level of phosphorylated Akt (p-Akt) and phosphorylated ILK (p-ILK), p-JNK, and p-ERK and localization of Nrf-2. JNK inhibitor and ILK inhibitor decreased HO-1 expression to different degrees. Moreover, specific siRNAs of ILK, Nrf-2, and HO-1, and inhibitors of HO-1 and ILK significantly increased ROS generation and Caspase9/3 expression in the presence of salidroside and HG. CONCLUSIONS The results suggest that salidroside reduces HG-induced ROS generation and apoptosis and improves podocytes viability by upregulating HO-1 expression. ILK/Akt, JNK, ERK1/2, p38 MAPK, and Nrf-2 are involved in salidroside-decreased podocyte apoptosis in HG condition. |Animals [MESH] |Apoptosis/drug effects [MESH] |Cell Survival/drug effects [MESH] |Cells, Cultured [MESH] |Gene Expression/drug effects [MESH] |Glucose/*administration & dosage/metabolism [MESH] |Glucosides/metabolism/*pharmacology [MESH] |Heme Oxygenase-1/biosynthesis/genetics/*metabolism [MESH] |MAP Kinase Signaling System [MESH] |Mice [MESH] |Mitogen-Activated Protein Kinases/metabolism [MESH] |Oxidative Stress/drug effects [MESH] |Phenols/metabolism/*pharmacology [MESH] |Phosphorylation [MESH] |Podocytes/*drug effects/metabolism [MESH] |Reactive Oxygen Species/metabolism [MESH] |Transcriptional Activation [MESH] |Up-Regulation/drug effects [MESH]Salidroside Reduces High-Glucose-Induced Podocyte Apoptosis and Oxidat(epmc).pdf DeepDyve Pubget Overpricing