PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29720871-13 2018 We also observed that quercetin could inhibit palmitic acid-induced cell apoptosis via suppressing the activation of caspase-3, -9, -12; increasing the ratio of Bcl-2/BAX and reversing the impaired mitochondrial membrane potential. Palmitic Acid 46-59 caspase 3 Mus musculus 117-130 28805970-6 2017 In mouse, insulinoma MIN6 cells, palmitic acid induced the activity of caspase 3/7 after a 72-h exposure, while pharmacologically active concentrations of MR1704 did not. Palmitic Acid 33-46 caspase 3 Mus musculus 71-80 26672616-5 2016 PA treatment also induced increased protein expression of inositol requiring protein 1alpha (IRE1alpha), phosphorylated eukaryotic initiation factor-alpha (eIF2alpha), and activating transcription factor 4 (ATF4) as well as activation of caspase-3. Palmitic Acid 0-2 caspase 3 Mus musculus 238-247 27449757-8 2016 We demonstrate that OXA attenuates PA-induced hypothalamic cell death via reduced caspase-3/7 apoptosis, stabilization of Bcl-2 gene expression, and reduced Bax/Bcl-2 gene expression ratio. Palmitic Acid 35-37 caspase 3 Mus musculus 82-91 22542939-6 2012 After the 24h of PA exposure, cells also underwent marked apoptosis and showed increased activation of the apoptosis protease, caspase-3. Palmitic Acid 17-19 caspase 3 Mus musculus 127-136 26157144-8 2015 NR4A1 overexpression in MIN6 cells reduced C/EBP homologous protein (CHOP) expression and Caspase3 activation induced by TG or PA. Palmitic Acid 127-129 caspase 3 Mus musculus 90-98 25846498-4 2015 In human and mouse hepatocytes palmitic acid at a lipotoxic concentration triggered early activation of endoplasmic reticulum (ER) stress-related kinases, induced the apoptotic transcription factor CHOP, activated caspase 3 and increased the percentage of apoptotic cells. Palmitic Acid 31-44 caspase 3 Mus musculus 214-223 26472223-9 2015 In vitro, stable XBP1-knockdown Huh7 cells (Huh7-KD) and scramble control cells (Huh7-SCR) were generated and treated with palmitic acid (PA) for 24 h. PA-treated Huh7-KD cells had increased cytotoxicity measured by lactate dehydrogenase release, apoptotic nuclei, and caspase3/7 activity assays compared with Huh7-SCR cells. Palmitic Acid 152-154 caspase 3 Mus musculus 269-277 26113535-6 2015 We show that Foxc2 reduces the expression of Bax, caspase-9, and caspase-3 in both serum-starved and palmitic acid-induced cell apoptotic models, which confirms the anti-apoptotic role of Foxc2. Palmitic Acid 101-114 caspase 3 Mus musculus 65-74 25841776-6 2015 Similar results were found in mouse hepatocytes in which LA attenuated PA-mediated activation of caspase 3 and reduced lipid accumulation by decreasing PA uptake and increasing fatty acid oxidation and lipophagy, thereby preventing lipoapoptosis. Palmitic Acid 71-73 caspase 3 Mus musculus 97-106 22542939-9 2012 Collectively, these results demonstrated that the JNK-mediated signaling mechanism of PA-induced beta-cell apoptosis involves up-regulated expression of PANDER and activation of caspase-3. Palmitic Acid 86-88 caspase 3 Mus musculus 178-187 31472681-10 2019 RESULTS: Exposure to 100-400 muM PA reduced cell viability, activated caspase 3, and enhanced the expression levels of the apoptosis-related protein BCL-2-associated X protein (BAX) and ER stress markers glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in MLTC-1 cells. Palmitic Acid 33-35 caspase 3 Mus musculus 70-79 31077207-8 2019 Our results showed that 200-800 muM PA treatment reduces cell viability, induces cell apoptosis, enhances the expression of apoptosis-related genes (Caspase 3 and B-cell lymphoma-2 (BCL-2) associated X protein (BAX)), and activates the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)). Palmitic Acid 36-38 caspase 3 Mus musculus 149-158 31472681-12 2019 Curcumin (20 muM) significantly suppressed PA- or TG-induced decrease in cell viability, caspase 3 activity, and the expression levels of BAX, CHOP, and GRP78. Palmitic Acid 43-45 caspase 3 Mus musculus 89-98