<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zang Y</submitter><funding>Youth project of Shanghai Municipal Commission of Health and Family Planning</funding><funding>Planned Science Program of the Shanghai University of Traditional Chinese Medicine</funding><funding>Science and Technology Innovation Project of Putuo District Health System</funding><funding>Exploration Program of Putuo Hospital</funding><funding>National Natural Science Foundation of China</funding><funding>Key Medical Discipline Project of Shanghai Municipal Health Bureau</funding><pagination>1453-1464</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7925475</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>48(2)</volume><pubmed_abstract>Loss of podocytes is a hallmark of diabetic nephropathy, and a growing body of evidence indicates that podocytes are susceptible to palmitic acid (PA). We have previously shown that AS-IV inhibited PA-induced podocyte apoptosis by activating sarcoendoplasmic reticulum Ca&lt;sup>2+&lt;/sup> ATPase (SERCA), which indicate calcium regulation may involve in the process. Immunofluorescence staining, Western blot and flow cytometry were used to measure the protective efficacy of AS-IV to ameliorate PA-induced ER stress and podocyte apoptosis. Meanwhile, AS-IV inhibited cytochrome c release, decreased mitochondrial membrane potential, accompany with the depletion of endoplasmic reticulum Ca&lt;sup>2+&lt;/sup> and elevation of cytosolic and mitochondrial Ca&lt;sup>2+&lt;/sup>. Sequestration of cytosolic calcium wit</pubmed_abstract><journal>Molecular biology reports</journal><pubmed_title>Astragaloside IV inhibits palmitic acid-induced apoptosis through regulation of calcium homeostasis in mice podocytes.</pubmed_title><pmcid>PMC7925475</pmcid><funding_grant_id>20154Y0133</funding_grant_id><funding_grant_id>81403235, 81803921</funding_grant_id><funding_grant_id>PTKWWS202001</funding_grant_id><funding_grant_id>2020360A</funding_grant_id><funding_grant_id>2020LK070</funding_grant_id><funding_grant_id>ZK2019A12</funding_grant_id><pubmed_authors>Shan X</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Peng W</pubmed_authors><pubmed_authors>Zang Y</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Deng W</pubmed_authors><pubmed_authors>Cao A</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Astragaloside IV inhibits palmitic acid-induced apoptosis through regulation of calcium homeostasis in mice podocytes.</name><description>Loss of podocytes is a hallmark of diabetic nephropathy, and a growing body of evidence indicates that podocytes are susceptible to palmitic acid (PA). We have previously shown that AS-IV inhibited PA-induced podocyte apoptosis by activating sarcoendoplasmic reticulum Ca&lt;sup>2+&lt;/sup> ATPase (SERCA), which indicate calcium regulation may involve in the process. Immunofluorescence staining, Western blot and flow cytometry were used to measure the protective efficacy of AS-IV to ameliorate PA-induced ER stress and podocyte apoptosis. Meanwhile, AS-IV inhibited cytochrome c release, decreased mitochondrial membrane potential, accompany with the depletion of endoplasmic reticulum Ca&lt;sup>2+&lt;/sup> and elevation of cytosolic and mitochondrial Ca&lt;sup>2+&lt;/sup>. Sequestration of cytosolic calcium wit</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Feb</publication><modification>2025-04-21T16:58:55.743Z</modification><creation>2025-04-21T16:58:55.743Z</creation></dates><accession>S-EPMC7925475</accession><cross_references><pubmed>33606151</pubmed><doi>10.1007/s11033-021-06204-4</doi></cross_references></HashMap>