{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["19(1)"],"submitter":["Cisternas P"],"pubmed_abstract":["<b>Background/Objectives:</b> Astrocytes are key regulators of brain energy homeostasis, integrating glucose metabolism with antioxidant support for neuronal function. Dysregulation of these processes contributes to neurodegenerative diseases, including Alzheimer's disease. Andrographolide, a bioactive diterpenoid from <i>Andrographis paniculata</i>, has been reported to exert neuroprotective effects through the modulation of Wnt/β-catenin signaling and neuronal metabolism; however, its actions on astrocytic metabolic pathways remain insufficiently characterized. <b>Methods:</b> Here, we investigated the effects of andrographolide on metabolic and redox parameters in primary mouse cortical astrocytes. <b>Results:</b> Andrographolide increased glucose uptake and antioxidant capacity without affecting AMPK activation or the activity of core glycolytic enzymes. Instead, it selectively enhanced glucose-6-phosphate dehydrogenase activity, promoting glucose flux through the pentose phosphate pathway in a partially Wnt-dependent manner. This metabolic reprogramming was associated with increased NADPH availability and glutathione levels, together with a reduced ATP/ADP ratio, consistent with a shift toward redox maintenance rather than maximal energy production. <b>Conclusions:</b> Collectively, these findings highlight astrocytic metabolic plasticity as a relevant and underexplored target of andrographolide and support the concept that natural compounds can enhance brain resilience by modulating glial redox metabolism."],"journal":["Pharmaceuticals (Basel, Switzerland)"],"pagination":["133"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12845274"],"repository":["biostudies-literature"],"pubmed_title":["Metabolic Reprogramming by Andrographolide: Enhanced Pentose Phosphate Pathway and Antioxidant Capacity in Cortical Astrocytes."],"pmcid":["PMC12845274"],"pubmed_authors":["Ormazabal P","Cisternas P","Bastias-Perez M","Inestrosa NC","Gherardelli C","Brito-Valenzuela J"],"additional_accession":[]},"is_claimable":false,"name":"Metabolic Reprogramming by Andrographolide: Enhanced Pentose Phosphate Pathway and Antioxidant Capacity in Cortical Astrocytes.","description":"<b>Background/Objectives:</b> Astrocytes are key regulators of brain energy homeostasis, integrating glucose metabolism with antioxidant support for neuronal function. Dysregulation of these processes contributes to neurodegenerative diseases, including Alzheimer's disease. Andrographolide, a bioactive diterpenoid from <i>Andrographis paniculata</i>, has been reported to exert neuroprotective effects through the modulation of Wnt/β-catenin signaling and neuronal metabolism; however, its actions on astrocytic metabolic pathways remain insufficiently characterized. <b>Methods:</b> Here, we investigated the effects of andrographolide on metabolic and redox parameters in primary mouse cortical astrocytes. <b>Results:</b> Andrographolide increased glucose uptake and antioxidant capacity without affecting AMPK activation or the activity of core glycolytic enzymes. Instead, it selectively enhanced glucose-6-phosphate dehydrogenase activity, promoting glucose flux through the pentose phosphate pathway in a partially Wnt-dependent manner. This metabolic reprogramming was associated with increased NADPH availability and glutathione levels, together with a reduced ATP/ADP ratio, consistent with a shift toward redox maintenance rather than maximal energy production. <b>Conclusions:</b> Collectively, these findings highlight astrocytic metabolic plasticity as a relevant and underexplored target of andrographolide and support the concept that natural compounds can enhance brain resilience by modulating glial redox metabolism.","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-11T03:13:52.176Z","creation":"2026-06-11T03:08:39.041Z"},"accession":"S-EPMC12845274","cross_references":{"pubmed":["41599730"],"doi":["10.3390/ph19010133"]}}