ArticleMetabolic brain disease2026
Chiglitazar alleviates cognitive dysfunction in diabetic mice by restoring mitochondrial function via the PPARs/Nrf2 signaling pathway.
Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiabetes is a chronic metabolic disorder associated with hyperglycemia, which often leads to cognitive dysfunction and mitochondrial impairment. Chiglitazar is a novel peroxisome proliferator-activated receptor (PPAR) agonist. However, the precise mechanism through which Chiglitazar alleviates cognitive dysfunction in diabetic mice remains unclear.
methodsA diabetic mouse model was established through intraperitoneal injection of streptozotocin (STZ), and high-glucose-induced neuronal injury model. The Morris water maze assessed spatial memory. HE and Nissl staining evaluated cortical and hippocampal structural changes. Western blot measured PPARs, Nrf2, and TFAM protein levels. mtDNA, ATP, SOD, and MDA levels were analyzed, and mitochondrial ultrastructure was assessed via transmission electron microscopy (TEM).
resultsDiabetic mice exhibited hyperglycemia and cognitive impairment, with longer escape latencies and reduced time in the target quadrant. HE and Nissl staining showed neuronal loss and structural damage, which Chiglitazar ameliorated. mtDNA, ATP, and SOD levels decreased, while MDA increased in diabetic mice and the high-glucose-induced neuronal injury model, Chiglitazar ameliorated this phenomenon. Western blot results showed that Chiglitazar increased the protein expression levels of PPARα, PPARγ, PPARδ, Nrf2 and TFAM. TEM revealed severe mitochondrial damage in high-glucose conditions. Chiglitazar treatment alleviated these ultrastructural abnormalities.
conclusionChiglitazar regulates the PPARs/Nrf2 pathway and reverses mitochondrial dysfunction to improve cognitive function in diabetic mice.
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