ArticleInternational journal of pharmaceutics: X2026
SRT1720-loaded exosome-mimetic nanovesicles promote mitophagy via SIRT1/PARKIN activation to ameliorate diabetic cerebral infarction in a preclinical rat model.
Article in International journal of pharmaceutics: X, 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
Mitochondrial dysfunction and impaired mitophagy-a key event in diabetic hyperglycemia-aggravated ischemic injury - lead to accumulation of dysfunctional mitochondria and neuronal apoptosis, which are vital processes involved in diabetic cerebral infarction (DCI). Herein, we developed SRT1720-loaded exosome-mimetic nanovesicles (SRT1720@M) to leverage the potential of SIRT1/PARKIN pathway activation to inhibit these processes and counteract DCI. The lipid fusion approach was used to fabricate exosome-loaded SRT1720@M. The properties of SRT1720@M were established by employing UV-Vis, transmission electron microscopy (TEM), dynamic light scattering, and Fourier-transform infrared (FTIR) spectroscopy. Oxygen-glucose deprivation/reperfusion (OGD/R) and high-glucose (HG)-treated primary hippocampal neurons were used as an in vitro DCI model treated with SRT1720@M. qPCR, Western blotting and immunofluorescence were used for expression analyses, whereas cell viability, phagocytosis, inflammation, and ATP/L-LA levels were assessed by CCK-8, ELISA and TEM. A rat model of DCI was obtained by establishing middle cerebral artery occlusion (MCAO), from which infarct volume, neurological deficits, histopathology, behavioral indexes, and molecular markers were detected. SRT1720@M average size was ∼68 nm, with an encapsulation efficiency of 78.19%, loading capacity of 8.52%, and zeta potential of -54 mV. In vitro, SRT1720@M markedly improved cell viability (
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