[Astragaloside IV alleviates D-GAL-induced endothelial cell senescence by promoting mitochondrial autophagy via inhibiting the PINK1/Parkin pathway].

Nov 28, 2025Nan fang yi ke da xue xue bao = Journal of Southern Medical University

Astragaloside IV reduces aging in blood vessel cells caused by D-GAL by boosting mitochondrial cleanup through blocking the PINK1/Parkin pathway

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Abstract

AS-IV treatment significantly reduced the rate of D-GAL-induced senescence in human umbilical vein endothelial cells.

AS-IV alleviated the inhibitory effect of D-GAL on cell viability.
Treatment with AS-IV promoted the angiogenesis and migration abilities of HUVECs.
AS-IV significantly decreased the number of cells positive for senescence-associated β-galactosidase staining.
The treatment restored mitochondrial membrane potential and lowered reactive oxygen species levels in D-GAL-treated HUVECs.
AS-IV inhibited the fusion of autophagosomes and lysosomes, affecting autophagic flux.
Increased expression of senescence-related proteins was observed with the addition of MTK458 in HUVECs treated with both D-GAL and AS-IV.

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OBJECTIVES: To explore the mechanism by which astragaloside IV (AS-IV) alleviates D-galactose (D-GAL)-induced senescence in human umbilical vein endothelial cells (HUVECs).

METHODS: Cultured HUVECs were treated with D-GAL (40 g/L), AS-IV (200 μmol/L), D-GAL+AS-IV, or D-GAL+AS-IV+MTK458 (a mitochondrial autophagy agonist, 25 μmol/L) for 48 h, and the changes in cell proliferation, migration, and angiogenesis capacity were evaluated. Cell apoptosis, reactive oxygen species (ROS) levels, mitochondrial membrane potential, and expressions of autophagy-related proteins (LC3-II/LC3-I) and PINK1/Parkin pathway proteins in the treated cells were detected.

RESULTS: AS-IV treatment significantly reduced the inhibitory effect of D-GAL on HUVEC viability, effectively alleviated D-GAL-induced impairment of tube-forming ability, and promoted angiogenesis and migration ability of the cells. AS-IV also significantly reduced the rate of D-GAL-induced HUVECs positive for senescence-associated β-galactosidase (SA-β-Gal) staining and inhibited the expression of senescence-related genes P21 and P53. AS-IV restored mitochondrial membrane potential and reduced intracellular ROS levels in D-GAL-induced HUVECs, and inhibited the fusion of autophagosomes and lysosomes to prevent the completion of autophagic flux. In HUVECs treated with both D-GAL and AS-IV, the application MTK458 significantly increased the number of yellow spots and enhanced the expressions of P21, P53, PINK1, Parkin, LC3, and Beclin proteins.

CONCLUSIONS: AS-IV alleviates D-GAL-induced endothelial cell senescence by inhibiting the PINK1/Parkin pathway to regulate mitochondrial autophagy.

[Astragaloside IV alleviates D-GAL-induced endothelial cell senescence by promoting mitochondrial autophagy via inhibiting the PINK1/Parkin pathway].

Abstract

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