Protocatechuic aldehyde attenuates chondrocyte senescence via the regulation of PTEN-induced kinase 1/Parkin-mediated mitochondrial autophagy

Aug 8, 2024International journal of immunopathology and pharmacology

Protocatechuic aldehyde reduces cartilage cell aging by controlling mitochondrial cleanup through PINK1/Parkin pathways

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Abstract

PCA effectively reduced in models of knee osteoarthritis.

Chondrocyte senescence is linked to the progression of knee osteoarthritis.
Treatment with PCA increased mitochondrial membrane potential and enhanced mitochondrial autophagy.
The protective effects of PCA were diminished when the PINK1 gene was silenced.
Overexpression of PINK1 amplified the beneficial effects of PCA on LPS-induced chondrocytes.
PCA may attenuate chondrocyte senescence through regulation of the PINK1/Parkin pathway.

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This study aimed to investigate whether the beneficial effects of PCA on are mediated through the regulation of . Chondrocyte senescence plays a significant role in the development and progression of knee osteoarthritis (OA). The compound protocatechuic aldehyde (PCA), which is abundant in the roots of, has been reported to have antioxidant properties and the ability to protect against cellular senescence. To achieve this goal, a destabilization of the medial meniscus (DMM)-induced mouse OA model and a lipopolysaccharide (LPS)-induced chondrocyte senescence model were used, in combination with PINK1 gene knockdown or overexpression. After treatment with PCA, cellular senescence was assessed using Senescence-Associated β-Galactosidase (SA-β-Gal) staining, DNA damage was evaluated using Hosphorylation of the Ser-139 (γH2AX) staining, reactive oxygen species (ROS) levels were measured using Dichlorodihydrofluorescein diacetate (DCFH-DA) staining, mitochondrial membrane potential was determined using a 5,5',6,6'-TETRACHLORO-1,1',3,3'-*. TETRAETHYBENZIMIDA (JC-1) kit, and mitochondrial autophagy was examined using Mitophagy staining. Western blot analysis was also performed to detect changes in senescence-related proteins, PINK1/Parkin pathway proteins, and mitophagy-related proteins. Our results demonstrated that PCA effectively reduced chondrocyte senescence, increased the mitochondrial membrane potential, facilitated mitochondrial autophagy, and upregulated the PINK1/Parkin pathway. Furthermore, silencing PINK1 weakened the protective effects of PCA, whereas PINK1 overexpression enhanced the effects of PCA on LPS-induced chondrocytes. PCA attenuates chondrocyte senescence by regulating PINK1/Parkin-mediated mitochondrial autophagy, ultimately reducing cartilage degeneration. Salvia miltiorrhiza

Key numbers

600 μmol/ml

Decrease in senescent chondrocytes

PCA treatment concentration used for assessing senescence.

1.5×

Increase in mitochondrial membrane potential

Mitochondrial membrane potential improvement measured in PCA-treated cells.

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Protocatechuic aldehyde attenuates chondrocyte senescence via the regulation of PTEN-induced kinase 1/Parkin-mediated mitochondrial autophagy

Abstract

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