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Abstract <p>Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorderworldwide. Insulin resistance and islet β-cell dysfunction are majorcontributing factors. Quercetin is a natural compound has anti-inflammatoryand antioxidant effects. This study aimed to explore the effectsand mechanisms of quercetin in palmitic acid (PA)-induced isletβ-cell line MIN6 cell damage and focused on the role of quercetinin mitophagy mediated by PINK1/Parkin. We used flow cytometry toanalyze apoptosis and reactive oxygen species (ROS) production rate. Mitochondrial-lysosomalcolocalization and mitochondrial membrane potential (ΔΨ<sub>m</sub>)were detected using fluorescence microscopy and flow cytometry. Proteinlevel of Bax, PINK1, Parkin, p62 and Bcl-2 were detected using WesternBlot. ATP levels were measured using a luminescence-based assaykit. Oxygen consumption rate (OCR) was detected via the SeahorseXF24 Analyzer. Results showed that PA promoted the apoptosis ofMIN6 cells, inhibited PINK1-dependent mitophagy, enhanced the ROS productionrate and reduced the ATP content, ΔΨ<sub>m</sub> andOCR. Quercetin significantly inhibited apoptosis and enhanced PINK1-dependentmitophagy, reduced the ROS production rate, enhanced ATP, ΔΨ<sub>m</sub> andOCR. These protective effects of quercetin were partially reversedby the inhibition of mitophagy. In conclusion, quercetin alleviatesMIN6 cell injury partially by the activation of PINK1/Parkin-mediatedmitophagy.</p>

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Quercetin Attenuates Palmitate-Induced MIN6 Cell Injury via Activation of PINK1/Parkin-Mediated Mitophagy

  • 期刊论文

  • 发表日期：

    2026年2月26日

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  • H. Zhang,
  • Z. Guo

摘要

Abstract

Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorderworldwide. Insulin resistance and islet β-cell dysfunction are majorcontributing factors. Quercetin is a natural compound has anti-inflammatoryand antioxidant effects. This study aimed to explore the effectsand mechanisms of quercetin in palmitic acid (PA)-induced isletβ-cell line MIN6 cell damage and focused on the role of quercetinin mitophagy mediated by PINK1/Parkin. We used flow cytometry toanalyze apoptosis and reactive oxygen species (ROS) production rate. Mitochondrial-lysosomalcolocalization and mitochondrial membrane potential (ΔΨm)were detected using fluorescence microscopy and flow cytometry. Proteinlevel of Bax, PINK1, Parkin, p62 and Bcl-2 were detected using WesternBlot. ATP levels were measured using a luminescence-based assaykit. Oxygen consumption rate (OCR) was detected via the SeahorseXF24 Analyzer. Results showed that PA promoted the apoptosis ofMIN6 cells, inhibited PINK1-dependent mitophagy, enhanced the ROS productionrate and reduced the ATP content, ΔΨm andOCR. Quercetin significantly inhibited apoptosis and enhanced PINK1-dependentmitophagy, reduced the ROS production rate, enhanced ATP, ΔΨm andOCR. These protective effects of quercetin were partially reversedby the inhibition of mitophagy. In conclusion, quercetin alleviatesMIN6 cell injury partially by the activation of PINK1/Parkin-mediatedmitophagy.