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| Puerarin mitigates hypoxia-reoxygenation-induced cardiomyocyte injury by modulating the PPARγ/NF-κB pathway |
| Hits 92 Download times 54 Received:January 20, 2026 |
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| DOI
10.11656/j.issn.1673-9043.2026.06.08 |
| Key Words
puerarin;myocardial ischemia-reperfusion injury;PPARγ/NF-κB;hypoxia-reoxygenation;apoptosis;oxidative stress;inflammatory mediators |
| Author Name | Affiliation | E-mail | | CHONG Haiyun | School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China | | | JIA Yaqian | Cangzhou People's Hospital, Cangzhou 061001, China | | | CAO Yuejuan | Tianjin Union Medical Center, The First Affiliated Hospital of Nankai University, Tianjin 300121, China | drcyj@aliyun.com |
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| Abstract
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| [Objective] To investigate the protective effects and mechanisms of puerarin（Pue） against hypoxia/reoxygenation（H/R）-induced injury in H9c2 cardiomyocytes. [Methods] An H/R injury model was established in H9c2 cardiomyocytes（6h hypoxia/2h reoxygenation），followed by intervention with different concentrations of Pue（25，50，100 μmol/L）. Knockdown the expression of peroxisome proliferator activated receptor gamma（PPARγ） through small interfering RNA（siRNA） technology to validate its mechanism. Cell Counting Kit 8（CCK-8 method） was used to detect cell viability，Western Blot was used to detect the expression of cysteine aspartic acid protease-3（caspase-3），inducible nitric oxide synthase（iNOS），PPARγ and phosphorylated IκBα（p-IκBα） proteins，and enzyme linked immunosorbent assay（ELISA） was used to detect the levels of inflammatory factors interleukin-6（IL-6） and tumor necrosis factor alpha（TNF-α）. [Results] H/R treatment significantly downregulated PPARγ expression，upregulated Caspase-3，iNOS，and p-IκBα protein expression，and increased IL-6 and TNF-α release. Compared with the H/R group，the Pue group significantly upregulated PPARγ protein，inhibited the nuclear factor κB（NF-κB） pathway，and simultaneously suppressed the expression of apoptosis，oxidative stress-related proteins and inflammatory factors. Mechanistic studies revealed that after knocking down PPARγ，the aforementioned protective effects of Pue were significantly reversed. [Conclusion] Pue effectively inhibits H/R-induced cardiomyocyte apoptosis，oxidative stress and inflammatory responses by regulating the PPARγ/NF-κB signaling pathway，exerting significant cardioprotective effects. |
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