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    Article

    Resveratrol Suppresses “Metabolic Memory” by Inhibiting Inflammation and Apoptosis Through the ROS/TXNIP/NLRP3 Signaling Pathway

    Tingting Jiang1,2,3,4, 4 Junxiang Gu1,2,3,4, Qing Chang1,2,3,4★★ Corresponding author

    1. 1Department of Ophthalmology, Eye and ENT Hospital, Fudan University, Shanghai, CHINA.
    2. 2Shanghai Key Laboratory of Visual, Impairment and Restoration, Shanghai, CHINA.
    3. 3Key Laboratory of Myopia of National Health Commission, Fudan University, Shanghai, CHINA.
    4. 4Key Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai, China.

    CORRESPONDENCE

    Qing Chang

    Department of Ophthalmology, Eye and ENT Hospital, Fudan University, Shanghai, CHINA.

    qngchang@aliyun.com

    Received: 22-08-2023; Accepted: 18-12-2023.

    Volume 20, Issue 3 · pp. 898–907 · PUBLISHED 2024 · DOI: 10.1177/09731296241229242

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Aim: This research endeavored to explore the impact and underlying mechanisms of resveratrol on the phenomenon of “metabolic memory” in cultured human retinal vascular endothelial cells (HRVECs) under high-glucose (HG) conditions. Materials and Methods: According to the glucose level and treatment, cultured HRVECs were divided into seven groups: normal glucose (NG), HG, high glucose followed by NG (HN), mannitol (Man), resveratrol, thioredoxin-interacting protein (TXNIP)-small interfering ribonucleic acid (siRNA), and N-acetylcysteine (NAC). The expression levels of TXNIP, nucleotide oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, intercellular adhesion molecule 1 (ICAM-1), caspase-1, interleukin-1β (IL-1β), B-cell lymphoma 2 (Bcl-2), caspase-3, and Bcl-2-associated X (BAX), as well as reactive oxygen species (ROS) production, were measured. Cell apoptosis was assessed through a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Results: In HRVECs from the HG group, expression levels of TXNIP, NLRP3, caspase-1, ICAM-1, and IL-1β were upregulated. However, in the HN group, the above upregulations were not reversed. After the administration of resveratrol, the expression levels of TXNIP, NLRP3, and other inflammatory cytokines were significantly reduced. Resveratrol mitigated the elevated ROS production induced by HG conditions. In the NAC group, the expression of TXNIP and inflammatory cytokines was downregulated. TXNIP-siRNA treatment showed similar effects. Resveratrol inhibited apoptosis as well as reversed the downregulation of BCL-2 and the upregulation of caspase-3 and BAX induced by HG conditions. Conclusion: Resveratrol mitigated the HG-induced phenomenon of “metabolic memory” by inhibiting inflammation and apoptosis via modulation of the ROS/TXNIP/NLRP3 signaling pathway in cultured HRVECs. Therefore, resveratrol may have therapeutic potential to treat diabetic retinopathy and related metabolic memory complications.

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      Jiang, T., Gu, J., & Chang, Q. (2024). Resveratrol Suppresses “Metabolic Memory” by Inhibiting Inflammation and Apoptosis Through the ROS/TXNIP/NLRP3 Signaling Pathway. Pharmacognosy Magazine, 20(3), 898–907. https://doi.org/10.1177/09731296241229242