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Background <p>Acrylamide (ACR) is an environmental and dietary contaminant widely known to induce imbalance in several biological systems, including oxidative stress, inflammation, and metabolic dysregulation. This study investigated the protective effects of gypenosides (GYP) against ACR-induced toxicity in human retinal pigment epithelial (RPE) cells and zebrafish embryos.</p> Methods and Results <p> RPE cells and zebrafish embryos were treated with ACR, or ACR + GYP; the levels of reactive oxygen species (ROS), antioxidative enzymes, proinflammatory cytokines, and lipids were measured using biochemical approaches. Our findings demonstrate that ACR exposure significantly elevated ROS production, increased lipid peroxidation, suppressed antioxidant defences, and upregulated pro-inflammatory cytokines in RPE cells. Additionally, ACR disrupted lipid metabolism, significantly increasing cellular cholesterol, triglyceride, and phospholipid levels while altering cholesterol metabolism gene expression. Co-treatment with GYP effectively mitigated ACR-induced oxidative stress by normalising ROS levels, restoring antioxidant enzyme activities, and upregulating antioxidant gene expression. GYP also attenuated the ACR-triggered inflammatory response, significantly downregulating the expression of proinflammatory cytokine genes. Furthermore, GYP normalised lipid profiles and modulated lipid-related gene expression disrupted by ACR exposure. Parallel zebrafish experiments corroborated these protective effects. ACR exposure led to delayed hatching, impaired cardiac function, increased ROS production, and neutral lipid accumulation. These adverse effects were markedly ameliorated by GYP co-treatment, which reduced oxidative stress, downregulated proinflammatory markers, and restored lipid homeostasis.</p> Conclusion <p>The results highlighted that GYP, as a natural protective agent against ACR-induced cellular and metabolic toxicity in both in vitro and in vivo models, exhibited antioxidative, anti-inflammatory, and lipid-regulatory properties.</p>

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Gypenosides mitigate acrylamide-induced oxidative stress, inflammation and lipid metabolic dysregulation in retinal pigment epithelial cells and in zebrafish embryos

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月18日

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  • Gabriel Mbuta Tchiveleketea,
  • Michal R. Baran,
  • Manuel Evaristo Augusto Vilengalenga,
  • Sebastião Tumitânguab,
  • James Reilly,
  • Xinhua Shua

摘要

Background

Acrylamide (ACR) is an environmental and dietary contaminant widely known to induce imbalance in several biological systems, including oxidative stress, inflammation, and metabolic dysregulation. This study investigated the protective effects of gypenosides (GYP) against ACR-induced toxicity in human retinal pigment epithelial (RPE) cells and zebrafish embryos.

Methods and Results

RPE cells and zebrafish embryos were treated with ACR, or ACR + GYP; the levels of reactive oxygen species (ROS), antioxidative enzymes, proinflammatory cytokines, and lipids were measured using biochemical approaches. Our findings demonstrate that ACR exposure significantly elevated ROS production, increased lipid peroxidation, suppressed antioxidant defences, and upregulated pro-inflammatory cytokines in RPE cells. Additionally, ACR disrupted lipid metabolism, significantly increasing cellular cholesterol, triglyceride, and phospholipid levels while altering cholesterol metabolism gene expression. Co-treatment with GYP effectively mitigated ACR-induced oxidative stress by normalising ROS levels, restoring antioxidant enzyme activities, and upregulating antioxidant gene expression. GYP also attenuated the ACR-triggered inflammatory response, significantly downregulating the expression of proinflammatory cytokine genes. Furthermore, GYP normalised lipid profiles and modulated lipid-related gene expression disrupted by ACR exposure. Parallel zebrafish experiments corroborated these protective effects. ACR exposure led to delayed hatching, impaired cardiac function, increased ROS production, and neutral lipid accumulation. These adverse effects were markedly ameliorated by GYP co-treatment, which reduced oxidative stress, downregulated proinflammatory markers, and restored lipid homeostasis.

Conclusion

The results highlighted that GYP, as a natural protective agent against ACR-induced cellular and metabolic toxicity in both in vitro and in vivo models, exhibited antioxidative, anti-inflammatory, and lipid-regulatory properties.