Antioxidant and Anti-Inflammatory Mechanisms in Rodent Models

Rodent models have long served as indispensable tools for elucidating the cellular and molecular underpinnings of oxidative stress and inflammation, two interlinked processes that contribute to a wide range of pathological conditions including hepatic injury, nephrotoxicity and systemic inflammatory disorders. In these models, an imbalance between reactive oxygen species (ROS) production and the capacity of endogenous antioxidant defences—such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)—leads to lipid peroxidation, protein oxidation and DNA damage. Concurrently, activation of inflammatory cascades mediated by nuclear factor kappa-B (NF-κB), mitogen-activated protein kinases and pro-inflammatory cytokines (for example tumour necrosis factor-α and interleukin-1β) exacerbates tissue injury. Recent research has focused on phytochemical and synthetic agents that enhance antioxidant enzyme activity, scavenge free radicals and suppress inflammatory mediators. By restoring redox homeostasis and down-regulating pro-inflammatory pathways, such interventions demonstrate the potential to protect against chemically induced organ damage and to inform the development of novel therapeutics aimed at human diseases marked by oxidative stress and inflammation.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Antioxidant and Anti-Inflammatory Mechanisms in Rodent Models publication trend

The graph below shows the total number of articles in antioxidant and anti-inflammatory mechanisms in rodent models across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive oxygen species (ROS): Chemically reactive oxygen-containing molecules capable of damaging cellular components.

Superoxide dismutase (SOD): An enzyme that catalyses conversion of superoxide radicals into oxygen and hydrogen peroxide.

Glutathione peroxidase (GPx): An enzyme that reduces hydrogen peroxide and organic peroxides using reduced glutathione.

Lipid peroxidation: Oxidative degradation of lipids leading to cell membrane damage and dysfunction.

Nuclear factor kappa-B (NF-κB): A transcription factor that regulates expression of genes involved in inflammation and immune responses.

Cytokines: Small signalling proteins released by cells to regulate immune and inflammatory processes.

References

1. Phytochemical, antioxidant and hepatoprotective effects of Alnus nitida bark in carbon tetrachloride challenged Sprague Dawley rats. BMC Complementary Medicine and Therapies (2016).
2. CCl4 induced genotoxicity and DNA oxidative damages in rats: hepatoprotective effect of Sonchus arvensis. BMC Complementary Medicine and Therapies (2014).
3. Evaluation of antioxidant, anti-inflammatory, analgesic and antipyretic activities of the stem bark of Sapindus mukorossi. BMC Complementary Medicine and Therapies (2017).