The Effect of Hyperoside on Glutathione Reductase (GR) Activity in Mice Liver

Abstract

Intruduction: Glutathione reductase plays a significant role in the cellular response to oxidative stress, particularly in the context of maintaining redox homeostasis and facilitating the detoxification of reactive oxygen species (ROS). [1] The protective mechanism of hyperoside appears to involve the activation of the Nrf2 transcription factor, which is crucial for the expression of various antioxidant genes, including those coding for antioxidant enzymes. [2] The aim of the current study was to evaluate the effect of hyperoside on the GR activity in mice liver after aluminium consumption. Materials and methods: Experiments were conducted on 4-6 weeks old mice (20-25g), n-8. Mice were divided into four groups: control, hyperoside-treated, aluminum-treated, and aluminum-hyperoside-treated. Aluminum was injected into the abdominal cavity. To assess the effects of the treatments, glutathione reductase (GR) activity was measured spectrophotometrically. Statistical analysis was performed using Student's t-test, and p-values were calculated to determine significance. A p-value of less than 0.05 was considered statistically significant. Results and discussion: Aluminum exposure significantly reduced glutathione reductase (GR) activity in liver tissue compared to the control group (p <0.05), indicating oxidative stress. The aluminum-hyperoside combination, however, significantly mitigated this reduction, suggesting that hyperoside may help protect against aluminum-induced oxidative damage (p<0.05). Hyperoside, known for its antioxidant properties, may support GR activity by enhancing cellular defense mechanisms or directly neutralizing reactive oxygen species. These findings align with previous studies on flavonoids as protective agents against oxidative stress, one of which indicated that hyperoside significantly protects mouse livers from damage and inflammation, which are often associated with oxidative stress. [3] While these results highlight hyperoside's potential, further research is needed to explore its precise mechanisms, optimal dosage, and broader effects on oxidative stress markers. Conclusions: The findings of this study suggest that hyperoside may counteract aluminum-induced reductions in glutathione reductase activity, indicating a potential protective role against oxidative stress. How-ever, further research is required to fully understand its therapeutic potential, optimal dosage, and underlying mechanisms.