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Sakuranetin counteracts polyethylene microplastics induced nephrotoxic effects via modulation of Nrf2/Keap1 pathway

Journal of King Saud University - Science 2024 4 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Akbar Ali, Fatima Amin, Moazama Batool, Aisha Khatoon, Zubair Ahmad, Usman Atique

Summary

Researchers found that polyethylene microplastics caused kidney damage in rats by increasing oxidative stress and disrupting a key protective cellular pathway. However, when the natural plant compound sakuranetin was administered alongside the microplastics, it significantly reduced the kidney damage by restoring antioxidant defenses. The study suggests that certain natural compounds may help counteract some of the harmful effects of microplastic exposure on organ health.

Polymers
Body Systems
Models

Polyethylene microplastics (PEMPs) are widely distributed in environment and exerts deleterious effects on animal as well as human health. Sakuranetin (SKN) is a natural flavonoid that manifests profound therapeutic potential. Albino rats (n = 24) were partitioned into 4 groups i.e., Control, PEMPs 1.5 mg/kg, PEMPs 1.5 mg/kg + SKN 10 mg/kg and SKN 10 mg/kg administered group. After 30 days of treatment, our results revealed that PEMPs exposure reduced nuclear factor erythroid 2–related factor 2 (Nrf-2) and antioxidant genes while enhancing the expression of kelch-like ECH-associated protein 1(Keap-1). Besides, PEMPs intoxication reduced the level of renal biomarkers i.e., creatinine clearance and increased the level of creatinine, urea, neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). Additionally, it lessened the activities of glutathione S-transferase (GST), superoxide dismutase (SOD), glutathione reductase (GSR), catalase (CAT), glutathione peroxidase (GPx) and heme oxygenase-1 (HO-1) whereas the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) were increased. Conversely, it increased the levels of nuclear factor-kappa B (NF-kB), tumor necrosis factor-alpha (TNF-a), interleukin-1beta (IL-1b) and IL-6 as well as escalated the activity of cyclooxygenase-2 (COX-2). Furthermore, the expression of bcl-2-associated X protein (Bax) and caspase-3 were elevated, while the expression of B-cell lymphoma 2 (Bcl-2) was lowered. However, SKN treatment significantly (P < 0.05) restored aforementioned renal impairments. Therefore, it is proposed that SKN may be applied as a nephroprotective agent against the PEMPs-prompted renal toxicity.

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