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Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study

Journal of King Saud University - Science 2023 Score: 40 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Ali Hamza, Ali Hamza, Ali Hamza, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Ali Hamza, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Nimra Ather, Ali Hamza, Ali Hamza, Nimra Ather, Ali Hamza, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Ali Hamza, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Muhammad Umar Ijaz, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Ali Hamza, Asma Ashraf, Mikhlid H. Almutairi, Asma Ashraf, Ali Hamza, Mikhlid H. Almutairi, Mikhlid H. Almutairi, Ali Hamza, Usman Atique Usman Atique Asma Ashraf, Asma Ashraf, Usman Atique Usman Atique Muhammad Umar Ijaz, Asma Ashraf, Usman Atique Usman Atique Usman Atique Usman Atique Usman Atique

Summary

Exposure to polystyrene nanoplastics caused significant liver damage in rats, including oxidative stress, inflammation, and cell death, along with elevated liver enzymes that are markers of liver injury in clinical settings. Treatment with sinensetin — a natural plant flavonoid — substantially reversed these effects, restoring antioxidant enzyme activity and reducing inflammatory markers. The findings establish a potential protective role for natural compounds against nanoplastic-induced organ toxicity and illuminate the mechanisms by which nanoplastics harm the liver.

Polymers
Body Systems
Models

Polystyrene nanoplastics (PS-NPs) are environmental pollutants that induce oxidative stress (OS) in multiple organs particularly, liver. Sinensetin (SNS) is a naturally present flavones that shows diverse pharmaceutical properties i.e., anti-oxidant, anti-inflammatory and anti-apoptotic. Therefore, the present study was designed to evaluate the therapeutic role of SNS against PS-NPs induced hepatotoxicity. 48 rats were distributed into 4 groups i.e., control, PS-NPs (50 µgkg-1) treated, PS-NPs + SNS (50 µgkg-1 + 20 mgkg-1) co-treated and only SNS (20 mgkg-1) treated group. PS-NPs intoxication reduced the activities of catalase (CAT), glutathione-S-transferase (GST), superoxide dismutase (SOD), glutathione peroxidases (GPx) glutathione reductase (GSR) and glutathione (GSH) level, whereas increasing the levels of ROS and MDA. Additionally, PS-NPs increased the levels of liver serum enzymes i.e., alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Moreover, the level of inflammatory makers such as nuclear factor-kappa B (NF-κB), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2) activity were increased following the PS-NPS exposure. The intoxication of PS-NPs elevated Caspase-3, Bax and Caspase-9 levels, besides reducing the Bcl-2 level. Furthermore, the exposure of PS-NPs induced significant histopathological damages in hepatic tissue of rats. However, the supplementation of SNS considerably improved the PS-NPs induced damages as well as histological changes due to its hepatoprotective, anti-inflammatory, anti-apoptotic and anti-oxidant nature.

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