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Attenuative effects of poncirin against polyethylene microplastics-prompted hepatotoxicity in rats

Journal of King Saud University - Science 2024 4 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Naila Ghafoor, Naila Ghafoor, Tooba Mehar, Tooba Mehar, Moazama Batool, Moazama Batool, Moazama Batool, Muhammad Zaid Salar, Moazama Batool, Muhammad Zaid Salar, Moazama Batool, Muhammad Zaid Salar, Moazama Batool, Moazama Batool, Moazama Batool, Muhammad Zaid Salar, Mohammad Z. Ahmed, Muhammad Zaid Salar, Mohammad Z. Ahmed, Mohammad Z. Ahmed, Usman Atique Usman Atique Muhammad Zaid Salar, Mohammad Z. Ahmed, Mohammad Z. Ahmed, Usman Atique Usman Atique Usman Atique Usman Atique Mohammad Z. Ahmed, Mohammad Z. Ahmed, Usman Atique Usman Atique Usman Atique

Summary

Researchers tested whether poncirin, a natural plant compound, could protect rat livers from damage caused by polyethylene microplastics. They found that microplastic exposure caused significant oxidative stress, inflammation, and liver tissue damage, which poncirin was able to substantially reduce by activating protective antioxidant pathways. The study suggests that natural compounds like poncirin may help counteract some of the harmful effects of microplastic exposure on the liver.

Polymers
Body Systems
Models

Polyethylene microplastics (PE-MPs) are of significant concern due to their widespread use, pervasive persistence in the environment that induce multiple organ damage especially in the liver. Poncirin (PON) is a naturally present flavone with conspicuous pharmacological properties. the current investigation was formulated to ascertain the palliative role of PON against PE-MPs-provoked hepatic dysfunction. Twenty-four male albino rats were randomly divided into four groups: control, PE-MPs-treated (1.5 mg/kg), PE-MPs + PON co-treated (1.5 mg/kg and 20 mg/kg), and PON-treated (20 mg/kg). PE-MPs inebriation markedly lowered the expressions of antioxidant genes and Nrf-2, besides escalating Keap-1 expression. It also decreased antioxidants i.e., glutathione (GSH), glutathione S-transferase (GST), catalase (CAT), glutathione peroxidase (GPx), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), glutathione reductase (GSR) activities, while remarkably upsurged reactive oxygen species (ROS) along with malondialdehyde (MDA) contents. Additionally, a notable escalation was observed in the levels of hepatic serum markers i.e., alkaline phosphatase (ALP), alanine transaminase (ALT) and aspartate aminotransferase (AST). Furthermore, PE-MPs exposure increased the levels of inflammatory biomarkers, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), nuclear factor kappa B (NF-kB), interleukin-1β (IL-1β) levels and cyclooxygenase-2 (COX-2) activities. PE-MPs intoxication augmented the expressions of Caspase-3 and Bax along with decreasing the expression of Bcl-2. Nevertheless, PON treatment notably abated PE-MPs prompted liver injuries owing to its hepatoprotective efficacy. Thus, it may be inferred that PON could be a potential therapeutic option for treating hepatic damage caused by PE-MPs.

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