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