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Attenuative effects of poncirin against polyethylene microplastics-prompted hepatotoxicity in rats
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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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Researchers investigated whether tamarixetin, a naturally occurring flavonoid, could reduce liver damage caused by polystyrene microplastic exposure in rats. The study found that tamarixetin helped protect against microplastic-induced liver toxicity by activating antioxidant defense pathways, suggesting potential protective effects of certain plant-derived compounds against microplastic-related oxidative stress.
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Reno-protective potential of poncirin against polyethylene microplastics instigated kidney damage in rats via regulating Nrf-2/Keap-1 pathway
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In a rat study, daily exposure to polyethylene microplastics caused kidney damage — elevated creatinine, urea, and injury biomarkers — while a natural plant compound called poncirin partially reversed this damage by activating the Nrf-2/Keap-1 antioxidant defense pathway. While the doses used were high and results need human validation, the study adds to growing evidence that microplastics can harm the kidneys and that dietary antioxidants may offer some protection.
Protective role of poncirin against polyethylene microplastics instigatedcardiac toxicity via regulating Nrf2/keap1 pathway
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Researchers found that exposing rats to polyethylene microplastics caused significant heart damage — including oxidative stress, inflammation, and cell death — by disrupting the Nrf2 antioxidant defense pathway. Supplementing with poncirin, a natural plant flavonoid, substantially protected cardiac tissue by restoring antioxidant activity, suggesting a potential protective role against microplastic-induced heart toxicity.
Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study
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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.
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