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Palliative potential of robinetin to avert polystyrene microplastics instigated pulmonary toxicity in rats

Journal of King Saud University - Science 2024 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Muhammad Faisal Hayat, Muhammad Faisal Hayat, Anees Ur Rahman, Anees Ur Rahman, Moazama Batool, Moazama Batool, Moazama Batool, Moazama Batool, Amara Tahir, Amara Tahir, Moazama Batool, Moazama Batool, Moazama Batool, Moazama Batool, Usman Atique Usman Atique Zubair Ahmed, Zubair Ahmed, Usman Atique Usman Atique Usman Atique Usman Atique Zubair Ahmed, Usman Atique Zubair Ahmed, Usman Atique Usman Atique

Summary

Researchers investigated whether the flavonoid compound robinetin could protect against lung damage caused by polystyrene microplastic exposure in rats. They found that robinetin supplementation reduced oxidative stress markers and inflammatory responses in lung tissue that had been damaged by microplastic ingestion. The study suggests that certain natural compounds may help mitigate some of the harmful effects of microplastic exposure on respiratory tissues.

Polymers
Models

Polystyrene microplastics (PSMPs) are noxious environmental pollutants that pose a significant threat to vital body organs including the lungs. Robinetin (ROB) is a flavonoid which demonstrates various pharmacological potentials. This trial was designed to assess the protective ability of ROB to avert PSMPs provoked pulmonary toxicity in rats. Twenty-four rats were divided into four groups i.e., control, PSMPs (0.1 mg/kg), PSMPs (0.1 mg/kg) + ROB (30 mg/kg) and ROB (30 mg/kg) only supplemented group. PSMPs exposure led to a notable reduction in the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GSR) as well as GSH contents while causing a pronounced elevation in the concentration of MDA and ROS. Furthermore, PSMPs significantly augmented the levels of myeloperoxidase (MPO), macrophages, neutrophils, and lymphocytes in BALF. Moreover, the levels of IL-1β, TNF-α, NF-κB, IL-6 and COX-2 activities were increased following the PSMPs exposure. Nonetheless PSMPs remarkably decreased Bcl-2 levels, coupled with an escalation in Caspase-9, Caspase-3 and Bax levels. Despite this, severe histological alterations were observed in lungs tissues after PSMPs provision. Nevertheless, ROB provision markedly protected the lungs via regulating aforementioned dysregulations. This investigation validated the shielding strength of ROB to counteract PSMPs caused pulmonary toxicity.

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