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Upcycling PET Waste into Novel Bis-1,3,4-Oxadiazole Scaffolds as Promising Anti-Inflammatory Agents: Synthesis, Biological Evaluation, and Molecular Docking
Summary
Scientists found a clever way to turn plastic water bottle waste (PET) into new compounds that fight inflammation, potentially reducing plastic pollution while creating useful medicines. In lab and animal tests, some of these plastic-derived compounds worked even better than common anti-inflammatory drugs like indomethacin and celecoxib, with fewer signs of tissue damage. While this research is still early-stage (tested in rats, not humans), it points to an exciting way to recycle plastic waste into safer pain and inflammation treatments instead of letting it pollute our environment.
Abstract Upcycling polyethylene terephthalate (PET) waste into high-value intermediates offers a sustainable approach to reducing plastic pollution and dependence on fossil-derived feedstocks. Here, terephthalic acid recovered from PET waste was used as a sustainable building block to synthesize a series of 2-(1,3,4-oxadiazolylsulfanyl)-based derivatives, including N-(aryl)acetamides 10a–h, acetates 12a,b, acetonitrile 12c, benzyl 12d, or 1-phenylethanone 12e as promising anti-inflammatory candidates. Compounds 10a−h and 12a−e were developed as potential anti-inflammatory agents with improved safety profiles. The inhibitory properties of these compounds toward cyclooxygenase isoforms COX-1 and COX-2 were assessed in vitro, using celecoxib and indomethacin as benchmarks. The five lead compounds, selected for their strong COX-2 inhibition, were evaluated in vivo using the carrageenan-induced paw edema model in rats. Subsequently, molecular docking was conducted to evaluate the binding modes of compounds 10c and 10e–h within the COX-2 isoenzyme-binding pocket (PDB: 3LN1), revealing interactions consistent with their observed inhibitory potencies. Compounds 10g and 10f showed greater edema inhibition than indomethacin. Compound 10f was significantly more active than both indomethacin and celecoxib. Histopathological analysis confirmed that 10g and 10f significantly reduced inflammation, while preserving the glandular mucosal and submucosal architecture in the examined tissue.