Antioxidant Potential of Mangifera foetida Bark, Mangifera foetida Leaves, and Cinnamomum burmanii Leaves Extract in Mitigating Nanoplastic-Induced Toxicity and Disruption of Glycolipid Metabolism.

Pollution from plastic waste has become an urgent issue, requiring solutions to prevent and mitigate diseases caused by plastic waste, particularly those involving nanoplastics (NP). This study specifically focused on investigating the exogenous antioxidant activity of three plant extracts: Mangifera foetida bark (MFB), Mangifera foetida leaves (MFL), and Cinnamomum burmanii leaves (CBL), to enhance the body's defense system and reduce the risk of Type II diabetes. Twenty-five rats (Rattus norvegicus) were randomly assigned to five groups: normal control, negative control, and three treatments that received different plant extracts (200 mg/kg of MFB, MFL, and CBL, respectively) after being exposed to 10 μL/kg NP for 30 days. According to confocal microscopy analysis, NPs were observed entering cells and localizing in the nucleolus more than in the cytoplasmic hepatocyte. This study found that the administration of the plant extract could reduce the level of the proapoptotic enzyme not through the intrinsic pathway but via the extrinsic pathway. Administration of MFB, MFL, and CBL could reduce Caspase-3 significantly (1.07 ± 0.05, 1.03 ± 0.08, 1.05 ± 0.10 ng/L, respectively). This effect is mediated by the upregulation of genes related to glycolipid metabolism, including AKT2, GLUT2, PI3K, FAS, PEPCK, and PK. Administration of MFL significantly upregulated the expression levels of AK2, GLUT2, PI3K, and PK genes compared to the negative control. Administration of CBL extract enhanced the percentage of normal hepatocytes and the diameter of the central vein and decreased the percentage of necrosis, swelling, and the number of Kupffer cells. All treatment groups showed a slight decrease in the level of SGOT and SGPT. Thus, plant extracts could be effective materials exhibiting exogenous antioxidant activity against NP, directly inhibiting proapoptotic signals and regulating glycolipid metabolism. These extracts could be further developed as a preventive or therapeutic strategy to address NP exposure in environmental and clinical settings.