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Protective Effects of Cysteine-Rich Peptides against Microplastics-Induced Cardiorenal Injury via Nrf2/HO-1 and Bax/Cytc Pathways
Summary
Researchers found that microplastic exposure caused significant heart and kidney injury in mice, as shown by elevated biomarkers of organ damage. Treatment with cysteine-rich peptides reduced these injury markers by more than 30%, working through activation of protective antioxidant pathways and suppression of cell-death signaling. The study suggests that certain bioactive peptides may help counteract organ damage associated with microplastic exposure.
This study investigated the protective effects of cysteine (Cys)-rich peptides on microplastic (MPs)-induced cardiorenal injury in C57BL/6 mice. Our results indicated that MPs exposure caused significant cardiorenal injury, as evidenced by >60% increases in α1-microglobulin (α1-MG), uric acid (UA), atrial natriuretic peptide (ANP), and monocyte chemoattractant protein-1 (MCP-1) (p < 0.001). Both Cys-rich hydrolysate (AMP-CA) and the peptide LGNGCP (LP-6) exerted protective effects against MPs-induced cardiorenal injury, as evidenced by >30% reductions in α1-MG, UA, and ANP (p < 0.001). Furthermore, AMP-CA and LP-6 restored the impaired activities of antioxidant enzymes. Further investigation revealed that AMP-CA and LP-6 significantly upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), while suppressing the expression of Bcl-2-associated X protein (Bax) and cytochrome c (Cytc) in MPs-exposed mice (p < 0.05). Our findings suggest that Cys-rich peptides ameliorate MPs-induced cardiorenal injury by activating the Nrf2/HO-1 pathway and inhibiting the Bax/Cytc pathway.
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