上睑下垂
背景(考古学)
肌酐
肾
川地68
血尿素氮
药理学
细胞凋亡
化学
促炎细胞因子
医学
内科学
生物
炎症
程序性细胞死亡
生物化学
免疫组织化学
古生物学
作者
Qihui Kuang,Likun Gao,Lixiang Feng,Xi Xiong,Jian Yang,Wei Zhang,Li‐Zhi Huang,Lili Li,Pengfei Luo
摘要
Abstract The widespread presence of microplastics (MPs) in the environment poses a significant threat to biological survival and human health. However, our understanding of the toxic effects of MPs on the kidneys remains limited. This study aimed to investigate the underlying mechanism of the toxic effects of MPs on the kidneys using an ischemia–reperfusion (IR) mouse model. Four‐week‐old ICR mice were exposed to 0.5 μm MPs for 12 weeks prior to IR injury. The results showed that MPs exposure could aggravate the IR‐induced damage to renal tubules and glomeruli. Although there were no significant changes in blood urea nitrogen and serum creatinine levels 7 days after IR, MPs treatment resulted in a slight increase in both parameters. In addition, the expression levels of inflammatory factors (MCP‐1 and IL‐6) at the mRNA level, as well as macrophage markers (CD68 and F4/80), were significantly higher in the MPs + IR group than in the Sham group after IR. Furthermore, MPs exposure exacerbated IR‐induced renal fibrosis. Importantly, the expression of pyroptosis‐related genes, including NLRP3, ASC, GSDMD, cleaved caspase‐1, and IL‐18, was significantly upregulated by MPs, indicating that MPs exacerbate pyroptosis in the context of renal IR. In conclusion, our findings suggest that MPs exposure can aggravate renal IR‐induced pyroptosis by activating NLRP3‐GSDMD signaling.
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