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聚烯微塑料通过涉及NF-κB,ERK/p38 MAPK和sirtuin-1的炎症和氧化途径加剧实验性慢性病

Sumaya Beegam¹, Suhail Al-Salam², Nur Elena Zaaba¹

¹Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 15551, Al Ain, United Arab Emirates.

|December 8, 2025

概括

聚乙烯微塑料 (PSMPs) 在患有慢性病 (CKD) 的小鼠中恶化损伤. 暴露于PSMPs增加了炎症,氧化应激和纤维化,突出显示了病患者的风险.

科学领域:

环境科学环境科学
毒理学毒理学毒理学
腎臟病學 (nephrology) 是一種醫學.

背景情况:

人类暴露于微塑料 (MPs) 的情况很普遍,主要是通过摄入.
聚烯MPs (PSMPs) 在食物和水中被检测到,并可能导致脏变化.
对于PSMPs对慢性病 (CKD) 的影响尚不清楚.

研究的目的:

为了研究PSMPs对氨酸诱导的CKD的小鼠模型的影响.
确定PSMP是否会在已确定的CKD中加剧功能障碍和损伤.

主要方法:

通过使用腺素诱导CKD的小鼠,并暴露在2微米PSMP (0.2或0.4毫克/天) 中4周.
评估了功能,组织学和炎症的分子标志物,氧化应激,DNA损伤和亡.
分析了NF-κB和MAPK通路的激活,以及Sirtuin-1的表达.

主要成果:

在健康小鼠中,PSMPs损害了功能 (减少肌素清除量,增加血尿素/肌素,白尿).
在CKD小鼠中,PSMP显著恶化了功能障碍,并加剧了管管损伤,炎症和纤维化.
暴露于PSMP会增加脏炎症,氧化应激,DNA损伤和亡,激活NF-κB和ERK/p38 MAPK通路,同时抑制Sirtuin-1.

结论:

暴露于PSMPs会通过促进炎症,氧化应激和纤维化而加剧慢性病中的损伤.
激活NF-κB和ERK/p38信号,以及抑制Sirtuin-1,可以调解PSMP诱导的损伤.
这些发现强调了微塑料暴露对病患者的潜在健康风险.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.慢性脏疾病慢性脏疾病造成的DNA损伤是DNA损伤.纤维化纤维化纤维化炎症炎症是一种炎症.微塑料是一种微塑料.

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