The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China.
Department of Endocrinology, Guangdong Geriatrics Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, China.
Dis Markers. 2023 Feb 18;2023:2516472. doi: 10.1155/2023/2516472. eCollection 2023.
Polystyrene microplastics (mic-PS) have become harmful pollutants that attracted substantial attention about their potential toxicity. Hydrogen sulfide (HS) is the third reported endogenous gas transmitter with protective functions on numerous physiologic responses. Nevertheless, the roles for mic-PS on skeletal systems in mammals and the protective effects of exogenous HS are still indistinct. Here, the proliferation of MC3T3-E1 cell was analyzed by CCK8. Gene changes between the control and mic-PS treatment groups were analyzed by RNA-seq. The mRNA expression of bone morphogenetic protein 4 (Bmp4), alpha cardiac muscle 1 (Actc1), and myosin heavy polypeptide 6 (Myh6) was analyzed by QPCR. ROS level was analyzed by 2',7'-dichlorofluorescein (DCFH-DA). The mitochondrial membrane potential (MMP) was analyzed by Rh123. Our results indicated after exposure for 24 h, 100 mg/L mic-PS induced considerable cytotoxicity in the osteoblastic cells of mice. There were 147 differentially expressed genes (DEGs) including 103 downregulated genes and 44 upregulated genes in the mic-PS-treated group versus the control. The related signaling pathways were oxidative stress, energy metabolism, bone formation, and osteoblast differentiation. The results indicate that exogenous HS may relieve mic-PS toxicity by altering , , and mRNA expressions associated with mitochondrial oxidative stress. Taken together, this study demonstrated that the bone toxicity effects of mic-PS along with exogenous HS have protective function in mic-PS-mediated oxidative damage and mitochondrial dysfunction in osteoblastic cells of mice.
聚苯乙烯微塑料（mic-PS）已成为有害污染物，其潜在毒性引起了广泛关注。硫化氢（HS）是第三种被报道的内源性气体递质，对许多生理反应具有保护作用。然而，mic-PS 对哺乳动物骨骼系统的作用以及外源性 HS 的保护作用尚不清楚。在这里，通过 CCK8 分析 MC3T3-E1 细胞的增殖。通过 RNA-seq 分析对照和 mic-PS 处理组之间的基因变化。通过 QPCR 分析骨形态发生蛋白 4（Bmp4）、α 型心肌肌球蛋白 1（Actc1）和肌球蛋白重链 6（Myh6）的 mRNA 表达。通过 2'，7'-二氯荧光素（DCFH-DA）分析 ROS 水平。通过 Rh123 分析线粒体膜电位（MMP）。我们的结果表明，暴露 24 小时后，100mg/L 的 mic-PS 在小鼠成骨细胞中引起了相当大的细胞毒性。在 mic-PS 处理组与对照组相比，有 147 个差异表达基因（DEGs），包括 103 个下调基因和 44 个上调基因。相关信号通路为氧化应激、能量代谢、骨形成和成骨细胞分化。结果表明，外源性 HS 可能通过改变与线粒体氧化应激相关的 、 和 mRNA 表达来缓解 mic-PS 毒性。综上所述，本研究表明，外源性 HS 可以减轻 mic-PS 介导的氧化损伤和小鼠成骨细胞线粒体功能障碍，对 mic-PS 的骨毒性具有保护作用。
