Carbon black (CB) has been demonstrated to have adverse effects on the lung tissue. Few studies explored the effects of CB on the cerebellum, widely recognized to contribute to gait and balance coordination and timing in the motor domain. Some studies have reported that inflammatory response and damaged autophagy are important mechanisms of CB toxicity and can be repaired after the recovery. The present study aimed to determine whether long-term CB exposure could induce the inflammation and damaged autophagy of the cerebellum. The rats were randomly divided into four groups. The control group received the filtered air for 90 days; the carbon black (CB) group received CB particles for 90 days; the recovery (R) group received CB for 90 days and recovered for another 14 days; the recovery control (RC) group received filtered air for 104 days. The purpose of the R group was to test whether neuroinflammation and autophagy could be repaired after short-term recovery. The western blot and immunohistochemistry revealed that long-term CB exposure induced augmented level of pro-inflammatory cytokines (Interleukin-1β, IL-1β; Interleukin-6, IL-6; and Tumor Necrosis Factor-α, TNF-α) and anti-inflammatory cytokine (Interleukin-10, IL-10). The autophagic markers (Beclin1 and LC3) were increased in both CB group and R group. These findings clearly demonstrated that long-term CB exposure induced inflammation and autophagy in the cerebellum, which were not obviously improved after short-term recovery.

炭黑 (CB) 已被证明对肺组织有不利影响。很少有研究探讨 CB 对小脑的影响，人们普遍认为它有助于运动领域的步态和平衡协调与时间。有研究报道炎症反应和受损的自噬是CB毒性的重要机制，恢复后可以修复。本研究旨在确定长期 CB 暴露是否会诱发小脑的炎症和受损的自噬。将大鼠随机分为四组。对照组接受过滤空气90天；炭黑 (CB) 组接受 CB 颗粒 90 天；恢复（R）组接受CB 90天，再恢复14天；恢复控制 (RC) 组接受过滤空气 104 天。R组的目的是测试神经炎症和自噬能否在短期恢复后得到修复。蛋白质印迹和免疫组织化学显示，长期 CB 暴露诱导促炎细胞因子（白介素 1β、IL-1β；白介素 6、IL-6 和肿瘤坏死因子-α、TNF-α）和抗炎细胞因子水平升高。 -炎性细胞因子（白细胞介素10，IL-10）。CB组和R组的自噬标志物（Beclin1和LC3）均升高。这些发现清楚地表明，长期 CB 暴露诱导小脑炎症和自噬，短期恢复后没有明显改善。蛋白质印迹和免疫组织化学显示，长期 CB 暴露诱导促炎细胞因子（白介素 1β、IL-1β；白介素 6、IL-6 和肿瘤坏死因子-α、TNF-α）和抗炎细胞因子水平升高。 -炎性细胞因子（白细胞介素10，IL-10）。CB组和R组的自噬标志物（Beclin1和LC3）均升高。这些发现清楚地表明，长期 CB 暴露诱导小脑炎症和自噬，短期恢复后没有明显改善。蛋白质印迹和免疫组织化学显示，长期 CB 暴露诱导促炎细胞因子（白介素 1β、IL-1β；白介素 6、IL-6 和肿瘤坏死因子-α、TNF-α）和抗炎细胞因子水平升高。 -炎性细胞因子（白细胞介素10，IL-10）。CB组和R组的自噬标志物（Beclin1和LC3）均升高。这些发现清楚地表明，长期 CB 暴露诱导小脑炎症和自噬，短期恢复后没有明显改善。