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| Activation of alveolar macrophage in rats under different modes of PM2.5 exposure and its mechanism |
| ZHU Li-na1,2, YANG Lin-hui1,2, LIN Ben-cheng2, SHI Yue2, LIU Huan-liang2, XI Zhu-ge2 |
1. College of Oceanography and Ecological Science, Shanghai Ocean University, Shanghai 201306, China;
2. Military Medical Sciences Academy, Academy of Military Sciences, Tianjin 300050, China |
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Abstract To explore the effects of two distinct PM2.5 exposure patterns on alveolar macrophages activation in rats, namely long-term low-concentration continuous exposure and high-concentration intermittent exposure. The rats were divided into three groups: a blank control group, a 4-fold concentrated PM2.5 continuous exposure group (4FC group) and an 8-fold concentrated PM2.5 intermittent exposure group (8-FI group). Exposure was facilitated using a whole-body dynamic exposure system over 84 days. The pathological changes in lung tissue were observed using hematoxylin and eosin (HE) staining. The oxidative stress indexes in bronchoalveolar lavage fluid (BALF) were determined by colorimetry. The mRNA levels of M2 polarization markers in lung tissue were measured by RT-qPCR. The protein expression levels related to the PI3K/AKT and JAK1/STAT6 signaling pathways, which are involved in macrophage activation, were assessed by Western blot. The results showed that, compared with the control group, the experimental group showed obvious symptoms of lung injury, accompanied by a significant elevation oxidation index in BALF. The mRNA levels of M2polarization marker and the protein expression of PI3K/AKT and JAK1/STAT6 signaling pathways were significantly upregulated, with the 8FI group showing higher levels than the 4FC group. These findings demonstrate that long-term inhalation of PM2.5 can promote the activation of alveolar macrophages via the stimulation of the PI3K/AKT and JAK1/STAT6 signaling pathways, ultimately leading to lung injury. And intermittent inhalation of PM2.5 with high concentration has a more serious effect on alveolar macrophages activation than continuous inhalation to low concentration. At the cellular level, the effect of PM2.5 on alveolar macrophages activation and related signaling pathways were further verified.
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Received: 30 July 2024
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