Ximin Chen1, Yuexiao Chen1, Yuan Chen1, Xin Wang2, Mei He3. 1. Beijing Institute of Nutritional Sources, Beijing, China. 2. Beijing Institute of Nutritional Sources, Beijing, China. wangxin@bonnysci.com. 3. Beijing Institute of Nutritional Sources, Beijing, China. hemei2003@163.com.
Abstract
BACKGROUND: Particulate matter (PM) is the sum of organic and inorganic substances suspended in air. Particles with a diameter equal to or smaller than 2.5 μm (PM2.5) can induce extensive oxidative stress damage in lung tissues. Lutein can prevent oxidative stress and the production of pro-inflammatory cytokines. However, its role in lung injury induced by PM2.5 is still unclear. This study used lutein to intervene in lung injury induced by PM2.5 in rats to confirm the protective function of lutein in PM2.5- induced lung injury. METHODS: A total of 80 rats were divided into five groups according to body weight (bw). Rats in the blank control group and the PM2.5 exposure group were treated with normal saline. The low-, medium-, and high-dose lutein groups were treated with 12.5, 25.0, and 50.0 mg/kg·bw lutein continuously for 28 days. In addition, on days 22-28, 10 mg/kg PM2.5 was introduced by intratracheal instillation into the PM2.5 exposure group and all lutein dose groups continuously for 7 days to establish PM2.5 injury models. Lung tissues were collected and subjected to hematoxylin-eosin (HE) staining to observe histomorphological changes. Bronchoalveolar lavage fluid (BALF) was collected to detect the expression of cell damage indicators including lactate dehydrogenase (LDH), acidic phosphatase (ACP), alkaline phosphatase (AKP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). In addition, the levels of serum oxidative stress indicators in rats, including methane dicarboxylic aldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide synthase (NOS), and 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as cytokines, including IL-6, IL-8, and TNF-α, were analyzed. RESULTS: Lung tissues of rats after PM2.5 exposure exhibited different degrees of pathological changes. In serum, oxidative damage indicators MDA, NOS, and 8-OHdG and inflammatory cytokines IL-6, IL-8, and TNF-α significantly increased whereas GSH levels significantly decreased (P<0.05). In BALF, cell damage indicators ACP and AKP and inflammatory cytokines IL-6, IL-8, and TNF-α all increased (P<0.05). After lutein intervention, oxidative damage and cellular inflammatory cytokines in serum and BALF all significantly decreased (P<0.05) whereas serum GSH levels increased (P<0.05). CONCLUSIONS: PM2.5 caused significant oxidative damage and inflammatory injury in rat lungs. Lutein alleviated these effects, playing a protective role in lung tissues.
BACKGROUND: Particulate matter (PM) is the sum of organic and inorganic substances suspended in air. Particles with a diameter equal to or smaller than 2.5 μm (PM2.5) can induce extensive oxidative stress damage in lung tissues. Lutein can prevent oxidative stress and the production of pro-inflammatory cytokines. However, its role in lung injury induced by PM2.5 is still unclear. This study used lutein to intervene in lung injury induced by PM2.5 in rats to confirm the protective function of lutein in PM2.5- induced lung injury. METHODS: A total of 80 rats were divided into five groups according to body weight (bw). Rats in the blank control group and the PM2.5 exposure group were treated with normal saline. The low-, medium-, and high-dose lutein groups were treated with 12.5, 25.0, and 50.0 mg/kg·bw lutein continuously for 28 days. In addition, on days 22-28, 10 mg/kg PM2.5 was introduced by intratracheal instillation into the PM2.5 exposure group and all lutein dose groups continuously for 7 days to establish PM2.5 injury models. Lung tissues were collected and subjected to hematoxylin-eosin (HE) staining to observe histomorphological changes. Bronchoalveolar lavage fluid (BALF) was collected to detect the expression of cell damage indicators including lactate dehydrogenase (LDH), acidic phosphatase (ACP), alkaline phosphatase (AKP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). In addition, the levels of serum oxidative stress indicators in rats, including methane dicarboxylic aldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide synthase (NOS), and 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as cytokines, including IL-6, IL-8, and TNF-α, were analyzed. RESULTS: Lung tissues of rats after PM2.5 exposure exhibited different degrees of pathological changes. In serum, oxidative damage indicators MDA, NOS, and 8-OHdG and inflammatory cytokines IL-6, IL-8, and TNF-α significantly increased whereas GSH levels significantly decreased (P<0.05). In BALF, cell damage indicators ACP and AKP and inflammatory cytokines IL-6, IL-8, and TNF-α all increased (P<0.05). After lutein intervention, oxidative damage and cellular inflammatory cytokines in serum and BALF all significantly decreased (P<0.05) whereas serum GSH levels increased (P<0.05). CONCLUSIONS: PM2.5 caused significant oxidative damage and inflammatory injury in rat lungs. Lutein alleviated these effects, playing a protective role in lung tissues.