Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5
The public health harms caused by fine particulate matter (PM2.5) have become a global focus, with PM2.5 exposure recognized as a critical risk factor for global morbidity and mortality. Chronic inflammation is the common pathophysiological feature of respiratory diseases induced by PM2.5 and is the...
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| Format: | Article |
| Language: | English |
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Elsevier
2022-12-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651322011691 |
| _version_ | 1811315921686364160 |
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| author | Lili Deng Mingyue Ma Shuying Li Lin Zhou Sun Ye Juan Wang Qiaoqiao Yang Chunling Xiao |
| author_facet | Lili Deng Mingyue Ma Shuying Li Lin Zhou Sun Ye Juan Wang Qiaoqiao Yang Chunling Xiao |
| author_sort | Lili Deng |
| collection | DOAJ |
| description | The public health harms caused by fine particulate matter (PM2.5) have become a global focus, with PM2.5 exposure recognized as a critical risk factor for global morbidity and mortality. Chronic inflammation is the common pathophysiological feature of respiratory diseases induced by PM2.5 and is the most critical cause of all these diseases. However, presently there is a lack of effective preventive and therapeutic approaches for inflammatory lung injuries caused by PM2.5 exposure. Baicalin is a herb-derived effective flavonoid compound with multiple health benefits. This study established a murine lung inflammatory injury model via inhalation of PM2.5 aerosols. The data showed that after baicalin intervention, lung injury pathological score of baicalin (4.16 ± 0.54, 3.33 ± 0.76, 4.00 ± 0.45) and claricid (3.00 ± 0.78) treatments were markedly lower than PM2.5-treated mice (6.17 ± 0.31), and pathological damage was alleviated. Compared to the PM2.5 group, the spleen and lung indexes in the baicalin and claricid groups were significantly reduced. The inflammatory cytokines of TNF-α, IL-18, and IL-1β in serum, alveolar lavage fluid, and lung tissue were significantly decreased in the baicalin and claricid groups. The expressions of inflammatory pathway-related genes and proteins HMGB1, NLRP3, ASC, and caspase-1 were up-regulated in the PM2.5 group. The expressions of these genes and proteins were significantly decreased following baicalin treatment. The lung function indicators showed that the MV (65.94 ± 8.19 mL), sRaw (1.79 ± 0.08 cm H2O.s), and FRC (0.52 ± 0.01 mL) in the PM2.5 group were higher than in the control and baicalin groups, and respiratory function was improved by baicalin. PM2.5 exposure markedly altered the bacterial composition at the genus level. The dominant flora relative abundances of uncultured_bacterium_f_Muribaculaceae, Streptococcus, and Lactobacillus, were decreased from the control group (9.20%, 8.53%, 6.21%) to PM2.5 group (6.26%, 5.49%, 4.77%), respectively. Following baicalin intervention, the relative abundances were 9.72%, 6.65%, and 3.57%, respectively. Therefore, baicalin could potentially prevent and improve mice lung inflammatory injury induced by PM2.5 exposure. Baicalin might provide a protective role by balancing oropharyngeal microbiota and affecting the expression of the HMGB1/Caspase1 pathway. |
| first_indexed | 2024-04-13T11:40:05Z |
| format | Article |
| id | doaj.art-b5e72412138e4cfb96780ab66900935a |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-13T11:40:05Z |
| publishDate | 2022-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-b5e72412138e4cfb96780ab66900935a2022-12-22T02:48:20ZengElsevierEcotoxicology and Environmental Safety0147-65132022-12-01248114329Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5Lili Deng0Mingyue Ma1Shuying Li2Lin Zhou3Sun Ye4Juan Wang5Qiaoqiao Yang6Chunling Xiao7College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang 110033, China; Department of Nutrition and Food Hygiene, School of Public Health, Shenyang Medical College, Shenyang, Liaoning 110034, ChinaDepartment of Toxicology, School of Public Health, Shenyang Medical College, Shenyang, Liaoning 110034, China; Key Lab of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No.146, North Huanghe Street, Yuhong District, Shenyang, Liaoning 110034, ChinaKey Lab of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No.146, North Huanghe Street, Yuhong District, Shenyang, Liaoning 110034, ChinaDepartment of Nutrition and Food Hygiene, School of Public Health, Shenyang Medical College, Shenyang, Liaoning 110034, ChinaKey Lab of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No.146, North Huanghe Street, Yuhong District, Shenyang, Liaoning 110034, ChinaKey Lab of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No.146, North Huanghe Street, Yuhong District, Shenyang, Liaoning 110034, ChinaDepartment of Toxicology, School of Public Health, Shenyang Medical College, Shenyang, Liaoning 110034, ChinaCollege of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang 110033, China; Key Lab of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No.146, North Huanghe Street, Yuhong District, Shenyang, Liaoning 110034, China; School of Health Management, Shenyang Polytechnic College, Shenyang, Liaoning, 110045, China; Corresponding author at: College of Integrated Chinese and Western Medical, Liaoning University of Traditional Chinese Medicine, Shenyang 110033, China.The public health harms caused by fine particulate matter (PM2.5) have become a global focus, with PM2.5 exposure recognized as a critical risk factor for global morbidity and mortality. Chronic inflammation is the common pathophysiological feature of respiratory diseases induced by PM2.5 and is the most critical cause of all these diseases. However, presently there is a lack of effective preventive and therapeutic approaches for inflammatory lung injuries caused by PM2.5 exposure. Baicalin is a herb-derived effective flavonoid compound with multiple health benefits. This study established a murine lung inflammatory injury model via inhalation of PM2.5 aerosols. The data showed that after baicalin intervention, lung injury pathological score of baicalin (4.16 ± 0.54, 3.33 ± 0.76, 4.00 ± 0.45) and claricid (3.00 ± 0.78) treatments were markedly lower than PM2.5-treated mice (6.17 ± 0.31), and pathological damage was alleviated. Compared to the PM2.5 group, the spleen and lung indexes in the baicalin and claricid groups were significantly reduced. The inflammatory cytokines of TNF-α, IL-18, and IL-1β in serum, alveolar lavage fluid, and lung tissue were significantly decreased in the baicalin and claricid groups. The expressions of inflammatory pathway-related genes and proteins HMGB1, NLRP3, ASC, and caspase-1 were up-regulated in the PM2.5 group. The expressions of these genes and proteins were significantly decreased following baicalin treatment. The lung function indicators showed that the MV (65.94 ± 8.19 mL), sRaw (1.79 ± 0.08 cm H2O.s), and FRC (0.52 ± 0.01 mL) in the PM2.5 group were higher than in the control and baicalin groups, and respiratory function was improved by baicalin. PM2.5 exposure markedly altered the bacterial composition at the genus level. The dominant flora relative abundances of uncultured_bacterium_f_Muribaculaceae, Streptococcus, and Lactobacillus, were decreased from the control group (9.20%, 8.53%, 6.21%) to PM2.5 group (6.26%, 5.49%, 4.77%), respectively. Following baicalin intervention, the relative abundances were 9.72%, 6.65%, and 3.57%, respectively. Therefore, baicalin could potentially prevent and improve mice lung inflammatory injury induced by PM2.5 exposure. Baicalin might provide a protective role by balancing oropharyngeal microbiota and affecting the expression of the HMGB1/Caspase1 pathway.http://www.sciencedirect.com/science/article/pii/S0147651322011691BaicalinPM2.5InflammationRespiratory FunctionMicrobiota |
| spellingShingle | Lili Deng Mingyue Ma Shuying Li Lin Zhou Sun Ye Juan Wang Qiaoqiao Yang Chunling Xiao Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 Ecotoxicology and Environmental Safety Baicalin PM2.5 Inflammation Respiratory Function Microbiota |
| title | Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 |
| title_full | Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 |
| title_fullStr | Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 |
| title_full_unstemmed | Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 |
| title_short | Protective effect and mechanism of baicalin on lung inflammatory injury in BALB/cJ mice induced by PM2.5 |
| title_sort | protective effect and mechanism of baicalin on lung inflammatory injury in balb cj mice induced by pm2 5 |
| topic | Baicalin PM2.5 Inflammation Respiratory Function Microbiota |
| url | http://www.sciencedirect.com/science/article/pii/S0147651322011691 |
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