High-fat intake alleviates lung injury induced by Paragonimus proliferus infection in rats through up-regulating CYP 4A1 expression in lung tissues
10.16250/j.32.1374.2022243
- VernacularTitle:高脂摄入上调肺组织CYP 4A1表达缓解丰宫 并殖吸虫感染所致大鼠肺损伤
- Author:
Siqi LIU
1
,
2
;
Qingqing WANG
1
,
2
;
Weiqun WANG
3
;
Lei WU
1
;
Zhiqiang MA
4
;
Lin WANG
4
;
Guoji CHANG
1
;
Jie DING
1
;
Lijuan HUA
1
;
Huayi CHEN
1
;
Shenghao LI
1
;
Wenlin WANG
3
Author Information
1. Department of Hepatology, Clinical Center for Infectious Diseases of Yunnan Province/The Third People’s Hospital of Kunming, Kunming, Yunnan 650041, China
2. Co-first authors
3. Department of Pathogen Biology, Faculty of Basic Medicine, Kunming Medical University, Kunming, Yunnan 650504, China
4. Changpo Laboratory, Clinical Center for Infectious Diseases of Yunnan Province/The Third People’s Hospital of Kunming, Yunnan Province, China
- Publication Type:Journal Article
- Keywords:
Paragonimus proliferus;
Cytochrome P450 4A1;
High-fat diet;
Lung injury;
Rat
- From:
Chinese Journal of Schistosomiasis Control
2023;35(2):171-176
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the improvements of high-fat intake on lung injury induced by Paragonimus proliferus infection in rats, and to preliminarily explore the mechanisms underlying the role of cytochrome P450 4A1 (CYP 4A1) in the improve ments. Methods SD rats were randomly assigned into three groups, including the normal control group (n = 10), the infection and normal diet group (n = 12) and the infection and high-fat diet group (n = 12). Rats in the normal control group were fed with normal diet and without any other treatments, and animals in the infection and normal diet group were subcutaneously injected with 8 excysted metacercariae of P. proliferus via the abdominal wall, followed by feeding with normal diet, while rats in the infection and high-fat diet group were subcutaneously injected with 8 excysted metacercariae of P. proliferus via the abdominal wall, followed by feeding with high-fat diet. All rats were sacrificed 28 weeks post-infection, and serum samples and lung specimens were collected. Following hematoxylin-eosin (HE) staining of rat lung specimens, the rat lung injury was observed under an optical microscope, and alveolitis was evaluated using semi-quantitative scoring. Serum interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were measured using enzyme-linked immunosorbent assay (ELISA), and the cytochrome P450 4A1 (CYP 4A1) expression was quantified in rat lung specimens at transcriptional and translational levels using quantitative real-time PCR (qPCR) and Western blotting assays. Results Alveolar wall thickening, edema and inflammatory cell infiltration were alleviated 28 weeks post-infection with P. proliferus in rats in the infection and high-fat diet group relative to the infection and normal diet group, and no alveolar consolidation was seen in the infection and high-fat diet group. The semi-quantitative score of alveolitis was significantly higher in the infection and normal diet group [(2.200 ± 0.289) points] than in the normal control group [(0.300 ± 0.083) points] and the infection and high-fat diet group [(1.300 ± 0.475) points] (both P values < 0.05), and higher serum IL-1β [(151.586 ± 20.492)] pg/mL and TNF-α levels [(180.207 ± 23.379) pg/mL] were detected in the infection and normal diet group than in the normal control group [IL-1β: (103.226 ± 3.366) pg/mL; TNF-α: (144.807 ± 1.348) pg/mL] and the infection and high-fat diet group [IL-1β: (110.131 ± 12.946) pg/mL; TNF-α: (131.764 ± 27.831) pg/mL] (all P values < 0.05). In addition, lower CYP 4A1 mRNA (3.00 ± 0.81) and protein expression (0.40 ± 0.02) was quantified in lung specimens in the infection and normal diet group than in the normal control group [(5.03 ± 2.05) and (0.84 ± 0.14)] and the infection and high-fat diet group [(11.19 ± 3.51) and (0.68 ± 0.18)] (all P values < 0.05). Conclusion High-fat intake may alleviate lung injuries caused by P. proliferus infection in rats through up-regulating CYP 4A1 expression in lung tissues at both translational and transcriptional levels.
