scholarly journals miR-19a-3p inhibition alleviates sepsis-induced lung injury via enhancing USP13 expression

2021 ◽  
Author(s):  
Hangqi Ren ◽  
Wei Mu ◽  
Qiaolian Xu
Keyword(s):  
Lung Injury ◽  
Cell Model ◽  
Lung Damage ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Regulation Mechanism ◽  
Tnf Α ◽  
And Control ◽  
Relationship Of

Sepsis is a systemic inflammatory response syndrome caused by various pathogenic microorganisms or toxins. Lung damage is one of the causes of death in patients with sepsis. This study aimed to investigate the role of miR-19a-3p and its regulation mechanism in sepsis-induced lung injury. MH-S cells were treated with lipopolysaccharide (LPS) to establish sepsis-induced lung injury cell model. C57BL/6 mice were injected with miR-19a-3p antagomiR and LPS to construct animal model. LPS-treated and control cells were transfected with miR-19a-3p mimic, miR-19a-3p inhibitor or USP13 expression vector . The expression levels of miR-19a-3p and USP13 were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The concentration of inflammatory cytokines was measured with enzyme-linked immunosorbent assay (ELISA). The relationship of miR-19a-3p and USP13 was validated using dual-luciferase reporter assay. The lung damage was assessed with hematoxylin-eosin staining (HE). The results showed that LPS treatment increased the concentration of TNF-α, IL-6 and IL-1β in MH-S cells. In LPS treated MH-S cells, the level of miR-19a-3p gradually increased over time. Both miR-19a-3p knockdown and USP13 overexpression in MH-S cells inhibited the LPS-induced production of TNF-α, IL-6 and IL-1β. Moreover, miR-19a-3p negatively regulated the expression of USP13 in MH-S cells. Furthermore, miR-19a-3p inhibitor suppressed lung damage in sepsis model mice. In conclusion, miR-19a-3p knockdown could alleviate sepsis-induced lung injury through enhancing USP13 expression.

scholarly journals MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.

scholarly journals miR-20a attenuates acute lung injury in septic rats via targeting TLR4

2021 ◽  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Lung Tissue ◽  
Cecal Ligation ◽  
Normal Group ◽  
Lung Damage ◽  
Luciferase Reporter ◽  
Arterial Bleeding ◽  
Tnf Α

Background: Sepsis is most likely to cause lung damage in patients, and the detection rate and mortality rate are high. Here, we investigated the expression of miR-20a in sepsis-induced acute lung injury (ALI) rats and its effect on inflammatory response, and reveal its possible molecular mechanism. Method: The model of acute lung injury caused by sepsis in rats was established by cecal ligation and puncture. The expression of miR-20a in lung tissue was determined by RT-qPCR. Acute lung injury rats were injected with 5 nmol miR-20a agomir or agomir NC every day for 3 days. Rats were sacrificed by arterial bleeding and lung tissues were removed. Serum interleukin (IL) -1β, IL-6, and tumor necrosis factor alpha (TNF-α) were detected by ELISA. HE staining was used to observe the pathology of lung tissue and calculate the pathological score of lung injury. Western blot to determine the level of TLR4 and nuclear transcription factor κB p65 (NF-κB p65) protein in lung tissue. The luciferase reporter assay was used to verify the binding effect of miR-20a on the 3 non-coding TLR4. Results: We found that compared with that in Normal group, the expression of miR-20a in lung tissues of rats with ALI was decreased (p < 0.05). In miR-20a agomir group, the plasma level of IL-1β, IL-6, and TNF-α was significantly lower than that in agomir NC group and ALI group (p < 0.05), while higher than those in Normal group (p < 0.05). The HE staining results showed that the pathological score of lung injury in rats in miR-20a agomir group was lower than that of agomir NC group and ALI group (p < 0.05). Compared with agomir NC group and ALI group, the expression of TLR4 and NF-κB p65 in miR-20a agomir group was decreased (p < 0.01). The luciferase reporting experiment confirmed that TLR4 was a target gene of miR-20a. Conclusion: To sum up, miR-20a exerts a protective effect on sepsis-induced ALI rats through its anti-inflammatory effect. The targeting of TLR4 by miR-20a may be an effective method to reduce the inflammatory response in sepsis-induced ALI.

scholarly journals MiR-429 Inhibits the Angiogenesis of Human Brain Microvascular Endothelial Cells through SNAI2-Mediated GSK-3β/β-Catenin Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yameng Sun ◽  
Shenghao Ding ◽  
Yiling Fan ◽  
Fei Shen ◽  
Qing Dong ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Model ◽  
Glucose Deprivation ◽  
Tube Formation ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Oxygen And Glucose Deprivation ◽  
Downstream Target ◽  
Gsk 3Β

MicroRNA (miRNA) dysfunction has been confirmed as a key event of ischemic stroke appearance. This study is aimed at revealing the role of miR-429 in the angiogenesis of HBMECs. The HBMECs were treated with oxygen and glucose deprivation (OGD) to establish the ischemic cell model. The qRT-PCR was used to measure the expression levels of the miR-429 in the serums of the patients or cells, and CCK-8, wound healing assay, and tube formation assay were used to observe the effects of miR-429 on the phenotype of HBMECs. Moreover, the Targetscan, dual-luciferase reporter assay, and Western blot were used to reveal the downstream target and regulation mechanism of miR-429 in OGD-induced HBMECs. The results showed that miR-429 was significantly upregulated in the serums of the patients, and overexpressed miR-429 could extremely inhibit the viability, migration, and tube formation of OGD-induced HBMECs. Furthermore, it was found that SNAI2 was a downstream factor of miR-429, and SNAI2 could rescue the effects of miR-429 on OGD-induced HBMECs. Besides, the Western blot showed that miR-429 could affect the activity of GSK-3β/β-catenin pathway via inhibiting the expression of SNAI2. In conclusion, this study suggests that miR-429 inhibits the angiogenesis of HBMECs through SNAI2-mediated GSK-3β/β-catenin pathway.

MicroRNA (miR)-429 Promotes Inflammatory Injury by Targeting Kruppel-like Factor 4 (KLF4) in Neonatal Pneumonia

2020 ◽  
Vol 17 (1) ◽  
pp. 102-109
Author(s):  
Lan Zhang ◽  
HuanLi Yan ◽  
Huiping Wang ◽  
Li Wang ◽  
Boling Bai ◽  
...  
Keyword(s):  
Cell Viability ◽  
Peripheral Blood ◽  
Cell Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Common Disease ◽  
Human Lung Fibroblast ◽  
Inflammatory Injury ◽  
Tnf Α

Background: Neonatal pneumonia is a common disease in the neonatal period with a high incidence and death. This study aimed to investigate the molecular mechanism and effect of microRNA (miR)-429 in neonatal pneumonia. Methods: The peripheral blood was collected from neonatal pneumonia and healthy patients, respectively. Human lung fibroblast WI-38 cells were treated with lipopolysaccharide (LPS) to establish neonatal pneumonia cell model. Then, the miR-429 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR). In addition, the relationship between miR- 429 and kruppel-like factor 4 (KLF4) was confirmed by dual luciferase reporter assay. Cell viability, the level of interleukin 6 (IL-6), IL-1β and tumor necrosis factor α (TNF-α) and apoptosis were measured by Cell Counting Kit-8 (CCK-8), enzyme linked immunosorbent assay (ELISA) and flow cytometry. Meanwhile, apoptosis and nuclear factor kappa-B (NF-κB) pathway related proteins expression were analyzed by western blot. Results: MiR-429 expression level was increased in neonatal peripheral blood and LPS-stimulated WI-38 cells. Then, miR-429 overexpression increased apoptosis, the level of IL-6, IL-1β, TNF-α, Bax and cleaved caspase-3, while reduced cell viability in LPS-stimulated WI-38 cells. Besides, KLF4 was identified as the target gene of miR-429, and reversed the changes caused by miR-429 overexpression. Finally, miR-429 suppressor down-regulated p-NF-κB level in LPS-stimulated cells and KLF4 knockdown reversed these reductions. Conclusion: MiR-429 promotes inflammatory injury, apoptosis and activates the NF-κB signaling pathway by targeting KLF4 in neonatal pneumonia, and then these results provide evidence for clinical diagnosis and treatment for neonatal pneumonia.

scholarly journals The Role of Vagus Nerve on Dexmedetomidine Induced Survival and Lung Protection in a Sepsis Model in Rats.

2021 ◽  
Author(s):  
Yumo Li ◽  
Binbin Wu ◽  
Cong Hu ◽  
Jie Hu ◽  
Qingquan Lian ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Vagus Nerve ◽  
Vagal Nerve ◽  
Lung Injury Score ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Lung Protection ◽  
Tnf Α

Abstract BackgroundSepsis often results in acute lung injury (ALI). Sedative dexmedetomidine (Dex) was reported to protect cells and organs due to its direct cellular effects. This study aims to investigate the role of vagus nerves on Dex induced lung protection in a model of lipopolysaccharide (LPS)-induced ALI in rats. MethodsThe bilateral cervical vagus nerve of male Sprague-Dawley rats was sectioned or just exposed without section as sham surgery. The ALI was induced by intraperitoneal injection of LPS (1 or 10 mg/kg). After LPS administration, Dex antagonist yohimbine (YOH) (1 mg/kg) and/or Dex (25 μg/kg) was injected intraperitoneally at 0, 4, 8 and 12 hours to rats with or without vagotomy. The severity of ALI was determined with survival curve analysis and lung pathological scores of haematoxylin and eosin (H-E) staining sections. The plasma concentrations of interleukin 1beta (IL-1β), tumour necrosis factor-alpha (TNF-α), catecholamine (CA) and acetylcholine (Ach) were measured with enzyme-linked immunosorbent assay (ELISA). ResultsThe median survival time of LPS-induced ALI rats was significantly prolonged by Dex (22 hours, 50% CI, [31.25, 90.63]) compared that in the LPS group (14 hours, 50% CI, [18.75, 81.25], P < 0.05), and the acute lung injury score was significantly reduced by Dex (6.5, 50% CI, [5.75, 7.5] vs 11.5, 50% CI, [10.75, 12.50] in the LPS group, P < 0.01). However, these protective effects of Dex were significantly reduced by either YOH administration or vagotomy. Dex significantly decreased LPS-induced plasma IL-1β (pg/ml) (20.75 ± 0.78 vs. 30.22 ± 2.62, P < 0.01), TNF-α (pg/ml) (205.30 ± 9.39 vs. 273.40 ± 14.50, P < 0.01), and CA (pg/ml) (825.70 ± 43.46 vs. 1188.00 ± 64.40, P < 0.01) but increased the secretion of Ach (pg/ml) (507.20 ± 49.52 vs. 296.50 ± 62.44, P < 0.01); these effects of Dex was partially abolished by vagotomy. ConclusionsOur data suggested that Dex increased vagal nerve tone which partially contributed to its anti-inflammatory and lung protective effects. The indirect anti-inflammation and direct cytoprotection of Dex are likely through high vagal nerve tone and α 2 -adrenoceptor activation, respectively.

scholarly journals Plasma extracellular vesicle delivery of miR-210-3p by targeting ATG7 to promote sepsis-induced acute lung injury by regulating autophagy and activating inflammation

2021 ◽  
Author(s):  
Guang Li ◽  
Bo Wang ◽  
Xiangchao Ding ◽  
Xinghua Zhang ◽  
Jian Tang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Recipient Cell ◽  
Cecal Ligation ◽  
Cell Permeability ◽  
Cell Counting ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Density

AbstractExtracellular vesicles (EVs) can be used for intercellular communication by facilitating the transfer of miRNAs from one cell to a recipient cell. MicroRNA (miR)-210-3p is released into the blood during sepsis, inducing cytokine production and promoting leukocyte migration. Thus, the current study aimed to elucidate the role of plasma EVs in delivering miR-210-3p in sepsis-induced acute lung injury (ALI). Plasma EVs were isolated from septic patients, after which the expression of various inflammatory factors was measured using enzyme-linked immunosorbent assay. Cell viability and apoptosis were measured via cell counting kit-8 and flow cytometry. Transendothelial resistance and fluorescein isothiocyanate fluorescence were used to measure endothelial cell permeability. Matrigel was used to examine the tubulogenesis of endothelial cells. The targeting relationship between miR-210-3p and ATG7 was assessed by dual-luciferase reporter assays. The expression of ATG7 and autophagy-related genes was determined to examine autophagic activation. A sepsis mouse model was established by cecal ligation and puncture (CLP)-induced surgery. The level of miR-210-3p was highly enriched in septic EVs. MiR-210-3p enhanced THP-1 macrophage inflammation, BEAS-2B cell apoptosis, and HLMVEC permeability while inhibiting angiogenesis and cellular activity. MiR-210-3p overexpression reduced ATG7 and LC3II/LC3I expression and increased P62 expression. Improvements in vascular density and autophagosome formation, increased ATG7 expression, and changes in the ratio of LC3II/LC3I were detected, as well as reduced P62 expression, in adenovirus-anti-miR-210-3p treated mice after CLP injury. Taken together, the key findings of the current study demonstrate that plasma EVs carrying miR-210-3p target ATG7 to regulate autophagy and inflammatory activation in a sepsis-induced ALI model.

scholarly journals Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jianwei Zhang ◽  
Lei Han ◽  
Feng Chen
Keyword(s):  
Inflammatory Response ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Mapk Pathway ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Western Blot Assay ◽  
Protein Levels ◽  
Tnf Α

Abstract Background Let-7a-5p is demonstrated to be a tumor inhibitor in nasopharyngeal carcinoma. However, the role of let-7a-5p in chronic rhinosinusitis with nasal polyps (CRSwNP) has not been reported. This study is designed to determine the pattern of expression and role of let-7a-5p in CRSwNP. Methods The expression level of let-7a-5p, TNF-α, IL-1β, and IL-6 in CRSwNP tissues and cells were detected by RT-qPCR. Western blot assay was carried out to measure the protein expression of the Ras-MAPK pathway. Dual luciferase reporter assay and RNA pull-down assay were used to explore the relationship between let-7a-5p and IL-6. Results Let-7a-5p was significantly downregulated in CRSwNP tissues and cells. Moreover, the mRNA expression of TNF-α, IL-1β and IL-6 was increased in CRSwNP tissues, while let-7a-5p mimic inhibited the expression of TNF-α, IL-1β and IL-6. Besides that, let-7a-5p was negatively correlated with TNF-α, IL-1β and IL-6 in CRSwNP tissues. In our study, IL-6 was found to be a target gene of let-7a-5p. Additionally, let-7-5p mimic obviously reduced the protein levels of Ras, p-Raf1, p-MEK1 and p-ERK1/2, while IL-6 overexpression destroyed the inhibitory effect of let-7a-5p on the Ras-MAPK pathway in CRSwNP. Conclusion We demonstrated that let-7a-5p/IL-6 interaction regulated the inflammatory response through the Ras-MAPK pathway in CRSwNP.

scholarly journals Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qingsong Sun ◽  
Man Luo ◽  
Zhiwei Gao ◽  
Xiang Han ◽  
Weiqin Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Cell Apoptosis ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Interacting Protein ◽  
Wide Range

Abstract Background Acute lung injury (ALI) is a pulmonary disorder that leads to acute respiration failure and thereby results in a high mortality worldwide. Increasing studies have indicated that toll-like receptor 4 (TLR4) is a promoter in ALI, and we aimed to explore the underlying upstream mechanism of TLR4 in ALI. Methods We used lipopolysaccharide (LPS) to induce an acute inflammatory response in vitro model and a murine mouse model. A wide range of experiments including reverse transcription quantitative polymerase chain reaction, western blot, enzyme linked immunosorbent assay, flow cytometry, hematoxylin–eosin staining, RNA immunoprecipitation, luciferase activity and caspase-3 activity detection assays were conducted to figure out the expression status, specific role and potential upstream mechanism of TLR4 in ALI. Result TLR4 expression was upregulated in ALI mice and LPS-treated primary bronchial/tracheal epithelial cells. Moreover, miR-26a-5p was confirmed to target TLR4 according to results of luciferase reporter assay. In addition, miR-26a-5p overexpression decreased the contents of proinflammatory factors and inhibited cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI by regulating TLR4. Afterwards, OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was identified to bind with miR-26a-5p. Functionally, OIP5-AS1 upregulation promoted the inflammation and miR-26a-5p overexpression counteracted the influence of OIP5-AS1 upregulation on cell inflammatory response and apoptosis. Conclusion OIP5-AS1 promotes ALI by regulating the miR-26a-5p/TLR4 axis in ALI mice and LPS-treated cells, which indicates a promising insight into diagnostics and therapeutics in ALI.

Long Noncoding RNA SNHG1 Promotes Lipopolysaccharide-Induced Activation and Inflammation in Microglia via Targeting miR-181b

2021 ◽  
pp. 1-11
Author(s):  
Jun Dong ◽  
Tingkai Fu ◽  
Yunxue Yang ◽  
Zhenxin Mu ◽  
Xingang Li
Keyword(s):  
Inflammatory Cytokines ◽  
Long Noncoding Rna ◽  
Calcium Binding ◽  
Noncoding Rna ◽  
Morphological Changes ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammation Response ◽  
Tnf Α ◽  
Cox 2

<b><i>Introduction:</i></b> Long noncoding RNA small nuclear host gene 1 (SNHG1) was involved in neuroinflammation in microglial BV-2 cells; however, its interaction with microRNA (miR)-181b in lipopolysaccharide (LPS)-induced BV-2 cells remained poor. <b><i>Methods:</i></b> BV-2 cells were treated with LPS and then were subjected to observation on morphology and immunofluorescence staining. After transfection, levels of inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were determined with enzyme-linked immunosorbent assay (ELISA). The potential binding sites between SNHG1 and miR-181b were confirmed using dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction and Western blot were applied for detecting the mRNA and protein expressions of proinflammatory cytokines, ionized calcium-binding adapter molecule 1 (Iba1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). <b><i>Results:</i></b> LPS led to the morphological changes and activation of BV-2 cells. The transfection of SNHG1 overexpression vector further promoted LPS-induced SNHG1 upregulation, inflammatory cytokines (IL-1β, IL-6, and TNF-α) generation and Iba-1, COX-2, and iNOS expressions, whereas silencing SNHG1 did the opposite. miR-181b functions as a downstream miRNA of SNHG1. In LPS-treated cells, the inhibition of miR-181b induced by SNHG1 promoted inflammation response and the expressions of Iba-1, COX-2, and iNOS. <b><i>Conclusion:</i></b> SNHG1 was involved in LPS-induced microglial activation and inflammation response via targeting miR-181b, providing another evidence of the roles of SNHG1 implicated in neuroinflammation of microglia.

3-methyadenine inhibits lipopolysaccharides-induced pulmonary inflammation at the early stage of silicosis via blocking NF-κB signaling pathway

2021 ◽  
pp. 074823372110394
Author(s):  
Yujing Zhang ◽  
Shuai Huang ◽  
Shiyi Tan ◽  
Mingke Chen ◽  
Shang Yang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Late Stage ◽  
Caspase 3 ◽  
Inflammatory Responses ◽  
Early Stage ◽  
Pulmonary Inflammation ◽  
Mechanism Study ◽  
Silica Dust ◽  
Tnf Α

Occupational exposure to silica dust is related to pulmonary inflammation and silicosis. Lipopolysaccharides (LPSs) could aggravate apoptosis in alveolar macrophages (AMs) of human silicosis through autophagy, yet how the reduction of autophagy attenuated LPS-induced lung injury and the related mechanisms need to be investigated. In the study, we aim to understand the role of 3-methyladenine (3-MA), an inhibitor of autophagy, in LPS-mediated inflammatory responses and fibrosis. We collected AMs from observers/silicosis patients. The results showed that LPS induced NF-κB-related pulmonary inflammation in observers and silicosis patients, as confirmed by an increase in the expression of IL-1β, IL-6, TNF-α, and p65, which could be inhibited by 3-MA treatment. In mice models, at the early stage (7d) of silicosis, but not the late (28d) stage, blocking autophagy reversed the increased levels of IL-1β, IL-6, TNF-α, and p65 caused by LPS. Mechanism study revealed that LPS triggered the expression of LC3 II, p62, and cleaved caspase-3 at the early stage exposed to silica, which could be restored by 3-MA, while there was no difference in the expression of LAMP1 either at the early or late stage of silicosis in different groups. Similarly, 3-MA treatment did not prevent fibrosis characterized by destroyed alveoli, collagen deposition, and increased expression of α-SMA and Col-1 induced by LPS at the late stage of silicosis. The results suggested that 3-MA has a role in the protection of lung injury at the early stage of silicosis and provided an experimental basis for preventive strategies of pulmonary inflammation and silicosis.

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