scholarly journals Astragaloside IV Attenuates Lipopolysaccharides-Induced Pulmonary Epithelial Cell Injury through Inhibiting Autophagy

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 90-101
Author(s):  
Biwang Liu ◽  
Huan Zhao ◽  
Yonghui Wang ◽  
Huizhong Zhang ◽  
Yanmiao Ma
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Cell Model ◽  
Beclin 1 ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Astragaloside Iv ◽  
Tnf Α ◽  
Therapeutic Function

Background: Astragaloside IV has shown its promising effect on acute respiratory distress syndrome (ARDS). Objectives: We aim to explore whether astragaloside IV is effective for ARDS treatment in a lipopolysaccharides (LPS)-induced cell model and whether autophagy is involved in the therapeutic function of astragaloside IV. Methods: MLE-12 cells were induced by LPS to construct an ARDS model in vitro. Cell viability was estimated by cell counting kit-8 and cell apoptosis by flow cytometry. Lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by enzyme-linked immunosorbent assay kit. The expression of tumour necrosis factor (TNF)-α, interleukin (IL)-6, zonula occludens (ZO)-1, Beclin-1 and autophagy-related (atg) 5 mRNA was evaluated by quantitative PCR, and the expression of ZO-1, microtubule-associated proteins 1A/1B light chain 3B (LC3B) I and, LC3B II protein by Western blot. Results: LPS effectively inhibited cell viability and LC3B I expression and enhanced LC3B II, Beclin-1 and atg5 expressions in MLE-12 cells. In LPS-induced ARDS cell model, astragaloside IV up-regulated cell viability, SOD activity and ZO-1 and LC3B I expressions but down-regulated cell apoptosis, TNF-α, IL-6, LC3B II, Beclin-1 and atg5 expressions and LDH and MDA levels. 3-methyladenine promoted cell viability and ZO-1 expression, down-regulated Beclin-1 and atg5 expression, while Rapamycin (Rap) had an opposite effect. Astragaloside IV suppressed cell viability and ZO-1 expression after the Rap treatment. Conclusions: Astragaloside IV might suppress autophagy initiation directly or indirectly through suppressing the oxidative stress and inflammatory response, which further enhances the cell viability and tight junction and reduces apoptosis in LPS-stimulated pulmonary endothelial ARDS cell model, thus exerting its therapeutic function in ARDS.

scholarly journals MiR-146b-3p protects against AR42J cell injury in cerulein-induced acute pancreatitis model through targeting Anxa2

2021 ◽  
Vol 16 (1) ◽  
pp. 255-265
Author(s):  
Kunpeng Zhang ◽  
Xiaoyu Zhang
Keyword(s):  
Acute Pancreatitis ◽  
Cell Viability ◽  
Cell Injury ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Qrt Pcr ◽  
Ar42j Cells ◽  
Tnf Α ◽  
Ar42j Cell

Abstract Background Acute pancreatitis (AP) is a common inflammatory disorder. MicroRNAs play crucial roles in the pathogenesis of AP. In this article, we explored the detailed role and molecular mechanisms of miR-146b-3p in AP progression. Methods The rat AR42J cells were treated with cerulein to establish the AP model in vitro. The miR-146b-3p and Annexin A2 (Anxa2) mRNA levels were assessed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were tested using the Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. Caspase-3 activity and the production of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay and qRT-PCR. Targeted interaction between miR-146b-3p and Anxa2 was verified by the dual-luciferase reporter and RNA immunoprecipitation assays. Western blot analysis was performed to detect the expression of Anxa2 protein. Results Our data revealed that miR-146b-3p was significantly downregulated in AP samples. The enforced expression of miR-146b-3p alleviated cerulein-induced injury in AR42J cells, as evidenced by the promotion in cell viability and the repression in cell apoptosis, as well as the reduction in IL-1β, IL-6, and TNF-α production. Anxa2 was directly targeted and inhibited by miR-146b-3p. Moreover, the alleviative effect of miR-146b-3p overexpression on cerulein-induced AR42J cell injury was mediated by Anxa2. Conclusions The current work had led to the identification of miR-146b-3p overexpression that protected against cerulein-induced injury in AR42J cells at least in part by targeting Anxa2, revealing a promising target for AP diagnosis and treatment.

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 Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

2021 ◽  
Keyword(s):  
Cell Viability ◽  
Methyl Jasmonate ◽  
Cell Apoptosis ◽  
Cell Model ◽  
Tubular Epithelial Cell ◽  
Cell Protein ◽  
Epithelial Cell Line ◽  
Tnf Α ◽  
Iκbα Phosphorylation ◽  
Anti Inflammatory

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

scholarly journals Endoplasmic reticulum stress regulates cell injury in lipopolysaccharide-induced nerve cells

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094976
Author(s):  
Min Li ◽  
Ying Zhang ◽  
Jixing Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Er Stress ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Injury ◽  
Cell Counting ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Stress Markers

Objective Sepsis-associated encephalopathy (SAE) is a common complication of sepsis, and excessive endoplasmic reticulum (ER) stress is closely correlated with the cell injury caused by sepsis. This study aimed to analyze the possible role of ER stress in SAE cell models. Methods PC12 and MES23.5 cells were treated with increasing concentrations of lipopolysaccharides (LPS). The Cell Counting Kit-8 assay was used to detect cell viability and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was performed to assess cell apoptosis. In addition, the protein expression levels of ER stress markers [GRP78, CHOP, inositol-requiring enzyme 1 (IRE1), and PKR-like ER kinase (PERK)] and apoptosis-related proteins (Bax, Bcl-2, caspase-3, and cleaved caspase-3) were analyzed using western blotting. Results LPS treatment activated ER stress markers in both the PC12 and MES23.5 cells. The overexpression of GRP78 significantly reduced cell viability and enhanced cell apoptosis in a time-dependent manner. An ER stress inhibitor, 4-PBA, significantly enhanced cell viability and inhibited the cell apoptosis induced by LPS. Therefore, an enhanced unfolded protein response (UPR) and UPR suppression may regulate cell apoptosis. Conclusions UPR was shown to be involved in regulating LPS-induced neuron injury. UPR could be a potential therapeutic target in SAE.

scholarly journals Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

2021 ◽  
Keyword(s):  
Cell Viability ◽  
Methyl Jasmonate ◽  
Cell Apoptosis ◽  
Cell Model ◽  
Tubular Epithelial Cell ◽  
Cell Protein ◽  
Epithelial Cell Line ◽  
Tnf Α ◽  
Iκbα Phosphorylation ◽  
Anti Inflammatory

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

scholarly journals Exosomal circ-BRWD1 contributes to osteoarthritis development through the modulation of miR-1277/TRAF6 axis

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Zhenye Guo ◽  
Huan Wang ◽  
Feng Zhao ◽  
Min Liu ◽  
Feida Wang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Injury ◽  
Cell Damage ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mechanism Analysis ◽  
Western Blot Assay ◽  
The Impact

Abstract Background Circular RNAs (circRNAs) can act as vital players in osteoarthritis (OA). However, the roles of circRNAs in OA remain obscure. Herein, we explored the roles of exosomal circRNA bromodomain and WD repeat domain containing 1(circ-BRWD1) in OA pathology. Methods In vitro model of OA was constructed by treating CHON-001 cells with interleukin-1β (IL-1β). Quantitative real-time polymerase chain reaction (qRT-PCR) assay was used for circ-BRWD1, BRWD, miR-1277, and TNF receptor-associated factor 6 (TRAF6) levels. RNase R assay was conducted for the feature of circ-BRWD1. Transmission electron microscopy (TEM) was employed to analyze the morphology of exosomes. Western blot assay was performed for protein levels. Cell Counting Kit-8 (CCK-8) assay, flow cytometry analysis, and 5-Ethynyl-2′-deoxyuridine (EDU) assay were adopted for cell viability, apoptosis, and proliferation, respectively. Enzyme-linked immunosorbent assay (ELISA) was carried out for the concentrations of interleukin-6 (IL-6) and interleukin-8 (IL-8). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to analyze the interaction between miR-1277 and circ-BRWD1 or TRAF6. Results Circ-BRWD1 was increased in OA cartilage tissues, IL-1β-treated CHON-001 cells, and the exosomes derived from IL-1β-treated CHON-001 cells. Exosome treatment elevated circ-BRWD1 level, while exosome blocker reduced circ-BRWD1 level in IL-1β-treated CHON-001 cells. Silencing of circ-BRWD1 promoted cell viability and proliferation and repressed apoptosis, inflammation, and extracellular matrix (ECM) degradation in IL-1β-stimulated CHON-001 cells. For mechanism analysis, circ-BRWD1 could serve as the sponge for miR-1277 to positively regulate TRAF6 expression. Moreover, miR-1277 inhibition ameliorated the effects of circ-BRWD1 knockdown on IL-1β-mediated CHON-001 cell damage. Additionally, miR-1277 overexpression relieved IL-1β-induced CHON-001 cell injury, while TRAF6 elevation restored the impact. Conclusion Exosomal circ-BRWD1 promoted IL-1β-induced CHON-001 cell progression by regulating miR-1277/TRAF6 axis.

scholarly journals Cullin3 Aggravates The Inflammatory Response of PDLSCs Via Regulation of Shh Signaling and Nrf2

2021 ◽  
Author(s):  
Wanhong Chen ◽  
Jiangling Su ◽  
Shixiong Cai ◽  
Chun Shi
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Western Blots ◽  
Alizarin Red ◽  
Shh Signaling ◽  
Protein Levels ◽  
Alkaline Phosphatase Staining

Abstract Objective: Sonic Hedgehog (Shh) was found to be correlated with inflammation degree of patients with periodontitis. Cullin3 is an important ubiquitin ligase for controlling Shh signaling. In this study, we exerted ourselves to clarify the roles of Shh and Cullin3 in P. gingivalis-LPS (Pg-LPS)-treated periodontal ligament stem cells (PDLSCs). Methods: Cell viability was detected using cell counting kit-8 (CCK-8). The inflammatory cytokines of PDLSCs were estimated by enzyme-linked immunosorbent assay (ELISA). The protein levels of Shh, Gli1 and NF-E2-related factor2 (Nrf2) were determined via western blots. Alkaline phosphatase staining and Alizarin red staining were performed to evaluate the differentiation and mineralization capabilities of PDLSCs. The apoptotic cells were screened by TUNEL staining. Results: Pg-LPS inhibited cell viability and triggered inflammation of PDLSCs. Overexpression of Cullin3 impeded the differentiation and mineralization capabilities of PDLSCs. Moreover, Cullin3 overexpression aggravated inflammation and cell apoptosis induced by Pg-LPS. Of note, while the protein levels of Shh, Gli1 and Nrf2 were elevated in PDLSCs treated with Pg-LPS, overexpression of Cullin3 decreased the expressions of them. Conclusion: Shh/Gli1 and Nrf2 were involved in the inflammation and cell apoptosis of PDLSCs, which was dominated by Cullin3.

scholarly journals Schizandrin A Alleviates LPS-Induced Injury in Human Keratinocyte Cell Hacat Through a MicroRNA-127-Dependent Regulation

2018 ◽  
Vol 49 (6) ◽  
pp. 2229-2239 ◽  
Author(s):  
Shujie Li ◽  
Ruijin Xie ◽  
Chengrui Jiang ◽  
Mei Liu
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Skin Diseases ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hacat Cells ◽  
Protective Effects ◽  
Human Keratinocyte ◽  
Tnf Α ◽  
Keratinocyte Cell

Background/Aims: Inflammatory skin diseases are the most common problems in dermatology. Schizandrin A (SchA) has been reported to have anti-inflammatory properties. Herein, we aimed to investigate the protective effects of SchA on lipopolysaccharide (LPS)-induced injury in keratinocyte HaCaT cells. Methods: Inflammation injury in HaCaT cells was induced by LPS treatment. Cell viability, apoptotic cell rate, and apoptosis-related proteins were analyzed by cell counting kit-8 (CCK-8) assay, Annexin V-(fluorescein isothiocyanate (FITC)/ Propidium Iodide (PI) double staining method, and western blot, respectively. The pro-inflammatory factors were analyzed by western blot and quantified by enzyme linked immunosorbent assay (ELISA). Expression of miR-127 in SchA-treated cells was analyzed by qRT-PCR. The effects of SchA on activations of p38MAPK/ERK and JNK pathways were analyzed by western blot. Results: SchA protected HaCaT cells from LPS-induced inflammation damage via promoting cell viability, suppressing apoptosis. Meanwhile, SchA inhibited IL-1β, IL-6, and TNF-α expression. miR-127 expression was up-regulated in LPS-treated HaCaT cells but down-regulated after SchA treatment. Overexpression of miR-127 inhibited cell growth and induced expression of IL-1β, IL-6 and TNF-α. Additionally, miR-127 overexpression impaired the protective effects of SchA, implying miR-127 might be correlated to the anti-inflammation property of SchA and also involved in inactivation of p38MAPK/ERK and JNK pathways by SchA. Conclusion: miR-127 is involved in the protective functions of SchA on LPS-induced inflammation injury in human keratinocyte cell HaCaT, which might inactivates of p38MAPK/ERK and JNK signaling pathways in HaCaT cells.

scholarly journals LncRNA PFAL suppresses TNF-α-induced inflammation by upregulating miR-18a in WI-38 cells

2021 ◽  
Vol 19 (12) ◽  
pp. 2513-2520
Author(s):  
Yichun Xie ◽  
Hongqun Wang
Keyword(s):  
Cell Viability ◽  
Inflammatory Cytokines ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Inflammatory Diseases ◽  
Jnk Pathway ◽  
Inflammatory Injury ◽  
Mortality And Morbidity ◽  
Injury Model ◽  
Tnf Α

Purpose: Pneumonia is a serious respiratory disease among children with high mortality and morbidity all over the world. Long non-coding RNAs have been proven to play a vital role in many inflammatory diseases including pneumonia. In the present study, the protective impact of lncRNA PFAL on cell viability, cell apoptosis and secretion of inflammatory cytokines, as well as the underlying molecular mechanism in TNF-α-induced inflammatory injury model of pneumonia were investigated.Methods: WI-38 cell line was treated with 20 ng/ml TNF-α to establish an inflammatory injury model of pneumonia. LncRNA PFAL or miR-18a was up- or down-regulated in the WI-38 cells by transfection procedure. Cell viability was assessed using CCK-8 assay, while the rate of cell apoptosis was measured by utilizing flow cytometry. The mRNA expression levels of lncRNA PFAL, miR-18a, apoptosis-related and JNK pathway genes were determined with RT-qPCR. Moreover, the production of inflammatory cytokines such as IL-6 and MCP-1 were detected by using Western blot analysis.Results: The results indicated that cell viability was significantly (P<0.05) reduced, while the rate of cell apoptosis was increased in the TNF-α-induced WI-38 cells. Also, TNF-α treatment enhanced the expression of inflammatory cytokines that included IL-6 and MCP-1 in WI-38 cells. Overexpression of PFAL suppressed the injury induced by TNF-α and miR-18a was positively regulated by PFAL. Moreover, the inhibition of miR-18a weakens the effect of PFAL overexpression in TNF-α-induced cell injury. Furthermore, PFAL and miR-18a were involved in the regulation of JNK pathway.Conclusion: Overexpression of PFAL suppresses TNF-α-induced WI-38 cell injury by up-regulating miR-18a via the inactivation of JNK signaling pathway. Keywords: Inflammation, JNK pathway, miR-18a, PFAL, Pneumonia, TNF-α

scholarly journals MiR-103a-3p antagonism attenuates pneumonia via inactivating the PI3K/AKT/NF-κB signaling pathway by targeting PTEN

2020 ◽  
Author(s):  
Lin Xu ◽  
Qingying Song ◽  
Zhanghong Ouyang ◽  
Xiangyan Zhang ◽  
Cheng Zhang
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Expression Levels ◽  
Tensin Homolog ◽  
Factor Α

Abstract Pneumonia accounts for approximately 15% mortalities in adolescents worldwide. MicroRNAs (miRNAs) regulate numerous diseases including pneumonia. miRNA and mRNA expression levels were detected by real time polymerase chain reaction (RT-qPCR). Protein expression levels were determined by enzyme-linked immunosorbent assay (ELISA) and western blot. The interaction between phosphatase and tensin homolog on chromosome ten (PTEN) and miR-103a-3p was explored by dual luciferase reporter assay. Cell viability and cell apoptosis were detected by cell Counting Kit-8 (CCK-8) and flow cytometry. Herein, we discovered that PTEN was decreased and miR-103a-3p was overexpressed in Ana-1 cells of in vitro pneumonia model. miR-103a-3p downregulated the expression levels of PTEN. AntagomiR-103a-3p reversed the increased cell apoptosis and decreased cell viability and inflammatory cytokine expression levels (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6) induced by LPS in Ana-1 cells by PTEN. AntagomiR-103a-3p inhibited the activation of PTEN/PI3K/AKT/NF-κB signaling pathway induced by LPS in Ana-1 cells. Taken together, our findings exhibited that miR-103a-3p attenuated LPS induced pneumonia by blocking the activation of PTEN/PI3K/AKT/NF-κB signaling pathway and the following cell apoptosis as well as release of proinflammatory cytokines, suggesting that miR-103a-3p might serve as a novel therapeutic target for the treatment of pneumonia.

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