scholarly journals HMGB1 and inflammatory cytokines in experimental acute lung injury induced in rabbits

2020 ◽  
Vol 72 (4) ◽  
pp. 1329-1338
Author(s):  
C.S. Kurokawa ◽  
J.P. Araújo Júnior ◽  
R.B. Pires ◽  
M.F. Carpi ◽  
M.A. Moraes ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokines ◽  
Lung Tissue ◽  
Tnf Alpha ◽  
Control Group ◽  
Early Expression

ABSTRACT The aim of this work was to measure HMGB1, TNF-alpha, and IL-8 in bronchoalveolar lavage (BAL), serum and TLR2 and TLR4mRNA expression in lung tissue of rabbits with two grades of acute lung injury (ALI). The animals were randomly assigned to groups with severe (S) and mild/moderate (MM) ALI, induced with warm saline, and a control group. HMGB1, TNF-alpha, IL-8, TLR2mRNA and TLR4mRNA were measured after ALI induction. The results showed increased levels of IL-8, TNF-alpha, HMGB1 and TLR4mRNA in the ALI groups. HMGB1, IL-8 and TNF-alpha concentrations in BAL were higher in S compared MM. Increased TLR4mRNA was observed in S and MM versus control. The results suggest an early participation of HMGB1 in ALI together with IL-8 and TNF-alpha and association with severity. TLR4 has early expression and role in ALI pathophysiology but is not associated with severity.

scholarly journals IL-6 knockout alleviates inflammatory response and improve acute lung injury via regulating macrophage polarization in sepsis

2021 ◽  
Author(s):  
Jinxin Zhang ◽  
Kuo Shen ◽  
Jiangang Xie ◽  
Shanshou Liu ◽  
Xiaozhi Bai ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Western Blot ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokines ◽  
Lung Tissue ◽  
General Condition ◽  
Death Rate ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid

Abstract BackgroundSepsis is a fatal disease with a high rate of morbidity and mortality, during which acute lung injury is the earliest and most serious complication. Macrophage plays a crucial role in the initiation and progress of sepsis. This study meant to explore the effect of IL-6 knockout in CLP induced sepsis.MethodsIn this study, cecal ligation and puncture (CLP) was performed on wildtype and interleukin 6 (IL-6) knockout C57 mice. General condition and death rate of sepsis mice were observed. organ samples (lungs, livers, kidneys and hearts) and serum were collected for histology observation and inflammatory cytokine detection. Lung tissue injury detection were conducted via lung injury score, wet/dry ration and protein concentrations measurement of Bronchoalveolar lavage fluid (BALF). In in vivo studies, RAW264.7 macrophages were transfected with IL-6 specific siRNA and treated with LPS. After exposed to IL-6 specific siRNA and LPS, expression of inflammatory cytokines interleukin 1 (IL-1), tumor necrosis factor- (TNF-), IL-6 and interleukin 10 (IL-10) were detected by RT-qPCR, concentration of IL-1 and TNF- in culture supernatant were detected by ELISA and M1 and M2 markers were detected by western blot and flow cytometry.ResultsWe constructed CLP induced sepsis models and found that inhibition of IL-6 could improve general condition and death rate of sepsis mice. Mice in IL-6 knockout group display improved tissue damage, especially in the lung tissue. IL-6 knockout relieved inflammatory cytokines storm in both serum and bronchoalveolar lavage fluid while polarized macrophage to an anti-inflammatory M2 phenotype. In cell model, inhibition of IL-6 could alleviate LPS induced expression of inflammatory cytokines IL-1, TNF-, and IL-6 in macrophages. Western blot and Flow cytometry results indicated that expression of M1 markers (iNOS and CD86) in LPS stimulated macrophages were significantly declined while M2 (Arg-1 and CD206) were enhanced when expression of IL-6 was blocked.Conclusion Inhibition of IL-6 alleviated LPS induced inflammation and exerted protective effect in sepsis via regulating macrophage function and polarization.

scholarly journals Acute lung injury inhibition by juglone in LPS induced sepsis mouse model involves Sirt1 activation

2020 ◽  
Vol 19 (5) ◽  
pp. 1001-1007
Author(s):  
Qiong Hu ◽  
Chunai Yang ◽  
Fenshuang Zheng ◽  
Hongdan Duan ◽  
Yangshan Fu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Inflammatory Cytokines ◽  
Alveolar Epithelial Cells ◽  
Control Group ◽  
Western Blot Assay ◽  
Edema Formation ◽  
Sirt1 Expression ◽  
Treatment Groups

Purpose: To investigate the effect of juglone on LPS induced lung injury in a mouse model and in TC 1cell line.Methods: Edema formation in lungs were measured by determination of lung wet/dry weight. Expressions of various proteins were assessed by western blot assay, while Sirt1 level was assessed using immunohistochemistry. Mice were randomly assigned to nine groups of 10 mice each: normal control, untreated and seven juglone treatment groups. Acute lung injury was induced in mice by injecting LPS (10 mg/kg) via intraperitoneal route (ip). The treatment groups were given 10, 20, 30, 40, 50, 60 and 100 μM of juglone, ip, respectively.Results: The levels of MMP-9, IL-6, IL-1β and iNOS were significantly higher in acute lung injury induced mice compared than the control group (p < 0.05). Treatment of the mice with juglone significantly decreased LPS-induced up-regulation of inflammatory cytokines in a dose-dependentmanner. The production of inflammatory cytokines was almost completely inhibited in the mice treated with 100 mg/kg dose of juglone, while treatment of the LPS-stimulated TC 1 cells with juglone upregulated the expression of Sirt1 mRNA. Down-regulation of Sirt1 expression by siRNA inhibited the effect of juglone on LPS-induced increase in inflammatory cytokine production.Conclusion: Juglone prevents lung injury in mice via up-regulation of Sirt1 expression. Therefore, juglone might be useful for the development of a treatment strategy for lung injury. Keywords: Inflammatory, Sirtuin, Edema, Cytokines, Lung injury, TC 1 lung alveolar epithelial cells, Sirt1

scholarly journals c-Fos is a mechanosensor that regulates inflammatory responses and lung barrier dysfunction during ventilator-induced acute lung injury

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Leilei Zhou ◽  
Chunju Xue ◽  
Zongyu Chen ◽  
Wenqing Jiang ◽  
Shuang He ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protein Expression ◽  
Tidal Volume ◽  
Lung Tissue ◽  
Inflammatory Reaction ◽  
Specific Inhibitor ◽  
Control Group ◽  
Fos Protein ◽  
Volume Group

Abstract Background As one of the basic treatments performed in the intensive care unit, mechanical ventilation can cause ventilator-induced acute lung injury (VILI). The typical features of VILI are an uncontrolled inflammatory response and impaired lung barrier function; however, its pathogenesis is not fully understood, and c-Fos protein is activated under mechanical stress. c-Fos/activating protein-1 (AP-1) plays a role by binding to AP-1 within the promoter region, which promotes inflammation and apoptosis. T-5224 is a specific inhibitor of c-Fos/AP-1, that controls the gene expression of many proinflammatory cytokines. This study investigated whether T-5224 attenuates VILI in rats by inhibiting inflammation and apoptosis. Methods The SD rats were divided into six groups: a control group, low tidal volume group, high tidal volume group, DMSO group, T-5224 group (low concentration), and T-5224 group (high concentration). After 3 h, the pathological damage, c-Fos protein expression, inflammatory reaction and apoptosis degree of lung tissue in each group were detected. Results c-Fos protein expression was increased within the lung tissue of VILI rats, and the pathological damage degree, inflammatory reaction and apoptosis in the lung tissue of VILI rats were significantly increased; T-5224 inhibited c-Fos protein expression in lung tissues, and T-5224 inhibit the inflammatory reaction and apoptosis of lung tissue by regulating the Fas/Fasl pathway. Conclusions c-Fos is a regulatory factor during ventilator-induced acute lung injury, and the inhibition of its expression has a protective effect. Which is associated with the antiinflammatory and antiapoptotic effects of T-5224.

scholarly journals Level of pro-inflammatory cytokines in patients with transfusion-related acute lung injury - Multiple comparisons between patients, controls and donor

2019 ◽  
Vol 10 (2) ◽  
pp. 1448-1455
Author(s):  
Adil Shaker Al-Tamimi ◽  
Israa A. Dheeb
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokines ◽  
Case Control Study ◽  
Serum Levels ◽  
Tnf Alpha ◽  
Blood Component ◽  
Ventilator Support ◽  
Control Study ◽  
Pro Inflammatory Cytokines

Transfusion-related acute lung injury recently regarded as the leading cause of death after transfusion. Several pro-inflammatory cytokines TNF, IL6 and IL8 have been linked to the pathogenesis of TRALI, supported by the findings of increased their serum levels in recipient patients. This is a prospective case-control study, twenty-five patients with a diagnosis of TRALI after transfusion of blood products were included and compared to another 25 transfused patients. Serum was obtained after the onset of TRALI in patients and controls. Other samples were obtained from the saved donor transfused bag or segments. All samples were utilized for cytokines assay. The intubation rate among TRALI patients was 48%. No difference was found in the regarding the type of transfusion and the cytokine level for each specific type of blood or blood component transfused between TRALI and controls. The overall TRALI associated mortality was 4%. Results revealed significantly increased TNF alpha IL-6 levels in sera of TRALI patients as compared with control and donor unit for patients with TRALI. Serum levels of IL-8 were significantly higher in patients with TRALI (mean42.11 pg/ml) as compared with sera of control and donor unit for TRALI patients. Serum level of TNF, IL-6 and-8 in patients with TRALI was significantly higher in patients with longer incubation time. Serum cytokines assay in patients with TRALI may add the significant advantage of assessing the severity, associated mortality and predicting the time of ventilator support.

scholarly journals Therapeutic Efficacy of Excretory-Secretory Products of Trichinella spiralis Adult Worms on Sepsis-Induced Acute Lung Injury in a Mouse Model

2021 ◽  
Vol 11 ◽  
Author(s):  
Huihui Li ◽  
Dapeng Qiu ◽  
Huijuan Yang ◽  
Yuan Yuan ◽  
Lingqin Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Lung Tissue ◽  
Therapeutic Efficacy ◽  
Trichinella Spiralis ◽  
Inflammatory Diseases ◽  
Secretory Products ◽  
Pro Inflammatory Cytokines

Acute lung injury (ALI) is a common complication of systemic inflammation or sepsis with high morbidity and mortality. Although many studies have confirmed that helminth-derived proteins had strong immunomodulatory functions and could be used to treat inflammatory diseases, there is no report on the therapeutic effect of excretory-secretory products of Trichinella spiralis adult worms (Ts-AES) on sepsis-induced ALI. In this study, the therapeutic efficacy of Ts-AES on sepsis-induced ALI and the underlying immunological mechanism and the signaling pathway were investigated. The results indicated that after being treated with Ts-AES, the survival rate of mice with CLP-induced sepsis was significantly increased to 50% for 72 hours after CLP surgery compared to PBS control group with all mice died. The sepsis-induced ALI was largely mitigated characterized by reduced inflammation cell infiltration and pathological changes in lung tissue, with decreased lung injury scores and lung wet/dry weight ratio. The therapeutic efficacy of Ts-AES is associated with stimulated Tregs response with increased regulatory cytokines IL-10 and TGF-β and downregulated pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). The expression of HMGB1, TLR2 and MyD88 in lung tissue was inhibited after treatment of Ts-AES. Our results demonstrated that Ts-AES play an important role in immunomodulation and confer a therapeutic effect on sepsis-induced ALI through inhibiting pro-inflammatory cytokines. The activation of Tregs and increased level of regulatory cytokines IL-10 and TGF-β are possibly involved in the immunomodulatory functions of Ts-AES through HMGB1/TLR2/MyD88 signal pathway. The findings suggest Ts-AES is a potential therapeutic agent for prevention and treatment of sepsis-induced ALI and other inflammatory diseases.

scholarly journals Keratinocyte Growth Factor-2 Reduces Inflammatory Response to Acute Lung Injury Induced by Oleic Acid in Rats by Regulating Key Proteins of the Wnt/β-Catenin Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shao Tenghao ◽  
Chen Ning ◽  
Wang Shenghai ◽  
Sun Qinlong ◽  
Wu Jiaqian ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Blood Cells ◽  
Keratinocyte Growth Factor ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Control Group

Reducing inflammation can effectively relieve acute lung injury (ALI). Objective. To test whether keratinocyte growth factor-2 (KGF-2) can reduce oleic acid-induced inflammation in ALI of rats and explore its possible mechanism. Methods. 45 Sprague-Dawley rats were randomly divided into control group, ALI group, and ALI + KGF-2 group. The animal model of acute lung injury was established by injecting 0.1 mL/kg oleic acid into the tail vein of rats. Rats in the control group were injected with equal volume of normal saline (NS). Each group needs pretreatment 72 hours before the preparation of the acute lung injury model. The control group and ALI group were instilled with 5 ml/kg NS through the airway, and the same amount of KGF-2 was instilled in the ALI + KGF-2 group. It takes 8 hours to successfully prepare the ALI model. Observe the pathological changes of lung tissue through light microscopy, ultrastructural changes through electron microscopy, and the lung wettability/dry weight (w/d) ratio and lung permeability index (LPI). By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. The expressions of Wnt5a, β-catenin, and APC in lung tissue were detected by immunohistochemistry and Western blot. The changes of key proteins in Wnt/β-catenin signaling pathway in the lung tissue of each group were observed. Result. Compared with the ALI group, after KGF-2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. It can also be observed that the expression of Wnt5a, β-catenin, and APC, a key protein in the Wnt/β-catenin signaling pathway, is reduced. The analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in BALF was positively correlated with the expression of Wnt5a, β-catenin, and APC. Conclusion. KGF-2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β-catenin signaling pathway.

Evidence of Abnormally Low Lymphocyte-To-Monocyte Ratio In COVID-19-Induced Severe Acute Respiratory Syndrome

2020 ◽  
Author(s):  
Paolo Lissoni
Keyword(s):  
Lung Injury ◽  
Respiratory Distress ◽  
Inflammatory Cytokines ◽  
Inflammatory Cells ◽  
Tnf Alpha ◽  
Control Group ◽  
Lymphocyte To Monocyte Ratio ◽  
System A ◽  
Infective Disease ◽  
Ventilator Therapy

It is known that lung injury due to COVID-19 responsible for the respiratory distress would mainly depend on host inflammatory response, depending on the excessive production of inflammatory cytokines, such as IL-6, and TNF-alpha, rather than direct virus-induced tissue damage, as well as for other forms of respiratory distress. Moreover, it is known that the inflammatory cytokines may induce profound changes in the behavior of the hematic cells, namely neutrophils, monocytes, and lymphocytes, with a following enhanced tissue infiltration by their inflammatory cells. According to the data available up to now, IL-6 and TNF-alpha would be the main cytokines involved in determining COVID-19-induced lung injury, as well as in other coronavirus infections, and most in general in all conditions of respiratory distress. Since it is known that the functionlessness of the whole immune system is namely depending on the interactions between lymphocyte and macrophage system, a preliminary study was planned to analyze the lymphocyte-to-monocyte ratio (LMR) in COVID-19 infective disease. The study included 17 consecutive patients, who underwent ventilator therapy for COVID-19-induced respiratory distress, and 100 healthy subjects, as a control group. Lymphocytopenia and monocytosis occurred in 14/17 (82%) and in 8/17(47%), respectively. Then, abnormally low values of LMR was found in 12/17 (71%) patients, and LMR men values observed in patients were significantly lower than in control (P<0.001). Therefore, by reflecting the interactions between lymphocyte and monocyte-macrophage systems, LMR could constitute a simple and less expensive biomarker to monitor the clinical evolution of COVID-19 infection.

scholarly journals Nebulized Heparin Attenuates Pulmonary Coagulopathy and Inflammation through Alveolar Macrophages in a Rat Model of Acute Lung Injury

2017 ◽  
Vol 117 (11) ◽  
pp. 2125-2134 ◽  
Author(s):  
Laura Chimenti ◽  
Marta Camprubí-Rimblas ◽  
Raquel Guillamat-Prats ◽  
Maria Gomez ◽  
Jessica Tijero ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Coagulation Cascade ◽  
Control Group ◽  
Proinflammatory Mediators

Objective Alveolar macrophages play a key role in the development and resolution of acute respiratory distress syndrome (ARDS), modulating the inflammatory response and the coagulation cascade in lungs. Anti-coagulants may be helpful in the treatment of ARDS. This study investigated the effects of nebulized heparin on the role of alveolar macrophages in limiting lung coagulation and inflammatory response in an animal model of acute lung injury (ALI). Methods Rats were randomized to four experimental groups. In three groups, ALI was induced by intratracheal instillation of lipopolysaccharide (LPS) and heparin was nebulized at constant oxygen flow: the LPS/Hep group received nebulized heparin 4 and 8 hours after injury; the Hep/LPS/Hep group received nebulized heparin 30 minutes before and 4 and 8 hours after LPS-induced injury; the LPS/Sal group received nebulized saline 4 and 8 hours after injury. The control group received only saline. Animals were exsanguinated 24 hours after LPS instillation. Lung tissue, bronchoalveolar lavage fluid (BALF) and alveolar macrophages isolated from BALF were analysed. Results LPS increased protein concentration, oedema and neutrophils in BALF as well as procoagulant and proinflammatory mediators in lung tissue and alveolar macrophages. In lung tissue, nebulized heparin attenuated ALI through decreasing procoagulant (tissue factor, thrombin–anti-thrombin complexes, fibrin degradation products) and proinflammatory (interleukin 6, tumour necrosis factor alpha) pathways. In alveolar macrophages, nebulized heparin reduced expression of procoagulant genes and the effectors of transforming growth factor beta (Smad 2, Smad 3) and nuclear factor kappa B (p-selectin, CCL-2). Pre-treatment resulted in more pronounced attenuation. Conclusion Nebulized heparin reduced pulmonary coagulopathy and inflammation without producing systemic bleeding, partly by modulating alveolar macrophages.

scholarly journals IL-6 knockout alleviates inflammatory response and improve acute lung injury via regulating macrophage polarization in sepsis

2021 ◽  
Author(s):  
Jinxin Zhang ◽  
Kuo Shen ◽  
Jiangang Xie ◽  
Shanshou Liu ◽  
Xiaozhi Bai ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Western Blot ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokines ◽  
Death Rate ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Tnf Α

Abstract Background Sepsis is a fatal disease with a high rate of morbidity and mortality, during which acute lung injury is the earliest and most serious complication. Macrophage plays a crucial role in the initiation and progress of sepsis. This study meant to explore the effect of IL-6 knockout in CLP induced sepsis. Methods In this study, cecal ligation and puncture (CLP) was performed on wildtype and interleukin 6 (IL-6) knockout C57 mice. General condition and death rate of sepsis mice were observed. organ samples (lungs, livers, kidneys and hearts) and serum were collected for histology observation and inflammatory cytokine detection. Lung tissue injury detection were conducted via lung injury score, wet/dry ration and protein concentrations measurement of Bronchoalveolar lavage fluid (BALF). In in vivo studies, RAW264.7 macrophages were transfected with IL-6 specific siRNA and treated with LPS. After exposed to IL-6 specific siRNA and LPS, expression of inflammatory cytokines interleukin 1 (IL-1), tumor necrosis factor-α (TNF-α), IL-6 and interleukin 10 (IL-10) were detected by RT-qPCR, concentration of IL-1 and TNF-α in culture supernatant were detected by ELISA and M1 and M2 markers were detected by western blot and flow cytometry. Results We constructed CLP induced sepsis models and found that inhibition of IL-6 could improve general condition and death rate of sepsis mice. Mice in IL-6 knockout group display improved tissue damage, especially in the lung tissue. IL-6 knockout relieved inflammatory cytokines storm in both serum and bronchoalveolar lavage fluid while polarized macrophage to an anti-inflammatory M2 phenotype. In cell model, inhibition of IL-6 could alleviate LPS induced expression of inflammatory cytokines IL-1, TNF-α, and IL-6 in macrophages. Western blot and Flow cytometry results indicated that expression of M1 markers (iNOS and CD86) in LPS stimulated macrophages were significantly declined while M2 (Arg-1 and CD206) were enhanced when expression of IL-6 was blocked. Conclusion Inhibition of IL-6 alleviated LPS induced inflammation and exerted protective effect in sepsis via regulating macrophage function and polarization.

scholarly journals Effects of Bacterial Translocation and Autophagy on Acute Lung Injury Induced by Severe Acute Pancreatitis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Hanlin Wang ◽  
Chang Li ◽  
Yingjian Jiang ◽  
Hongbo Li ◽  
Dianliang Zhang
Keyword(s):  
Oxidative Stress ◽  
Acute Pancreatitis ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Severe Acute Pancreatitis ◽  
Lung Tissue ◽  
Bacterial Translocation ◽  
Control Group ◽  
Sham Operation ◽  
Rdna Sequencing

Aim. To reveal the role of bacterial translocation (BT) and autophagy in severe acute pancreatitis-induced acute lung injury (SAP-ALI). Methods. Rats were separated into a control (sham-operation) group (n=10) and a SAP group (n=30). Sodium taurocholate (5%) was retrogradely injected into the cholangiopancreatic duct to induce SAP-ALI in rats. Then, 16S rDNA sequencing was used to detect bacterial translocation (BT). Hematoxylin eosin staining (HE) was used to detect morphological changes to the pancreas, intestine, and lung. And lung tissue wet/dry weight ratio (W/D ratio) was used to assess the extent of pulmonary edema. The expressions of LC3II and Beclin1 proteins were analyzed by western blot and immunofluorescence. Glutathione peroxidase (GPx), malondialdehyde (MDA), and superoxide dismutase (SOD) were used to assess oxidative stress in lung tissue. Results. Levels of TNF-α, IL-6, lipase, and amylase in the SAP group were significantly higher than those in the control group (P<0.01). Histopathological score and W/D ratio of the lung in the SAP-BT(+) group were significantly higher than that in the SAP-BT(-) group (P<0.01). LC3II expression was higher in the SAP-BT(-) group than that in the SAP-BT(+) group (P<0.01). The results were consistent with those of LC3II immunofluorescence assay. The expression of Beclin1 was similar to that of LC3II (P<0.01). MDA content in the SAP-BT(+) group was significantly higher than that in the SAP-BT(-) group (P<0.01), whereas SOD and GPX activities were opposite (P<0.01). Conclusions. BT can aggravate SAP-ALI with the increasing oxidative stress level, which may be related to the decrease of autophagy level.

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