scholarly journals Mechanism of MCP-1 in Acute Lung Injury and Advanced Therapy by Drug-Loaded Dextrin Nanoparticle

2018 ◽  
Vol 2018 ◽  
pp. 1-7
Author(s):  
Zheng Cao ◽  
Jing-Lan Liu ◽  
Shen Wu ◽  
Qiao Wang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Weight Ratio ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Inflammatory Factors ◽  
Saline Control ◽  
Mrna Levels ◽  
Blood Gas ◽  
Wet Weight

Objective. To observe the expression of monocyte chemotactic protein 1 (MCP-1) in acute lung injury (ALI) rat model, to characterize its effect on the development and progression of ALI, and to identify the potential new drug delivery approach during in vivo experiment. Method. The effects of different doses of lipopolysaccharide (LPS) on human pulmonary artery endothelial cells (HPAEC) were tested. For the animal experiments, thirty Sprague-Dawley (SD) rats were divided into physiological saline control group (NC group), the LPS model group (L group), the antagonist RS102895 combined with LPS group (R + L group), and the antagonist RS102895-loaded polyaldehyde dextran nanoparticles combined with LPS group (DNPR + L group). The blood gas analysis and dry/wet weight ratio were detected 24 hours after interventions. The levels of inflammatory factors, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were tested by ELISA. The expression of monocyte chemoattractant protein-1 (MCP-1) in lung tissues was examined through Western blot, and the change of MCP-1 mRNA expression level was detected by performing RT-PCR. Result. LPS was responsible for inducing ALI in rats, and the degree of cell damage was dose-dependent. Blood gas analysis of L group showed that PaO2 and PaO2/FiO2 levels were significantly lower than those of the NC group (P<0.05), while the dry/wet weight ratio of lung tissues in L group increased (P<0.05). Inflammatory factors including TNF-α and IL-1β and the expression of MCP-1 in both protein and mRNA levels were higher in L group than in the NC group (P<0.05). The inhibition of the interaction between MCP-1 and chemokines receptor 2 (CCR2) by antagonist RS102895 can significantly alleviate the ALI in rats, which is accompanied by a significant decrease of inflammatory factors and MCP-1 expression (P<0.05). Compared with R + L group, treatment with DNPR and LPS combination significantly improved the condition of rats and decreased the level of TNF-α, IL-1β, and MCP-1 expression (P<0.05). Conclusion. In ALI, RS102895 can inhibit the MCP-1/CCR2 interaction, therefore, retarding the progress of ALI. Because of the high transfection efficiency of inhibitor RS102895packgaed by polyaldehyde dextran nanoparticles, this phenomenon particularly reached a significant level. The results imply new insights for the treatment of ALI.

scholarly journals Comparison of SpO2/FiO2 and PaO2/FiO2 ratios as markers of acute lung injury

2017 ◽  
Vol 57 (1) ◽  
pp. 30 ◽  
Author(s):  
Dewi Shandi Laila ◽  
Chairul Yoel ◽  
Hakimi Hakimi ◽  
Munar Lubis
Keyword(s):  
Acute Lung Injury ◽  
Linear Regression ◽  
Lung Injury ◽  
Pulse Oximetry ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Blood Gas ◽  
Weak Correlation ◽  
Non Invasive ◽  
Arterial Blood

Background One of the diagnostic criteria for acute lung injury (ALI) is the PaO2/FiO2 (P/F) ratio. This measurement is obtained by blood gas analysis, which involves an invasive procedure (arterial blood draw). In order to reduce invasive procedures on critically ill patients, an alternative non-invasive marker for ALI is needed. The SpO2/FiO2 (S/F) ratio attained by pulse oximetry may be a suitable alternative.Objective To investigate for a correlation between S/F ratio and P/F ratio, in order to find an alternative non-invasive marker of ALI.Methods A cross-sectional study was conducted in the pediatric intensive care unit (PICU) at Haji Adam Malik Hospital, Medan from August 2012 to June 2013. Subjects (children aged 1 month – 18 years) underwent blood gas analysis when their pulse oximetry showed saturation of 80-97% within 24 hours of ventilator use. We measured PaO2, SpO2, and FiO2 and calculated S/F and P/F ratios. Data were analyzed by Spearman’s correlation and linear regression tests.Results Of 69 PICU patients, 39 children fulfilled the criteria for ALI. The S/F ratio and P/F ratio had a weak correlation (r=0.2; P=0.18). The linear regression equation was S/F ratio = 129.67 + 0.11 (P/F), with S/F ratio values of 162.67 and 151.67 correlating to P/F ratio values of 300 and 200, respectively.Conclusion  The S/F ratio has a weak correlation with P/F ratio for ALI in children.  

scholarly journals Protective effect of Cordyceps sinensis extract on lipopolysaccharide-induced acute lung injury in mice

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Shuiqiao Fu ◽  
Weina Lu ◽  
Wenqiao Yu ◽  
Jun Hu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Weight Ratio ◽  
Cordyceps Sinensis ◽  
Myeloperoxidase Activity ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Tnf Α ◽  
Cox 2

Abstract Background: To study the protective effect of Cordyceps sinensis extract (Dong Chong Xia Cao in Chinese [DCXC]) on experimental acute lung injury (ALI) mice. Methods and results: ALI model was induced by intratracheal-instilled lipopolysaccharide (LPS, 2.4 mg/kg) in BALB/c male mice. The mice were administrated DCXC (ig, 10, 30, 60 mg/kg) in 4 and 8 h after receiving LPS. Histopathological section, wet/dry lung weight ratio and myeloperoxidase activity were detected. Bronchoalveolar lavage fluid (BALF) was collected for cell count, the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and nitric oxide (NO) in BALF was detected by ELISA, the protein and mRNA expression of nuclear factor-κB p65 (NF-κB p65), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung tissue was detected by Western blot and RT-PCR. The result showed that DCXC could reduce the degree of histopathological injury, wet/dry weight ratio (W/D ratio) and myeloperoxidase activity (P<0.05) with a dose-dependent manner. The increased number of total cells, neutrophils and macrophages in BALF were significantly inhibited by DCXC treatment (P<0.05). The increased levels of TNF-α, IL-1β, IL-6 and NO in BALF after LPS administration was significantly reduced by DCXC (P<0.05). In addition, the increased protein and mRNA levels of iNOS, COX-2 and NF-κB p65 DNA binding ability in LPS group were dose-dependently reduced by DCXC treatment (P<0.05). Conclusion: DCXC could play an anti-inflammatory and antioxidant effect on LPS-induced ALI through inhibiting NF-κB p65 phosphorylation, and the expression of COX-2 and iNOS in lung. The result showed that DCXC has a potential protective effect on the ALI.

scholarly journals miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

2020 ◽  
Author(s):  
Li Ding ◽  
Xiang Gao ◽  
Shenghui Yu ◽  
Liufang Sheng
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Weight Ratio ◽  
Dry Weight ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Inflammatory Factor ◽  
Over Expression

Abstract Background: To investigate the mechanism of miR-128-3p and MAPK14 on the protective effect of dexmedetomidine on acute lung injury in septic mice. Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO2, PaCO2, MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to verify the targeting relationship between miR-128-3p and MAPK14. qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased. DEX treatment and up-regulation of miR-128-3p could significantly decrease the contents of MDA, MPO, inflammatory factor levels and significantly increase the SOD content in model mice, however, MAPK14 over-expression had opposite effects. miR-128-3p up-regulation enhanced the changes of above indicators caused by DEX treatment and MAPK14 over-expression could block the protective effect of DEX on acute lung injury in septic mice. miR-128-3p up-regulation reversed the effects of MAPK14 over-expression in model mice. Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

scholarly journals miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

2020 ◽  
Author(s):  
Li Ding ◽  
Xiang Gao ◽  
Shenghui Yu ◽  
Liufang Sheng
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Weight Ratio ◽  
Dry Weight ◽  
Serum Levels ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Targeted Inhibition

Abstract Background: To investigate the role of miR-128-3p and MAPK14 in the dexmedetomidine treatment of acute lung injury in septic mice. Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO 2 , PaCO 2 , MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to detect the targeting relationship of miR-128-3p and MAPK14, and qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased (all p < 0.05). Compared with the Model group, the contents of MDA, MPO, inflammatory factors in the DEX group and miR-128-3p mimic group were significantly decreased, and the content SOD was significantly increased, however, opposite results were occurred in oe-MAPK14 group (all p < 0.05). Compared with the DEX group, all the indicators in miR-128-3p mimic+DEX group showed significant improvement (all p < 0.05). Compared with the miR-128-3p mimic group, all the indicators were deteriorated in the miR-128-3p mimic+oe-MAPK14 group (all p < 0.05). The combination of DEX and oe-MAPK14 blocked the protective effect of dexmedetomidine on acute lung injury in septic mice. Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

scholarly journals miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

2020 ◽  
Author(s):  
Li Ding ◽  
Xiang Gao ◽  
Shenghui Yu ◽  
Liufang Sheng
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Weight Ratio ◽  
Dry Weight ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Inflammatory Factor ◽  
Over Expression

Abstract Background: To investigate the mechanism of miR-128-3p and MAPK14 on the protective effect of dexmedetomidine on acute lung injury in septic mice.Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO2, PaCO2, MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to verify the targeting relationship between miR-128-3p and MAPK14. qPCR and WB were used to detect the expression of miR-128-3p and MAPK14.Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased. DEX treatment and up-regulation of miR-128-3p could significantly decrease the contents of MDA, MPO, inflammatory factor levels and significantly increase the SOD content in model mice, however, MAPK14 over-expression had opposite effects. miR-128-3p up-regulation enhanced the changes of above indicators caused by DEX treatment and MAPK14 over-expression could block the protective effect of DEX on acute lung injury in septic mice. miR-128-3p up-regulation reversed the effects of MAPK14 over-expression in model mice.Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

scholarly journals Transcutaneous Electrical Acupoint Stimulation Attenuates Lung Injury Caused by Tourniquet-induced Limb Ischemia/reperfusion During Lower Extremity Surgery: A Randomized Controlled Trial

2020 ◽  
Author(s):  
Lirong Gong ◽  
Dinghuan Zhao ◽  
Cui Li ◽  
Yue Ji ◽  
Yongxing Kan ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lower Extremity ◽  
Ischemia Reperfusion ◽  
Blood Gas Analysis ◽  
Limb Ischemia ◽  
Gas Analysis ◽  
Blood Gas ◽  
Arterial Blood ◽  
Acupoint Stimulation ◽  
Extremity Ischemia

Abstract Background: Tourniquet-induced extremity ischemia-reperfusion injury is one of the major complications in patients with lower extremity surgery, while lung is the most vulnerable organ to insult subsequent to ischemia-reperfusion. Current scientific research data has shown that electric stimulation at special acupoints could suppress inflammasome activation and subsequently exert protective effects in the lungs. Thus, the effect of transcutaneous electrical acupuncture point stimulation (TEAS) on lung injury induced by limb ischemia/reperfusion remains to be elucidated. Methods: One hundred individuals scheduled for unilateral lower extremity surgery were randomly divided into 2 groups (n=50 each): transcutaneous electrical acupoint stimulation group (group T) and control group (group C). Patients in group T were given TEAS at FeiShu (BL13, bilateral) acupoints and ZuSanLi (ST36, non-surgical side) acupoint, while patients in group C received sham stimulation (no current) at the same acupoints for the same time as the TEAS group. Arterial blood samples were collected to assess blood gas analysis and other indicators. Results: The TEAS group showed significant improvements in blood gas analysis. Compared with group C, PaO2 and oxygenation index (OI) in group T were significantly increased at T4(4h after removing the tourniquet), while A-aDO2 and respiratory index (RI) were decreased at T4. There was an increase in the HO-1 levels in group T at T3(2h after removing the tourniquet) and T4 compared with group C. Compared with group T, SOD levels were significantly lower at T4 in group C. At T4, the levels of ICAM-1, IL-6 and IL8 were significantly lower in group T when compared to group C. At T3 and T4, IL-10 levels were higher when compared to group C, while TNF-a levels were significantly lower.Conclusions: Transcutaneous electrical acupoint stimulation attenuates lung injury following tourniquet-induced extremity ischemia-reperfusion in patients, and HO-1 is endowed of potential mechanism of cytoprotective effects against tourniquet-induced lung injury. Trial registration: Chinese Clinical Trial Registry, ChiCTR-IOR-16008264. Registered 11 April 2016, http://www.chictr.org.cn/ ChiCTR-IOR-16008264

scholarly journals Hyperbaric Oxygen Combined With Hydrogen-rich Saline Protect Against Acute Lung Injury Induced by Lipopolysaccharide in Rat Model

2021 ◽  
Author(s):  
Yintao Chang ◽  
Zhenzhen Zhang ◽  
Xiaochen Bao ◽  
Mingdong Wang ◽  
Yuxiang Jin ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hyperbaric Oxygen ◽  
Cell Apoptosis ◽  
Combined Treatment ◽  
Weight Ratio ◽  
Dry Weight ◽  
Inflammatory Factors ◽  
Therapeutic Effects ◽  
Pulmonary Tissue

Abstract Background: To investigate the effects of hydrogen-rich saline (HRS) combined with hyperbaric oxygen (HBO) on acute lung injury (ALI) and its clinical significance.Methods: 40 adult male Sprague-Dawlay rats were randomly divided into 5 groups: the sham, LPS, LPS + HBO, LPS + HRS and LPS + HBO + HRS. LPS at a rate of 3mg/kg was injected into the trachea of the experimental animals to develop ALI model, then the animals were respectively given simple HBO or HRS treatment or combined treatment. 3 days later, we study lung pathological, the levels of inflammatory factors , and cell apoptosis in the pulmonary tissue was detected by Tunel and cell apoptosis rate was calculated accordingly. Results: In the groups treated with HRS and HBO, pulmonary pathological data, wet-dry weight ratio and immflammatory factors in the pulmonary tissues and avelar lavage fluid were signficantly superiror to those of the sham group（P<0.05）. Cell apoptosis detection revealed that the simple treatment with HRS or HBO, or combined treatment with both, can all alleviate cell apoptosis, and the combined treatment with HRS and HBO was obviously superior to single treatment（P<0.05）.Conclusions: HRS and HBO could all decrease the release of immflammatory cytokines in lung tissue, reduce accumulation of oxidative products and alleviate apoptosis of pulmoanry cells, and could produce good therapeutic effects on ALI induced by LPS. HBO combined with HRS seems to have a synergistic effect on the decrease of cell apoptosis, and in the expression of immflammatory cytokines and the generation of related immflammatory products, the combined use of HBO and HRS showed a decreasing trend as compared with simple application.

Targeted Treatment Of Acute Chest Syndrome In Transgenic Sickle Mice

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 727-727 ◽  
Author(s):  
Samit Ghosh ◽  
Olufolake Adisa ◽  
Prasanthi Chappa ◽  
Fang Tan ◽  
Kesmic A Jackson ◽  
...  
Keyword(s):  
Lung Injury ◽  
Large Scale ◽  
Conflicts Of Interest ◽  
Weight Ratio ◽  
Gas Analysis ◽  
Acute Chest Syndrome ◽  
Blood Gas ◽  
Respiratory Dysfunction ◽  
Breath Rate ◽  
Arterial Blood

Abstract Acute chest syndrome (ACS) is a major cause of morbidity and mortality in sickle cell disease (SCD). The diagnosis, prevention and treatment of ACS pose major clinical concerns in SCD partly because the mechanism underlying the pathogenesis of this syndrome remains elusive. Our group first reported that excess intravascular hemin causes a lethal acute lung injury (ALI) in transgenic SCD mice reminiscent of ACS (Ghosh and Ofori-Acquah, Blood 116 Suppl 1:944, 2010). Subsequently, large-scale genomics studies by Bean et al., (Blood 120:3822-8, 2012) and Galarneau et al., (Blood, 122:434-42, 2013) have implicated hemin catabolism and inflammation in the pathogenesis of ACS. In addition, we have reported recently that raised plasma free hemin increases the odds of ACS in children with SCD (Adisa et al., Br J Haematol. 2013). Collectively, these studies support a new theme of ACS pathogenesis involving extracellular hemin. In the current study, we validated the respiratory dysfunction of this ACS model, tested the hypothesis that toll-like receptor 4 (TLR4) mediates the associated lung injury, and examined the efficacy of two strategies to treat the condition in mice. Arterial blood gas analysis of SS mice with the ACS-like disease confirmed severe hypoxemia (PaO2; 40.23 ±3.85 mmHg, SO2; 58.72±6.6%, p<0.001), and revealed worsening hypercapnia (PaCO2; 56.08±3.64 mmHg) and acidosis (mean pH; 7.21), which are all typical of severe ALI. Blood gas parameters remained normal in control AA mice exposed to the same concentration of extracellular hemin. Next, we generated two types of sickle bone marrow chimeric mice that lack expression of TLR4 in non-hematopoietic cells (SSNHTLR4-/-) or express TLR4 on all cell types (SSTLR4+/+). Induction of extracellular hemin crisis with 70 micromoles/kg of hemin resulted in rapid oxygen desaturation, reduced breath rate, pulmonary infiltration, high lung wet/dry weight ratio and sudden death in the SSTLR4+/+ chimeras (n=6). Although all the SSNHTLR4-/- mice acquired a similar phenotype of hemin crisis as the SSTLR4+/+ mice, defined by acute intravascular hemolysis (∼1g/dl drop in Hb, ∼1g/dl increase in cell-free Hb), exhaustion of plasma hemopexin, ∼3-fold increase in plasma free hemin, they did not develop any respiratory symptoms (n=7). Next, we tested two potential therapies, recombinant human hemopexin and TAK-242 a small molecule inhibitor of TLR4. Both agents protected SS mice from developing ACS when they were administered immediately after the induction of hemin crisis. When SS mice were treated after developing respiratory distress evident by significant reductions in oxygen saturation and breath rate, only the recombinant human hemopexin was effective in preventing respiratory failure. In conclusion, we show that TLR4 expressed by the vessel wall, most likely the endothelium, mediates the inflammatory response to excess free hemin associated with severe ACS in mice. Pharmacological inhibition of TLR4 signaling and hemin sequestration may be effective in preventing the development of ACS. In addition, hemin sequestration offers a targeted approach that may halt the progression of ACS in those with more advanced disease. Disclosures: No relevant conflicts of interest to declare.

Prevention of interleukin 2-induced acute lung injury in guinea pigs by pentoxifylline

1989 ◽  
Vol 67 (6) ◽  
pp. 2432-2437 ◽  
Author(s):  
A. Ishizaka ◽  
J. R. Hatherill ◽  
H. Harada ◽  
M. Yonemaru ◽  
H. Hoffmann ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Guinea Pigs ◽  
Interleukin 2 ◽  
Weight Ratio ◽  
Saline Control ◽  
Control Group ◽  
Lung Water ◽  
Lung Weight ◽  
Cell Counts

We administered recombinant human interleukin 2 (IL-2) to guinea pigs to investigate whether IL-2 would cause acute lung injury. In addition, we examined the effects of pentoxifylline (PTXF) on IL-2-induced acute lung injury. Three groups of animals were studied over a period of 8 h. The saline control group was injected intravenously with 2 ml of pyrogen-free saline; the IL-2 group was injected intravenously with 4 X 10(6) U/kg recombinant IL-2; and the IL-2-PTXF group was injected with a 20-mg/kg bolus of PTXF followed by a continuous infusion (6 mg.kg-1.h-1) started 60 min before injection of 4 X 10(6) U/kg IL-2. Lung water (wet-to-dry lung weight ratio), the concentration ratios of 125I-albumin in bronchoalveolar lavage (BAL) fluid and lung tissue compared with plasma (125I-albumin BAL-to-plasma, 125I-albumin lung-to-plasma), and cell counts in BAL fluid were examined. An intravenous injection of IL-2 caused an increased lung water (P less than 0.01), an increased 125I-albumin lung-to-plasma ratio (P less than 0.05), and a significant increase in the absolute number of neutrophils, lymphocytes, and macrophages in BAL fluid compared with the saline control. In contrast, the PTXF-pretreated group did not demonstrate IL-2-induced acute lung injury (lung water, 125I-albumin lung-to-plasma) or increased accumulation of neutrophils, lymphocytes, and macrophages in the BAL. These data suggest a possible role for PTXF in attenuating the side effects of IL-2.

Co(II) and Cu(II) coordination polymers: Crystal structures and treatment effect on acute lung injury treatment by inhibiting inflammatory response

2020 ◽  
Vol 19 (3) ◽  
pp. 207-215
Author(s):  
Xiao-Jing Li ◽  
Wei-Jun Yan
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Partial Pressure ◽  
Coordination Polymers ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Enzyme Linked Immunosorbent Assay ◽  
X Ray Diffraction ◽  
Elemental Analyses ◽  
Injury Treatment

Two coordination polymers named [Co(tib)(H2O)3]· ipa·2H2O (1, H2ipa = iso-phthalic acid) and [Cu3(tib)2(BTB)2]·DMF·2H2O (2, H3BTB = 4,4′,4′′-gbenzene-1,3,5-triyl-tribenzoic acid, DMF = N,N-dimethylformamide) were constructed using a solvothermal method by reaction of metal salts with the 1,3,5-tris(1-imidazolyl)benzene (tib) ligands and different carboxylate linkers as the co-ligands. The two complexes have been characterized by X-ray diffraction as well as the elemental analyses. Subsequently, the protective effect of compounds 1 and 2 on the acute lung injury and its related mechanism was explored. Firstly, the enzyme linked immunosorbent assay (ELISA) was performed to detect the release of the inflammatory cytokines. Then, the partial pressure of oxygen (PaO2) and the partial pressure of carbon dioxide (PaCO2) was measured with blood gas analysis.

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