scholarly journals Rabdosia japonicavar.glaucocalyxFlavonoids Fraction Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Chun-jun Chu ◽  
Nai-yu Xu ◽  
Xian-lun Li ◽  
Long Xia ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protein Concentration ◽  
Biochemical Analysis ◽  
Sandwich Elisa ◽  
Lavage Fluid ◽  
Therapeutic Effects ◽  
Proinflammatory Mediators ◽  
Lps Challenge ◽  
Complement Deposition

Rabdosia japonicavar.glaucocalyx(Maxim.) Hara, belonging to theLabiataefamily, is widely used as an anti-inflammatory and antitumor drug for the treatment of different inflammations and cancers.Aim of the Study. To investigate therapeutic effects and possible mechanism of the flavonoids fraction ofRabdosia japonicavar.glaucocalyx(Maxim.) Hara (RJFs) in acute lung injury (ALI) mice induced by lipopolysaccharide (LPS).Materials and Methods. Mice were orally administrated with RJFs (6.4, 12.8, and 25.6 mg/kg) per day for 7 days, consecutively, before LPS challenge. Lung specimens and the bronchoalveolar lavage fluid (BALF) were isolated for histopathological examinations and biochemical analysis. The level of complement 3 (C3) in serum was quantified by a sandwich ELISA kit.Results. RJFs significantly attenuated LPS-induced ALI via reducing productions of the level of inflammatory mediators (TNF-α, IL-6, and IL-1β), and significantly reduced complement deposition with decreasing the level of C3 in serum, which was exhibited together with the lowered myeloperoxidase (MPO) activity and nitric oxide (NO) and protein concentration in BALF.Conclusions. RJFs significantly attenuate LPS-induced ALIviareducing productions of proinflammatory mediators, decreasing the level of complement, and reducing radicals.

Protective Role of Urinary Trypsin Inhibitor in Acute Lung Injury Induced by Lipopolysaccharide

2005 ◽  
Vol 230 (4) ◽  
pp. 281-287 ◽  
Author(s):  
Ken-ichiro Inoue ◽  
Hirohisa Takano ◽  
Rie Yanagisawa ◽  
Miho Sakurai ◽  
Akinori Shimada ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Trypsin Inhibitor ◽  
Inflammatory Diseases ◽  
Lavage Fluid ◽  
Intercellular Adhesion Molecule ◽  
Urinary Trypsin Inhibitor ◽  
Intercellular Adhesion Molecule 1 ◽  
Lung Water ◽  
Lps Challenge

Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used as a drug for patients with acute inflammatory disorders such as disseminated intravascular coagulation, shock, and pancreatitis. However, direct contribution of UTI to inflammatory diseases has not been established. The present study analyzed acute inflammatory lung injury induced by lipopolysaccharide (LPS) in UTI-deficient (–/–) mice and corresponding wild-type (WT) mice. UTI (–/–) and WT mice were treated intratracheally with vehicle or LPS (125 μg/kg). The cellular profile of bronchoalveolar lavage fluid, lung water content, histology, and expression of proinflammatory molecules in the lung were evaluated. After LPS challenge, both genotypes of mice revealed neutrophilic lung inflammation and pulmonary edema. UTI (–/–) mice, however, showed more prominent infiltration of inflammatory cells and edema than WT mice. After LPS challenge in both genotypes of mice, the lung levels of mRNA and/or protein expression of interleukin-1β, macrophage inflammatory protein-1α, macrophage chemoattractant protein-1, keratinocyte chemoattractant, and intercellular adhesion molecule-1 (ICAM-1) were elevated in both groups, but to a greater extent in UTI (–/–) mice than in WT mice. These results suggest that UTI protects against acute lung injury induced by bacterial endotoxin, at least partly, through the inhibition of the enhanced local expression of proinflammatory cytokines, chemokines, and ICAM-1.

Therapeutic Effects of Baicalin on Lipopolysaccharide-Induced Acute Lung Injury in Rats

2008 ◽  
Vol 36 (02) ◽  
pp. 301-311 ◽  
Author(s):  
Kun-Lun Huang ◽  
Chien-Sheng Chen ◽  
Ching-Wang Hsu ◽  
Min-Hui Li ◽  
Hung Chang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Weight Ratio ◽  
Histological Finding ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Blue Dye ◽  
Therapeutic Effects ◽  
Lung Weight ◽  
Lactate Dehydrogenase Activity

Baicalin is a flavonoid present in many traditional Chinese medicines. A number of studies show that baicalin has anti-inflammatory actions and protects against a variety of tissue and organ injuries. The effect of baicalin in lipopolysaccharide (LPS)-induced acute lung injury is not well studied. In this study, typically acute lung injury was induced in rat by intratracheal injection of LPS, which increased lactate dehydrogenase activity and protein content in bronchoalveolar lavage fluid, wet/dry lung weight ratio, Evan's blue dye leakage, and neutrophil infiltration. Baicalin (20 mg/kg) was administrated 1 hour before or 30 min after LPS injection. Both pre and post-treatment with baicalin attenuated the increase of these parameters and improved histological finding. Our results suggest that baicalin has a therapeutic effect on LPS-induced acute lung injury.

scholarly journals Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1742 ◽  
Author(s):  
Ching-Ying Huang ◽  
Jeng-Shyan Deng ◽  
Wen-Chin Huang ◽  
Wen-Ping Jiang ◽  
Guan-Jhong Huang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Er Stress ◽  
Anterior Segment ◽  
Signal Transduction Pathway ◽  
Lavage Fluid ◽  
Cell Number ◽  
Lps Challenge ◽  
Induced Apoptosis

The anti-inflammatory effect of hispolon has identified it as one of the most important compounds from Sanghuangporus sanghuang. The research objectives were to study this compound using an animal model by lipopolysaccharide (LPS)-induced acute lung injury. Hispolon treatment reduced the production of the pro-inflammatory mediator NO, TNF-α, IL-1β, and IL-6 induced by LPS challenge in the lung tissues, as well as decreasing their histological alterations and protein content. Total cell number was also reduced in the bronchoalveolar lavage fluid (BALF). Moreover, hispolon inhibited iNOS, COX-2 and IκB-α and phosphorylated IKK and MAPK, while increasing catalase, SOD, GPx, TLR4, AKT, HO-1, Nrf-2, Keap1 and PPARγ expression, after LPS challenge. It also regulated apoptosis, ER stress and the autophagy signal transduction pathway. The results of this study show that hispolon regulates LPS-induced ER stress (increasing CHOP, PERK, IRE1, ATF6 and GRP78 protein expression), apoptosis (decreasing caspase-3 and Bax and increasing Bcl-2 expression) and autophagy (reducing LC3 I/II and Beclin-1 expression). This in vivo experimental study suggests that hispolon suppresses the LPS-induced activation of inflammatory pathways, oxidative injury, ER stress, apoptosis and autophagy and has the potential to be used therapeutically in major anterior segment lung diseases.

Diammonium glycyrrhizinate lipid ligand ameliorates lipopolysaccharide-induced acute lung injury by modulating vascular endothelial barrier function

2020 ◽  
Author(s):  
Mei-Mei Liu ◽  
Jin Zhou ◽  
Dan Ji ◽  
Jun Yang ◽  
Yan-Ping Huang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Protein Concentration ◽  
Weight Ratio ◽  
Dry Weight ◽  
Lavage Fluid ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Junction Protein

Abstract Background: The present study investigated the attenuating effect of diammonium glycyrrhizinate lipid ligand (DGLL) on acute lung injury (ALI) and pulmonary edema induced by lipopolysaccharide (LPS) in rats.Methods: Rat ALI model was established by LPS (10 mg/kg) intraperitoneal injection, and DGLL (30, 60, 120 mg/kg) was administrated orall 1 hour before LPS infusion. Six hours after LPS stimulation, lung injury was evaluated by histological staining. Pulmonary edema was evaluated by lung wet-dry weight ratio, the protein concentration of bronchoalveolar lavage fluid (BALF), and the evans blue (EB) extravasation in lung tissues. The expression of cytokines and adhesion molecules in lung tissues were detected by ELISA method. The myeloperoxidase (MPO) expression was detected by immunohistochemical staining. Western blot was used to detect the expression changes of the proteins associated with pulmonary inflammation and microvascular permeability.Results: DGLL significantly inhibited LPS induced ALI, manifested as attenuation of MPO positive cells and TNF-α, IL-6, ICAM-1 expression in rat lung tissue. In addition, DGLL abrogated LPS-induced pulmonary edema, decreased the protein concentration in BALF and EB extravasation. Meanwhile, DGLL inhibited the degradation of vascular endothelial cadherin (VE-Cadherin) and tight junction protein, including ZO-1, Occludin, and JAM-1.Conclusions: DGLL has an inhibitory effect on LPS-induced rat ALI, which is related to the inhibition of inflammatory cell infiltration and microvascular barrier disruption. These results provide a theoretical basis for DGLL in the potential clinical treatment of ALI.

scholarly journals Therapeutic Effect of the Tuber ofAlisma orientaleon Lipopolysaccharide-Induced Acute Lung Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Kyun Ha Kim ◽  
Min Jung Kwun ◽  
Jun-Yong Choi ◽  
Kyung-Seop Ahn ◽  
Sei-Ryang Oh ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Therapeutic Effect ◽  
Lung Inflammation ◽  
Lethal Dose ◽  
Ethanol Extract ◽  
Lavage Fluid ◽  
Luciferase Reporter ◽  
Therapeutic Effects ◽  
Alisma Orientale

AlthoughAlisma orientale, an ethnic herb, has been prescribed for treating various diseases in Asian traditional medicine, experimental evidence to support its therapeutic effects is lacking. Here, we sought to determine whetherA. orientalehas a therapeutic effect on acute lung injury (ALI). Ethanol extract of the tuber ofA. orientale(EEAO) was prepared and fingerprinted by HPLC for its constituents. Mice received an intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) for the induction of ALI. At 2 h after LPS treatment, mice received an intratracheal (i.t.) spraying of various amounts of EEAO to the lung. Bioluminescence imaging of transgenic NF-κB/luciferase reporter mice shows that i.t. EEAO posttreatment suppressed lung inflammation. In similar experiments with C57BL/6 mice, EEAO posttreatment significantly improved lung inflammation, as assessed by H&E staining of lung sections, counting of neutrophils in bronchoalveolar lavage fluid, and semiquantitative RT-PCR analyses of proinflammatory cytokines and Nrf2-dependent genes in the inflamed lungs. Furthermore, EEAO posttreatment enhanced the survival of mice that received a lethal dose of LPS. Together, our results provide evidence thatA. orientalehas a therapeutic effect on ALI induced by sepsis.

scholarly journals Estradiol attenuates LPS-induced acute lung injury via induction of aquaporins AQP1 and AQP5

2021 ◽  
Vol 19 ◽  
pp. 205873922110491
Author(s):  
Xiaobo Wang ◽  
Xiuyun Zhou ◽  
Xiumei Xia ◽  
Yili Zhang
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Weight Ratio ◽  
Lung Edema ◽  
Therapeutic Effects ◽  
Lps Challenge ◽  
And Oxidative Stress

Background Acute lung injury (ALI) is associated with increased inflammation and oxidative stress. Estradiol is produced by the ovaries and is the most active hormone of estrogen. Our aim was to investigate whether estradiol contributes to protect against lipopolysaccharide (LPS)-induced ALI via induction of aquaporins AQP1 and AQP5 and the underlying mechanisms. Methods and results For induction of ALI, LPS was applied once by intraperitoneal injection in SD rats 14 days after oophorectomy. To assess the therapeutic effects of estradiol on LPS-induced ALI, estradiol was subcutaneously injected for 1 h prior to LPS challenge. Estradiol can significantly attenuate the lung edema reflected by decreasing wet-to-dry weight ratio and permeability of lung and total protein concentration of bronchial lavage fluid (BALF). Results of histological detection showed that estradiol attenuated the lung injury reflected by reducing edema, congestion, and thickening pulmonary septal of lung tissues. In addition, estradiol attenuated TNF-α, IL-1β, and IL-6 and oxidative stress in lung tissues. Estradiol was more effective than estradiol associated with ERα antagonist or ERβ antagonist in protecting against LPS-induced ALI in rats. Mechanistically, we investigate whether estradiol regulates the expression of AQP1 and AQP5 in lung tissues. Of interest, estradiol upregulates AQP1 and AQP5 mRNA and protein expression. Taken together, these results demonstrate that estradiol can increase the expression of AQP1 and AQP5, which plays a critical role in ameliorating oxidative stress and downregulating inflammatory responses induced by LPS.Conclusion Therefore, these findings strongly suggest that AQP1 and AQP5 mediate the anti-inflammatory and antioxidant effects of estradiol.

Ethanolic extract of Achillea wilhelmsii C. Koch improves pulmonary function and inflammation in LPS-induced acute lung injury mice

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Niloofar Honari ◽  
Parastoo Shaban ◽  
Saeed Nasseri ◽  
Mehran Hosseini
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cell ◽  
Ethanolic Extract ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Lps Challenge ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Achillea Wilhelmsii

Abstract Objectives Acute lung injury (ALI) is a life-threatening pulmonary dysfunction associated with severe inflammation. There are still no effective pharmacological therapies for the treatment of ALI. In this concern, several anti-inflammatory agents could be used as add-on therapy to inhibit inflammation. Achillea wilhelmsii (AW) C. Koch is a well-known medicinal plant in the Iranian ethnomedical practices with anti-inflammatory activity. This study was aimed to evaluate the efficacy of ethanolic extract of AW on lipopolysaccharide (LPS)-induced ALI in mice. Methods The ALI model was established via the intra-tracheal (i.t.) administration of LPS (2 mg/kg) to male BALB/c mice. The ALI mice were divided into four groups (n=8 each) which intra-peritoneally (i.p.) treated with repeated doses of saline (model), dexamethasone (2 mg/kg), and AW (150–300 mg/kg) 1, 11 and 23 h post LPS administration. Twenty-four hours after the LPS challenge, bronchoalveolar lavage fluid (BALF) and lung tissue were evaluated for inflammatory cell influx, level of tumor necrosis factor-α (TNF-α) and histopathological changes. Results The AW (150–300 mg/kg) treated mice showed lower inflammatory cells infiltration in BALF and TNF-α level when compared to the model group. In addition, LPS induced several pathological alterations such as edema, alveolar hemorrhage and inflammatory cell infiltration into the interstitium and alveolar spaces. Treatment with AW significantly reduced LPS-induced pathological injury. Conclusions Taken together, the data here indicated that AW may be considered as a promising add-on therapy for ALI.

scholarly journals A role for bronchial epithelial autotaxin in ventilator-induced lung injury

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Ioanna Nikitopoulou ◽  
Ioanna Ninou ◽  
Nikolaos Manitsopoulos ◽  
Ioanna Dimopoulou ◽  
Stylianos E. Orfanos ◽  
...  
Keyword(s):  
Lung Injury ◽  
Protein Concentration ◽  
Bronchoalveolar Lavage Fluid ◽  
Pulmonary Inflammation ◽  
Small Animal ◽  
Lavage Fluid ◽  
Bronchial Epithelial ◽  
Ventilator Induced Lung Injury ◽  
Lung Histopathology ◽  
Genetic Deletion

Abstract Background The pathophysiology of acute respiratory distress syndrome (ARDS) may eventually result in heterogeneous lung collapse and edema-flooded airways, predisposing the lung to progressive tissue damage known as ventilator-induced lung injury (VILI). Autotaxin (ATX; ENPP2), the enzyme largely responsible for extracellular lysophosphatidic acid (LPA) production, has been suggested to play a pathogenic role in, among others, pulmonary inflammation and fibrosis. Methods C57BL/6 mice were subjected to low and high tidal volume mechanical ventilation using a small animal ventilator: respiratory mechanics were evaluated, and plasma and bronchoalveolar lavage fluid (BALF) samples were obtained. Total protein concentration was determined, and lung histopathology was further performed Results Injurious ventilation resulted in increased BALF levels of ATX. Genetic deletion of ATX from bronchial epithelial cells attenuated VILI-induced pulmonary edema. Conclusion ATX participates in VILI pathogenesis.

Protective effects of coumestrol on lipopolysaccharide-induced acute lung injury via the inhibition of proinflammatory mediators and NF-κB activation

2017 ◽  
Vol 34 ◽  
pp. 181-188 ◽  
Author(s):  
Heung Joo Yuk ◽  
Jae Won Lee ◽  
Hyun Ah Park ◽  
Ok-Kyoung Kwon ◽  
Kyeong-Hwa Seo ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effects ◽  
Proinflammatory Mediators
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