COX-2 inhibition attenuates lung injury induced by skeletal muscle ischemia reperfusion in rats

Wang, Liangrong; Shan, Yuanlu; Ye, Yuzhu; Zhuo, Qian; Xiong, Xiaoxing; Zhao, Xiangshan; Lin, Lina; Miao, Jianxia

doi:10.1016/j.intimp.2015.12.019

Cited by 14 publications

(5 citation statements)

References 39 publications

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“…Increased MPO activity is an indicator of neutrophil activation because MPO is found almost exclusively within neutrophils [ 20 ]. The proinflammatory cytokines including TNF- α , IL-1 β , and IL-6 are prominent in lung injury especially following hindlimb IR [ 1 , 21 ]. As demonstrated in our results, hindlimb IR in rat caused gastrocnemius muscle damage and morphologic abnormalities in remote lung tissue, accompanied by pulmonary edema and neutrophil infiltration.…”

Section: Discussionmentioning

confidence: 99%

“…Prolonged cessation of the blood flow in lower extremity would cause ischemic damage, while subsequent restoration of blood flow paradoxically provokes IR injury. It has been well documented that lower limb IR could lead to remote lung injury, which is primarily characterized by increased pulmonary capillary permeability, edema, and neutrophil infiltration [ 1 , 2 ]. Although the exact mechanisms underlying these processes are not fully understood, oxygen radical formation and oxidative stress are believed to play key roles [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Methylene Blue Attenuates Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

Wang

Chen

Lin

et al. 2018

Mediators of Inflammation

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Objective This study was aimed to investigate the protective effect of methylene blue against lung injury induced by reperfusion of ischemic hindlimb in a rat model. Methods Twenty-four healthy adult male Sprague-Dawley rats were equally randomized into three groups: sham (SM) group, ischemia reperfusion (IR) group, and methylene blue (MB) group. Rats in both IR and MB groups were subjected to 4 h of ischemia by clamping the left femoral artery and then followed by 4 h of reperfusion. Treatment with 1% methylene blue (50 mg/kg) was administrated intraperitoneally at 10 min prior to reperfusion in the MB group. After 4 h of reperfusion, malondialdehyde (MDA) level, myeloperoxidase (MPO), and superoxide dismutase (SOD) activities in lung tissue were detected; inflammatory cytokines, including IL-1β and IL-6, were measured in bronchoalveolar lavage fluid (BALF); correspondingly, the morphological changes and water content in both gastrocnemius muscle and lung samples were evaluated. Results Hindlimb IR caused remarkable morphological abnormalities and edema in both muscle and lung tissues. SOD activity was decreased, both the MPO activity and MDA level in lung tissue, as well as IL-1β and IL-6 levels in BALF, were increased in the IR group (p < 0.05). Compared with the IR group, SOD activity was increased, whereas MPO activity and MDA level in lung tissue and IL-1β and IL-6 levels in BALF were decreased in the MB group (p < 0.05). Also, the histological damage and edema in both lung and muscle tissues were significantly attenuated by the treatment of methylene blue. Conclusion Methylene blue attenuates lung injury induced by hindlimb IR in rats, at least in part, by inhibiting oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Methylene Blue Attenuates Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

Wang

Chen

Lin

et al. 2018

Mediators of Inflammation

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“…In line with this result, COX-2 seems to be crucially involved in the regulation of water-transporting aquaporins. 45 In addition, PGE 2 has been reported to stimulate other secretory processes. 46e48 The observed inhibitory action of parecoxib on vasculogenesis in endometriotic lesions may be attributable to different effects on EPCs.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Cyclooxygenase-2 Suppresses the Recruitment of Endothelial Progenitor Cells in the Microvasculature of Endometriotic Lesions

Rudzitis‐Auth

Nickels

Menger

et al. 2018

The American Journal of Pathology

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The incorporation of endothelial progenitor cells (EPCs) into newly developing blood vessels contributes to the vascularization of endometriotic lesions. We analyzed whether cyclooxygenase (COX)-2 signaling regulates this vasculogenic process. Endometriotic lesions were surgically induced in irradiated FVB/N mice, which were reconstituted with bone marrow from FVB/N-TgN [Tie2/green fluorescent protein (GFP)] 287 Sato mice. The animals received β-estradiol 17-valerate once a week and were treated daily with the selective COX-2 inhibitor parecoxib (25 mg/kg) or vehicle (control) for 7 and 28 days. Analyses involved the determination of lesion growth, cyst formation, homing of GFP/Tie2 EPCs, numbers of circulating EPCs, vascularization, cell proliferation, apoptosis, and immune cell infiltration by means of high-resolution ultrasonography, caliper measurements, flow cytometry, histologic analysis, and immunohistochemical analysis. In parecoxib-treated mice, blood circulating EPCs were higher, but numbers of recruited EPCs in endometriotic lesions were significantly lower when compared with controls. This finding was associated with an impaired early vascularization and stromal tissue growth as well as reduced glandular secretory activity of the lesions. Parecoxib-treated lesions further contained less proliferating and more apoptotic cells and exhibited lower numbers of infiltrating macrophages and neutrophilic granulocytes. These findings demonstrate that the inhibition of COX-2 suppresses vasculogenesis in endometriotic lesions, which may contribute to an impaired lesion vascularization and growth.

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“…A significant decrease in the number of various inflammatory cells in the administration group was found to be related to the inhibition of PTGS2 expression [ 42 ]. Wang et al demonstrated that the inhibition of PTGS2 could regulate the expression of aquaporin-1 and alleviate lung injury [ 43 ]. Furthermore, PTGS2 was directly enriched in related inflammation pathways, such as the TNF signaling pathway and the IL-17 signaling pathway, and in small cell lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanism of Xixin-Ganjiang Herb Pair Treating Chronic Obstructive Pulmonary Disease-Integrated Network Pharmacology and Molecular Docking

Huang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Background. Chronic obstructive pulmonary disease (COPD) is characterized by high morbidity, disability, and mortality, which seriously threatens human life and health. Xixin and Ganjiang are classic herb pairs of Zhongjing Zhang, which are often used to treat COPD in China. However, the substance basis and mechanism of action of Xixin-Ganjiang herb pair (XGHP) in the treatment of COPD remain unclear. Methods. On the website of TCMSP and the DrugBank, effective compounds and targets of XGHP were found. COPD targets were obtained from GeneCards, DisGeNET, and GEO gene chips. Intersecting these databases resulted in a library of drug targets for COPD. Then, intersection targets were used for protein-protein interaction (PPI) and pathway enrichment analysis. Finally, the binding activity between compounds and core genes was evaluated by molecular docking to verify the expression level of PTGS2 and PPARG in rats. Results. Twelve effective compounds and 104 core genes were found in the intersection library, and kaempferol, sesamin, β-sitosterol, PTGS2, and PPARG were particularly prominent in the network analysis. A total of 113 pathways were obtained and enrichment of the TNF signaling pathway, IL-17 signaling pathway, and C-type lectin receptor signaling pathway was particularly obvious. Molecular docking indicated that kaempferol, sesamin, and β-sitosterol were closely related to PTGS2 and PPARG and were superior to aminophylline. Key compounds in XGHP could restrict the expression of PTGS2 in the lung tissues of COPD rats and promote the expression of PPARG. Conclusion. Inhibition of the expression of inflammatory factor PTGS2 and promotion of the expression of PPARG may be an effective target of XGHP in the treatment of COPD.

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COX-2 inhibition attenuates lung injury induced by skeletal muscle ischemia reperfusion in rats

Cited by 14 publications

References 39 publications

Methylene Blue Attenuates Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

Methylene Blue Attenuates Lung Injury Induced by Hindlimb Ischemia Reperfusion in Rats

Inhibition of Cyclooxygenase-2 Suppresses the Recruitment of Endothelial Progenitor Cells in the Microvasculature of Endometriotic Lesions

Molecular Mechanism of Xixin-Ganjiang Herb Pair Treating Chronic Obstructive Pulmonary Disease-Integrated Network Pharmacology and Molecular Docking

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