scholarly journals Fingolimod attenuates renal ischemia/reperfusion-induced acute lung injury by inhibiting inflammation and apoptosis and modulating S1P metabolism

2021 ◽  
Vol 49 (8) ◽  
pp. 030006052110328
Author(s):  
Zu-an Shi ◽  
Ting-ting Li ◽  
Dao-ling Kang ◽  
Hang Su ◽  
Fa-ping Tu
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokine ◽  
Ischemia Reperfusion ◽  
Pulmonary Inflammation ◽  
Sphingosine Kinase ◽  
Renal Ischemia ◽  
Cytokine Levels ◽  
Sphingosine 1 Phosphate

Objective This study examined whether the immunomodulator fingolimod (FTY720) could alleviate renal ischemia/reperfusion (I/R)-induced lung injury and explored the potential mechanisms. Methods Renal I/R was established in a rat model, and FTY720 (0.5, 1, or 2 mg/kg) was injected intraperitoneally after 15 minutes of ischemia. Pro-inflammatory cytokine levels, oxidative stress, apoptosis, and the mRNA expression of the sphingosine-1-phosphate (S1P)-related signaling pathway genes sphingosine kinase-1 (SphK1) and sphingosine kinase-2 were analyzed in lung tissue. Results Increased pro-inflammatory cytokine levels; decreased total superoxide dismutase, catalase, and glutathione peroxidase levels; increased apoptosis; and increased S1P lyase and SphK1 expression were observed following renal I/R. FTY720 reversed renal I/R-induced changes and effectively attenuated lung injury. Conclusion FTY720 protected against acute lung injury in rats subjected to renal I/R by decreasing pulmonary inflammation and apoptosis, increasing oxidative stress, and modulating S1P metabolism.

scholarly journals Renal ischemia/reperfusion against nephrectomy for induction of acute lung injury in rats

Renal Failure ◽  
2016 ◽  
Vol 38 (9) ◽  
pp. 1503-1515 ◽  
Author(s):  
Zynab Karimi ◽  
Farzaneh Ketabchi ◽  
Nasim Alebrahimdehkordi ◽  
Hossein Fatemikia ◽  
Seyed Mohammad Owji ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia

scholarly journals Hypothermia Induced by Adenosine5′-Monophosphate Attenuates Acute Lung Injury Induced by LPS in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Zhimin Miao ◽  
Shulai Lu ◽  
Na Du ◽  
Weiting Guo ◽  
Jidong Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Bronchoalveolar Lavage ◽  
Inflammatory Cytokine ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Acute Injury ◽  
Pathological Changes ◽  
Inflammatory Reactions ◽  
Cytokine Levels

We have built a rat’s model to investigate whether the hypothermia induced by adenosine 5′-monophosphate (5′-AMP) (AIH) could attenuate acute lung injury induced by LPS in rats. We detected the inflammatory cytokine levels in the plasma and bronchoalveolar lavage fluid samples, and we analyzed the pathological changes in the lungs. We have found that AIH can effectively inhibit acute inflammatory reactions and protect the lung from acute injury induced by LPS in rats.

scholarly journals Penehyclidine hydrochloride inhibits renal ischemia/reperfusion-induced acute lung injury by activating the Nrf2 pathway

Aging ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 13400-13421 ◽  
Author(s):  
Zhaohui Liu ◽  
Yan Li ◽  
Lili Yu ◽  
Yulin Chang ◽  
Jingui Yu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nrf2 Pathway ◽  
Penehyclidine Hydrochloride

Sodium houttuyfonate relieves acute lung injury by nano micellar carrier and inhibits mitogen-activated protein kinase and nuclear factor kappa-B activation in mice

2021 ◽  
Vol 11 (5) ◽  
pp. 781-788
Author(s):  
Kai Yang ◽  
Shushu Yan ◽  
Jian Xie ◽  
Fang Xie ◽  
Zhenzhen Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Vascular Permeability ◽  
Delivery System ◽  
Lung Tissue ◽  
Good Effect ◽  
Pulmonary Vascular Permeability ◽  
Cytokine Levels ◽  
And Oxidative Stress

Acute lung injury (ALI) is characterized by increased pulmonary vascular permeability in response to the accumulation of inflammatory cells, release of inflammatory cytokines, and activated oxidative stress. The present study was performed to investigate the effect of sodium houttuyfonate (SH), an extract of Houttuynia cordata, on inflammatory response and oxidative stress in ALI induced by lipopolysaccharides (LPS). Male C57BL/6 mice were randomly allocated to control, LPS, dimethyl sulfoxide (DMSO), and SH groups. The ALI model was established by intratracheal LPS injection. Lung tissue was collected 6 h after LPS injection for histopathological analysis, measurement of wet-to-dry ratio, myeloperoxidase (MPO) and oxidative stress levels, and the p38, jun N-terminal kinase (JNK), extracellular regulated kinase (ERK), and p65 phosphorylation levels. Bronchoalveolar fluid (BALF) was collected for the detection of protein concentration, MPO and cytokine levels. The histopathological test showed that SH significantly alleviates damage to pulmonary tissue. Improved vascular permeability was indicated by reduced BALF protein level and lung wet-to-dry ratio in the SH group. MPO levels were decreased in lung tissue and BALF. Oxidative stress and inflammatory responses were inhibited by SH, as indicated by MDA, SOD and cytokine levels. The MAPK and NF-KB pathways were inhibited as shown by the attenuated phosphorylation of p38, JNK, ERK and p65. Sodium houttuyfonate exhibited a protective role against LPS-induced lung injury through anti-oxidative and anti-inflammatory effects. The MAPK and NF-K B pathways may be inhibited by sodium houttuyfonate. Sodium Houttuynin has a good effect on a variety of acute infectious diseases, but its solubility and stability are insufficient, which limits its efficacy. Nano delivery system can enhance the effective ingredients of traditional Chinese medicine, reduce the toxic and side effects of drugs, and improve their medicinal properties. Therefore, this paper adopts nano delivery system to assist drug use and improve research efficiency.

scholarly journals Prophylactic and therapeutic treatment with the flavonone sakuranetin ameliorates LPS-induced acute lung injury

2017 ◽  
Vol 312 (2) ◽  
pp. L217-L230 ◽  
Author(s):  
Márcia Isabel Bittencourt-Mernak ◽  
Nathalia M. Pinheiro ◽  
Fernanda P. R. Santana ◽  
Marina P. Guerreiro ◽  
Beatriz M. Saraiva-Romanholo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Collagen Fiber ◽  
Pulmonary Inflammation ◽  
Fiber Formation ◽  
Therapeutic Effects ◽  
Therapeutic Treatment ◽  
Fiber Deposition

Sakuranetin is the main isolate flavonoid from Baccharis retusa ( Asteraceae) leaves and exhibits anti-inflammatory and antioxidative activities. Acute respiratory distress syndrome is an acute failure of the respiratory system for which effective treatment is urgently necessary. This study investigated the preventive and therapeutic effects of sakuranetin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Animals were treated with intranasal sakuranetin 30 min before or 6 h after instillation of LPS. Twenty-four hours after ALI was induced, lung function, inflammation, macrophages population markers, collagen fiber deposition, the extent of oxidative stress, and the expression of matrix metalloprotease-9 (MMP-9), tissue inhibitor of MMP-9 (TIMP-1) and NF-κB were evaluated. The animals began to show lung alterations 6 h after LPS instillation, and these changes persisted until 24 h after LPS administration. Preventive and therapeutic treatment with sakuranetin reduced the neutrophils in the peripheral blood and in the bronchial alveolar lavage. Sakuranetin treatment also reduced macrophage populations, particularly that of M1-like macrophages. In addition, sakurnaetin treatment reduced keratinocyte-derived chemokines (IL-8 homolog) and NF-κB levels, collagen fiber formation, MMM-9 and TIMP-1-positive cells, and oxidative stress in lung tissues compared with LPS animals treated with vehicle. Finally, sakuranetin treatment also reduced total protein, and the levels of TNF-α and IL-1β in the lung. This study shows that sakuranetin prevented and reduced pulmonary inflammation induced by LPS. Because sakuranetin modulates oxidative stress, the NF-κB pathway, and lung function, it may constitute a novel therapeutic candidate to prevent and treat ALI.

scholarly journals The Roles of Autophagy in Acute Lung Injury Induced by Myocardial Ischemia Reperfusion in Diabetic Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Liying Zhan ◽  
Yuan Zhang ◽  
Wating Su ◽  
Qiongxia Zhang ◽  
Rong Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Myocardial Ischemia ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Lung Injury Score ◽  
Sod Activity ◽  
Autophagy Inhibitor ◽  
Myocardial Ischemia Reperfusion

Patients with diabetes are vulnerable to myocardial ischemia reperfusion (IR) injury, which may also induce acute lung injury (ALI) due to overaccumulation of reactive oxygen species (ROS) and inflammation cytokine in circulation. Despite autophagy plays a significant role in diabetes and pulmonary IR injury, the role of autophagy in ALI secondary to myocardial IR in diabetes remains largely elusive. We aimed to investigate pulmonary autophagy status and its roles in oxidative stress and inflammation reaction in lung tissues from diabetic rats subjected to myocardial IR. Control or diabetic rats were either treated with or without autophagy inducer rapamycin (Rap) or autophagy inhibitor 3-methyladenine (3-MA) before myocardial IR, which was achieved by occluding the left anterior descending coronary artery for 30 min and followed by reperfusion for 120 min. Diabetic rats subjected to myocardial IR showed more serious ALI with higher lung injury score and WET/DRY ratio and lower PaO2 as compared with control rats, accompanied with impaired autophagy indicated by reduced LC-3II/LC-3I ratio and Beclin-1 expression, decreased superoxide dismutase (SOD) activity, and increased 15-F2t-Isoprostane formation in lung tissues, as well as increased levels of leukocyte count and proinflammatory cytokines in BAL fluid. Improving autophagy with Rap significantly attenuated all these changes, but the autophagy inhibitor 3-MA exhibited adverse or opposite effects as Rap. In conclusion, diabetic lungs are more vulnerable to myocardial IR, which are involved in impaired autophagy. Improving autophagy could attenuate ALI induced by myocardial IR in diabetic rats, possibly through inhibiting inflammatory reaction and oxidative stress.

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