Intravenous Superoxide Dismutase Administration Reduces Contralateral Lung Injury Induced by Unilateral Lung Ischemia and Reperfusion in Rats Through Suppression of Activity and Protein Expression of Matrix Metalloproteases

Yeh, Diana; Tung, Shao-Hsien; Fu, Yurong; Yang, Y.-C.; Wang, J.J.

doi:10.1016/j.transproceed.2014.10.060

Cited by 14 publications

(12 citation statements)

References 11 publications

(11 reference statements)

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“…On the other hand, a series of antioxidant enzymes, such as SOD, GSH-PX, and CAT, have the function of eliminating the reactive free radicals to maintain the balance of oxidative and antioxidative stress response. Suppressing the activities of antioxidant enzymes could further aggravate in ammatory response and tissues damage during lung I/R [22,34]. Consistent with previous studies, lung I/R could increase the products of oxidative stress (ROS, MDA, 15-F2t-Isoprostane) and decrease the expression of antioxidant enzymes (SOD, GSH-PX, CAT).…”

Section: Discussionsupporting

confidence: 83%

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury through inhibiting alveolar macrophages pyroptosis via Keap1/Nrf2/HO-1 signal pathway

Lin

Jingyuan

Liang

et al. 2020

Preprint

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Background: Lung ischemia-reperfusion injury (LIRI) is a common and complex pathophysiological process that can lead to poor patient outcomes. Inflammasome-dependent macrophage pyroptosis contributes to organ damage caused by ischemia-reperfusion (I/R). Oxidative stress reaction and antioxidant enzymes also play an important role in LIRI. This experiment was conducted to investigate whether preconditioning with rHMGB1 could ameliorate LIRI and explore the mechanisms of its protective effect in a lung I/R mice model. Methods: Adult male mice were anesthetized and the left hilus pulmonis was clamped for 60 min, followed by 120 min of reperfusion. rHMGB1 was performed by intraperitoneal injection at 2 h before anesthesia. Brusatol (Nrf2 antagonist) was given intraperitoneally every other day for a total of five times before surgery. Measurements of pathohistological lung tissue damage, pulmonary wet/dry (W/D) ratios and inflammatory mediators were performed to assess the extent of lung injury after I/R. Alveolar macrophages (AMs) pyroptosis were evaluated by LDH release, caspase-1 expression in flow cytometry, GSDMD expression in immunofluorescent staining. The products of oxidative Stress (ROS, MDA, 15-F2t-Isoprostane) and the antioxidant enzymes (SOD, GSH-PX, CAT) were detected.Results: Preconditioning with rHMGB1 significantly ameliorated I/R-induced lung injury through measuring the morphology, wet/dry weight ratio, the expressions of IL-1β, IL-6, NF-κB and HMGB1 in lung tissue. rHMGB1 preconditioning remarkably alleviated AMs pyroptosis induced by lung I/R. rHMGB1 preconditioning significantly reduced oxidative stress and restored the activity of antioxidative enzymes. In addition, rHMGB1 preconditioning mediated the activity of Keap1/Nrf2/HO-1 pathway in LIRI. Furthermore, inhibiting Keap1/Nrf2/HO-1 pathway through brusatol administration could aggravate lung tissue damage and inflammatory response after lung I/R. And these effects by brusatol administration could be alleviated by rHMGB1 preconditioning in LIRI .Conclusions : rHMGB1 preconditioning protects against LIRI through suppressing AMs pyroptosis. The molecular mechanism could be partially explained by inhibiting oxidative stress and improving the activity of antioxidative enzymes via Keap1/Nrf2/HO-1 pathway upon rHMGB1 preconditioning.

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Section: Discussionsupporting

confidence: 83%

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury through inhibiting alveolar macrophages pyroptosis via Keap1/Nrf2/HO-1 signal pathway

Lin

Jingyuan

Liang

et al. 2020

Preprint

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“…The loss of antioxidant enzymes evidently causes free radical accumulation and further aggravates lung I/R injury [31, 32]. Interestingly, a previous study reported the antioxidative activity of MaR 1 in CCl4-induced liver injury [15].…”

Section: Discussionmentioning

confidence: 99%

Maresin 1 Ameliorates Lung Ischemia/Reperfusion Injury by Suppressing Oxidative Stress via Activation of the Nrf‐2‐Mediated HO‐1 Signaling Pathway

Sun

Zhao

et al. 2017

Oxidative Medicine and Cellular Longevity

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Lung ischemia/reperfusion (I/R) injury occurs in various clinical conditions and heavily damaged lung function. Oxidative stress reaction and antioxidant enzymes play a pivotal role in the etiopathogenesis of lung I/R injury. In the current study, we investigated the impact of Maresin 1 on lung I/R injury and explored the possible mechanism involved in this process. MaR 1 ameliorated I/R-induced lung injury score, wet/dry weight ratio, myeloperoxidase, tumor necrosis factor, bronchoalveolar lavage fluid (BALF) leukocyte count, BALF neutrophil ratio, and pulmonary permeability index levels in lung tissue. MaR 1 significantly reduced ROS, methane dicarboxylic aldehyde, and 15-F2t-isoprostane generation and restored antioxidative enzyme (superoxide dismutase, glutathione peroxidase, and catalase) activities. Administration of MaR 1 improved the expression of nuclear Nrf-2 and cytosolic HO-1 in I/R-treated lung tissue. Furthermore, we also found that the protective effects of MaR 1 on lung tissue injury and oxidative stress were reversed by HO-1 activity inhibitor, Znpp-IX. Nrf-2 transcription factor inhibitor, brusatol, significantly decreased MaR 1-induced nuclear Nrf-2 and cytosolic HO-1 expression. In conclusion, these results indicate that MaR 1 protects against lung I/R injury through suppressing oxidative stress. The mechanism is partially explained by activation of the Nrf-2-mediated HO-1 signaling pathway.

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“…It has well been accepted that skeletal muscle I/R injury is caused by free radicals produced from oxidative stress [7] and leukocytes play a key role in the pathogenesis of skeletal muscle I/R injury [8][9][10][11], which is preconditioned by the expression of adhesion molecular on leukocytes and endothelia [12][13][14]. Large scale of evidences have also demonstrated that the superoxide dismutase (SOD) is an important to control reactive oxygen species during I/R injury [15,16], but the relevance to human disease conditions mentioned above and the potential mechanism underlying I/R injury is not clarified. Moreover, looking for a therapeutic agent to replacement of SOD would be worthy of attempting due to the sources and cost for utilizing the SOD.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

Wang¹,

Tian²,

Xu³

et al. 2015

Cell Physiol Biochem

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Background/Aim: Ischemia/reperfusion (I/R) injury of skeletal muscles is common pathophysiology during surgeries and the superoxide dismutase (SOD) plays a critical role in this process. SOD-modeled coordination compound (MSODa) may simulate the protective effects as SOD. Methods: Therefore, this study was designed to explore the protective effects and underlying mechanism of MSODa on malondialdehyde (MDA) and integrin-β2 (CD11b/CD18) in plasma, myeloperoxidase (MPO) and intercellular cell adhesion molecule-1 (ICAM-1) in tissue, and morphological changes before and after I/R injury. The rat model of I/R in hind limb was established and randomly divided into sham, ischemia, I/R, I/R-treated with saline, SOD, and MSODa, respectively. Results: These results showed that averaged values for MDA, MPO, CD11b/CD18, and ICAM-1 were significantly increased (P < 0.01 vs ischemia alone) in a time-dependent fashion along with marked tissue remodeling, such as abnormal arrangement of muscular fibers, interstitial edema, vasodilation with no-reflow, inflammatory cells adherent and infiltration, structural changes in mitochondrial, and decrease in glycogens as well. However, all parameter changes induced by I/R injury were reversed, at least partially, by MSODa and SOD treatments and intriguingly, the beneficial/protective effects of MSODa was superior to SOD with an early onset. Conclusion: This novel finding demonstrates that MSODa improves I/R injury of skeletal muscles due at least partially to inhibition of adherent molecule expression and reduction of oxygen free radical formation during I/R pathophysiological processes and this protective action of MSODa was superior to SOD, highlighting the bright future for MSODa in clinical management of tissue I/R injury.

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Intravenous Superoxide Dismutase Administration Reduces Contralateral Lung Injury Induced by Unilateral Lung Ischemia and Reperfusion in Rats Through Suppression of Activity and Protein Expression of Matrix Metalloproteases

Cited by 14 publications

References 11 publications

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury through inhibiting alveolar macrophages pyroptosis via Keap1/Nrf2/HO-1 signal pathway

Preconditioning with rHMGB1 ameliorates lung ischemia–reperfusion injury through inhibiting alveolar macrophages pyroptosis via Keap1/Nrf2/HO-1 signal pathway

Maresin 1 Ameliorates Lung Ischemia/Reperfusion Injury by Suppressing Oxidative Stress via Activation of the Nrf‐2‐Mediated HO‐1 Signaling Pathway

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

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