Methane attenuates lung ischemia-reperfusion injury via regulating PI3K-AKT-NFκB signaling pathway

Wang, Fang; Wang, Feidi; Li, Fengtao; Wang, Dong; Li, Haopeng; He, Xijing; Zhang, Jingyao

doi:10.1080/10799893.2020.1727925

Cited by 16 publications

(17 citation statements)

References 28 publications

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“…2 E). Overall, enriched gene sets with an FDR < 0.1 aligned well with the analysis of DEGs and previous studies 27 , 28 , and convey the impression of a severe immune response, mediated via NK cells, TNF-α, NFkB, IL6, JAK1/2, STAT3 (Fig. 2 C), and potentially p38 MAPK (Fig.…”

Section: Resultssupporting

confidence: 84%

Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

Wallner

Drysch

Becerikli

et al. 2021

Sci Rep

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Ischemia reperfusion (IR) injury plays a pivotal role in many diseases and leads to collateral damage during surgical interventions. While most studies focus on alleviating its severity in the context of brain, liver, kidney, and cardiac tissue, research as regards to skeletal muscle has not been conducted to the same extent. In the past, myostatin (MSTN), primarily known for supressing muscle growth, has been implicated in inflammatory circuits, and research provided promising results for cardiac IR injury mitigation by inhibiting MSTN cell surface receptor ACVR2B. This generated the question if interrupting MSTN signaling could temper IR injury in skeletal muscle. Examining human specimens from free myocutaneous flap transfer demonstrated increased MSTN signaling and tissue damage in terms of apoptotic activity, cell death, tissue edema, and lipid peroxidation. In subsequent in vivo MstnLn/Ln IR injury models, we identified potential mechanisms linking MSTN deficiency to protective effects, among others, inhibition of p38 MAPK signaling and SERCA2a modulation. Furthermore, transcriptional profiling revealed a putative involvement of NK cells. Collectively, this work establishes a protective role of MSTN deficiency in skeletal muscle IR injury.

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Section: Resultssupporting

confidence: 84%

Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

Wallner

Drysch

Becerikli

et al. 2021

Sci Rep

View full text Add to dashboard Cite

show abstract

“…2E). Overall, enriched gene sets with an FDR < 0.1 aligned well with the analysis of DEGs and previous studies 26,27 , and convey the impression of a severe immune response, mediated via NK cells, TNF-α, NFkB, IL6, JAK1/2, STAT3 (Fig. 2C), and potentially p38 MAPK (Fig.…”

Section: Transcriptome Changes In Skeletal Muscle Following Ir Injurysupporting

confidence: 83%

Deficiency of GDF8 Protects Skeletal Muscle Cells from Ischemia Reperfusion Injury

Wallner

Drysch

Becerikli

et al. 2021

Preprint

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Ischemia reperfusion (IR) injury plays a pivotal role in many diseases and leads to collateral damage during surgical interventions. While most studies focus on alleviating its severity in the context of brain, liver, kidney, and cardiac tissue, research as regards to skeletal muscle has not been conducted to the same extent. In the past, GDF8 (myostatin), primarily known for supressing muscle growth, has been implicated in inflammatory circuits, and research provided promising results for cardiac IR injury mitigation by inhibiting GDF8 cell surface receptor ACVR2B. This generated the question if interrupting GDF8 signaling could temper IR injury in skeletal muscle. Examining human specimens from free myocutaneous flap transfer demonstrated increased GDF8 signaling and tissue damage in terms of apoptotic activity, cell death, tissue edema, and lipid peroxidation. In subsequent in vivo MstnLn/Ln IR injury models, we identified potential mechanisms linking GDF8 deficiency to protective effects, among others, inhibition of p38 MAPK signaling and SERCA2a modulation. Furthermore, transcriptional profiling revealed a putative involvement of NK cells. Collectively, this work establishes a protective role of GDF8 deficiency in skeletal muscle IR injury.

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“…In 2012, Boros et al (2012) found that CH 4 inhalation decreased intestinal I/R injury. More recently, CH 4 was shown to exert protective effects in the liver, spinal, and lung I/R injury ( Ye et al, 2015 ; Wang et al, 2017 , 2020 ). These results suggest that CH 4 may be a good therapeutic agent.…”

Section: Discussionmentioning

confidence: 99%

“…In 2020, Wang et al (2020) reported that intraperitoneal injection of methane-rich saline decreased lung I/R injury in rats and proved the importance of the PI3K-AKT-NFκB signaling pathway in the protective effects of CH 4 . Compared with those of Wang’ study ( Wang et al, 2020 ), a different method of CH 4 administration, inhalation, was chosen in this study. Although methane-rich saline is considered safer, inhalation is a more convenient route of administration and acts on the target organ (lung) directly.…”

Section: Discussionmentioning

confidence: 99%

Methane Inhalation Protects Against Lung Ischemia-Reperfusion Injury in Rats by Regulating Pulmonary Surfactant via the Nrf2 Pathway

et al. 2021

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Methane (CH4) exerted protective effects against lung ischemia-reperfusion (I/R) injury, but the mechanism remains unclear, especially the role of pulmonary surfactant. Therefore, this study aimed to explore the effects of CH4 inhalation on pulmonary surfactant in rat lung I/R injury and to elucidate the mechanism. Rats were randomly divided into three groups (n = 6): the sham, I/R control, and I/R CH4 groups. In the sham group, only thoracotomy was performed on the rats. In the I/R control and I/R CH4 groups, the rats underwent left hilum occlusion for 90 min, followed by reperfusion for 180 min and ventilation with O2 or 2.5% CH4, respectively. Compared with those of the sham group, the levels of large surfactant aggregates (LAs) in pulmonary surfactant, lung compliance, oxygenation decreased, the small surfactant aggregates (SAs), inflammatory response, oxidative stress injury, and cell apoptosis increased in the control group (P < 0.05). Compared to the control treatment, CH4 increased LA (0.42 ± 0.06 vs. 0.31 ± 0.09 mg/kg), oxygenation (201 ± 11 vs. 151 ± 14 mmHg), and lung compliance (16.8 ± 1.0 vs. 11.5 ± 1.3 ml/kg), as well as total antioxidant capacity and Nrf2 protein expression and decreased the inflammatory response and number of apoptotic cells (P < 0.05). In conclusion, CH4 inhalation decreased oxidative stress injury, inflammatory response, and cell apoptosis, and improved lung function through Nrf2-mediated pulmonary surfactant regulation in rat lung I/R injury.

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Methane attenuates lung ischemia-reperfusion injury via regulating PI3K-AKT-NFκB signaling pathway

Cited by 16 publications

References 28 publications

Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

Deficiency of GDF8 Protects Skeletal Muscle Cells from Ischemia Reperfusion Injury

Methane Inhalation Protects Against Lung Ischemia-Reperfusion Injury in Rats by Regulating Pulmonary Surfactant via the Nrf2 Pathway

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