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Year : 2020  |  Volume : 63  |  Issue : 6  |  Page : 276-285

Helium Protects Against Lipopolysaccharide-Induced Cardiac Dysfunction in Mice via Suppressing Toll-Like Receptor 4-Nuclear Factor κB-Tumor Necrosis Factor-Alpha/ Interleukin-18 Signaling

1 Department of Traditional Chinese Medicine, The Third Affiliated Hospital; Institute of Integrated Traditional Chinese and Western Medicine, Sun Yat-sen University, Guangzhou, China
2 Biofeedback Laboratory; School of Biomedical Engineering, Xinhua College of Sun Yat-sen University, Guangzhou, China
3 Biofeedback Laboratory, Xinhua College of Sun Yat-sen University; Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China
4 Research Center for Translational Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

Correspondence Address:
Prof. Hongzhi Yang
600 Tianhe Road, Guangzhou 510630, Guangdong
Associate Prof. Min Dai
600 Tianhe Road, Guangzhou 510630, Guangdong
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CJP.CJP_66_20

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The nonanesthetic noble gas helium (He) can protect many organs against ischemia and reperfusion injury, such as liver and heart. However, the role of He on cardiac dysfunction during sepsis is not clear. In this study, we established a lipopolysaccharide (LPS)-induced cardiac dysfunction mouse model to examine the influence of He on the impaired cardiac function, and further investigated the possible innate immune mechanisms that may be involved. LPS induced left ventricular dysfunction and cavity enlargement, as indicated by decreased percent ejection fraction, percent fractional shortening, left ventricular anterior wall thickness in systole, and left ventricular posterior wall thickness in systole, while increased left ventricular end-systolic diameter and left ventricular end-systolic volume. He improved the impaired left ventricular function and cavity enlargement in a dose-dependent manner, and it was beneficial at 1.0 mL/100 g. Mechanistically, He inhibited toll-like receptor 4 (TLR4) expression, reduced the phosphorylation of nuclear factor κB (NF-κB), and subsequently alleviated tumor necrosis factor-alpha (TNF-α) and interleukin-18 (IL-18) expression in heart. Therefore, He protects against LPS-induced cardiac dysfunction in mice partially via inhibiting myocardial TLR4-NF-κB-TNF-α/IL-18 signaling.

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