H2 Protects Against Lipopolysaccharide-Induced Cardiac Dysfunction via Blocking TLR4-Mediated Cytokines Expression
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BACKGROUND AND PURPOSE: Septic cardiomyopathy, which is one of the features of multi-organ dysfunction in sepsis, is characterized by ventricular dilatation, reduction in ejection fraction and reduced contractility, and if severe, can lead to death. To date, there is no specific therapy exists and its treatment represents a large unmet clinical need. Herein, we investigated the effects and underlying anti-inflammatory mechanisms of hydrogen gas in the setting of lipopolysaccharide (LPS)-induced cardiomyocytes injury. EXPERIMENTAL APPROACH: Hydrogen gas was intraperitoneal injected to mice in LPS plus hydrogen group, and hydrogen group for 3 days. On 4th, LPS was given by intraperitoneal injection to mice in LPS group, and to mice in LPS plus hydrogen group. In addition, H9c2 cardiomyocytes were treated with hydrogen-rich medium for 30 min before LPS. The transthoracic echocardiography was performed at 6 hours post‐LPS to assess left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), left ventricular ejection fraction (EF%), fractional shortening (FS%), left ventricular mass average weight (LV Mass AW), and LV Mass AW (Corrected). The histological and morphological analyses of left ventricular were performed by hematoxylin and eosin (H&E) staining, and Masson’s trichrome staining. The mRNA levels of hypertrophy marker ANP and BNP were examined by PCR in vitro. The expression of cytokines were assayed by ELISA and PCR. Moreover, western blotting was performed to examine the expression of TLR4, the activation of ERK1/2, p38, JNK, and the expression of NF-κB in nucleus after 6 hours of LPS challenge in vivo and in vitro. KEY RESULTS: LPS induced cardiac dysfunction, hydrogen therapy maintained cardiac function after LPS challenge. Furthermore, pretreatment with hydrogen resulted in cardioprotection during septic cardiomyopathy via inhibiting the expression of pro-inflammatory cytokines TNFα, IL-1β and IL-18, suppressing the phosphorylation of ERK1/2, p38 and JNK, reducing the nuclear translocation of NF-κB and LPS-induced the expression of TLR4. CONCLUSION AND IMPLICATIONS: Hydrogen therapy prevents LPS-induced cardiac dysfunction in part via downregulation of TLR4-mediated pro-inflammatory cytokines expression.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- H2 Protects Against Lipopolysaccharide-Induced Cardiac Dysfunction via Blocking TLR4-Mediated Cytokines Expression
- Date Crossref
- 05/08/2019
- Éditeur
- Frontiers Media SA
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Sun Yat-sen University Department of Traditional Chinese Medicine pays non établi dans la noticeUniversité ou école supérieure
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Guangzhou University of Chinese Medicine pays non établi dans la noticeUniversité ou école supérieure
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Sun Yat-sen Memorial Hospital pays non établi dans la noticeÉtablissement de santé
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Anhui Xinhua University pays non établi dans la noticeUniversité ou école supérieure
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Guangdong Pharmaceutical University Department of Science and Education pays non établi dans la noticeUniversité ou école supérieure
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Third Affiliated Hospital of Sun Yat-sen University pays non établi dans la noticeÉtablissement de santé
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Zhongshan School of Medicine Department of Physiology pays non établi dans la noticeUniversité ou école supérieure
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Second School of Clinical Medicine Department of Psychological Sleeping pays non établi dans la noticeUniversité ou école supérieure
Department of Traditional Chinese Medicine — Sun Yat-sen University, Guangzhou University of Chinese Medicine et Sun Yat-sen Memorial Hospital, avec 5 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.