| Autor: |
Xingxing Shi, Lixia Du, Zhongmin Fan, Binxiao Su, Yu Chen, Zongping Fang, Xijing Zhang |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
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| Zdroj: |
Intensive Care Research, Vol 2, Iss 1-2, Pp 34-43 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
2666-9862 |
| DOI: |
10.1007/s44231-022-00008-1 |
| Popis: |
Abstract Background Sepsis is the leading cause of death in hospitalized patients in the intensive care unit (ICU). Although substantial progress has been made in studies on the treatment of sepsis, the mortality rate remains extremely high. We have previously reported that electroacupuncture (EA) induced tolerance against sepsis, but the underlying mechanism remains unclear. Methods C57BL/6 mice were pretreated with EA before sepsis was induced by cecal ligation and puncture (CLP). Then the indexes associated with pulmonary edema and mortality were tested. And the changes of endogenous cholinergic anti-inflammatory pathway especially their typical receptor α7nAChR were detected. Finally, the mechanism of EA in sepsis was explored through regulating the expression of α7nAChR. Results The expression of α7nAChR was significantly decreased after sepsis, while EA prevented this reduction. Methyllycaconitine (MLA), an antagonist of α7nAChR, attenuated the beneficial effects of EA. On the other hand, as an α7nAChR agonist, GTS-21 produced similar protective effects against sepsis. Furthermore, the EA-induced enhancement of α7nAChR and inhibition of NF-κB expression in the lungs were reversed by MLA administration. Conclusions EA robustly protects the lungs against sepsis and inhibits NF-κB release by activating α7nAChR in mice. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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