Amelioratory effect of neoandrographolide on myocardial ischemic-reperfusion injury by its anti-inflammatory and anti-apoptotic activities.

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Tytuł:: Amelioratory effect of neoandrographolide on myocardial ischemic-reperfusion injury by its anti-inflammatory and anti-apoptotic activities.
Autorzy:: Liu Y; Department of Cardiology, the Eighty-first Hospital of PLA Affiliated with Anhui Medical University, Nanjing, China.
Liu Y; Department of Cardiology, the Eighty-first Hospital of PLA Affiliated with Anhui Medical University, Nanjing, China.
Zhang HL; Department of Cardiology, the Eighty-first Hospital of PLA Affiliated with Anhui Medical University, Nanjing, China.
Yu FF; Department of Respiratory, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Yin XR; Department of Obstetrics and Gynecology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Zhao YF; Department of Cardiology, the Eighty-first Hospital of PLA Affiliated with Anhui Medical University, Nanjing, China.
Ye F; Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Wu XQ; Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Źródło:: Environmental toxicology [Environ Toxicol] 2021 Dec; Vol. 36 (12), pp. 2367-2379. Date of Electronic Publication: 2021 Aug 16.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: New York, NY : John Wiley & Sons, c1999-
MeSH Terms:: Diterpenes*/pharmacology
Myocardial Reperfusion Injury*/drug therapy
Myocardial Reperfusion Injury*/prevention & control
Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Apoptosis ; Glucosides ; Male ; Mice ; Myocytes, Cardiac ; NF-kappa B/genetics ; Rats ; Tetrahydronaphthalenes
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Grant Information:: Military medical science and technology innovation project; Nanjing Municipal Science and Technology Bureau
Contributed Indexing:: Keywords: apoptosis; inflammatory response; myocardial ischemia/reperfusion; neoandrographolide
Substance Nomenclature:: 0 (Anti-Inflammatory Agents)
0 (Diterpenes)
0 (Glucosides)
0 (NF-kappa B)
0 (Tetrahydronaphthalenes)
XBY0Z806J2 (neoandrographolide)
Entry Date(s):: Date Created: 20210816 Date Completed: 20211104 Latest Revision: 20211104
Update Code:: 20240105
DOI:: 10.1002/tox.23350
PMID:: 34397165
: Czasopismo naukowe

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In the present study, we aimed to evaluate the cardioprotective effect of neoandrographolide (Neo) on myocardial ischemia/reperfusion injury (I/R) models and explore its possible mechanism. We randomly and equally divided male mice into sham-operation, I/R, and I/R + Neo groups. H9C2 cell line and primary neonatal rat cardiomyocytes were induced into the simulated I/R's status and used to further validate the Neo's role in vitro. Heart systolic function, indexes of myocardial injury (IMI), infarct size, pathological change, cell apoptosis, inflammatory cytokines, and indexes related to apoptotic and NF-κB signaling pathways were analyzed in vivo or in vitro after the Neo treatment. Compared to the I/R group, Neo significantly suppressed IMI, infarct size, inflammatory cell infiltration, cell apoptosis, inflammatory cytokines, bax, cleaved caspase-3, P-IKBa, and P-NF-κB protein expressions, and the translocation of NF-kB subunit p65 from the cytoplasm to the nucleus in vivo or in vitro. Still, ejected fraction, fractional shortening, and the bcl-2 protein expression were notably increased after the Neo treatment. Neo could be developed into a new drug for treating myocardial I/R by inhibiting myocardial inflammation and apoptosis, which was closely related to suppressing the activation of bax/bcl-2 and NF-κB signaling pathways.
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