Baicalin attenuates myocardial ischemia‐reperfusion injury through Akt/NF‐κB pathway

Abstract

Background: Baicalin can attenuate myocardial ischemia-reperfusion (I/R) on damage. However, the mechanisms are still not fully understood. The study aimed to investigate the antiapoptosis and anti-inflammatory effects of baicalin on myocardial I/R-induced injury. Methods:We established male rats I/R model, and baicalin was intragastric administration after ischemia onset. All experimental animals were randomly divided into five groups: group I, sham; group II, I/R; group III, 50 mg/kg; group IV, 100 mg/kg; and group V, 200 mg/kg baicalin. Postoperation, left ventricular (LV) function was recorded by transthoracic echocardiography. Myocardial infarct size, number of vessels and apoptosis were detected by histology and immunohistochemistry. Furthermore, the messenger RNA (mRNA) and protein levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-6, IL-8, IL-10, Bcl2, Bax, caspase-3, phosphatidylinositol 3-kinase (PI3K), Akt, p-Akt, and nuclear factor-κB (NF-κB) p65 in myocardial tissues were measured by quantitative real-time polymerase chain reaction and Western blot analysis assays. Result: When compared with I/R groups, baicalin could significantly improve LV hemodynamic parameters. Myocardial infarct size and apoptosis were significantly decreased, but the vessel density was increased. The mRNA levels of TNF-α, IL-1β, IL-6, and IL-8 were downregulated, but the levels of IL-10, proapoptotic genes caspase-3, and the ratio of Bax/Bcl2 were upregulated. Moreover, the protein expression of PI3K, p-Akt, and Akt were upregulated but NF-κB p65 was downregulated in the groups III, IV, and V than in group II. Conclusion:Our current study suggested that baicalin attenuated myocardial I/R-induced damage, inhibited myocardial apoptosis, and inflammation by activating PI3K/Akt but suppressing NF-κB signaling. K E Y W O R D S apoptosis, baicalin, ischemia-reperfusion, inflammation, PI3K/Akt/NF-κB signaling J Cell Biochem. 2019;120:3212-3219. wileyonlinelibrary.com/journal/jcb 3212 |

RETRACTED: Diosmetin exerts cardioprotective effect on myocardial ischaemia injury in neonatal rats by decreasing oxidative stress and myocardial apoptosis

“…Our results showed that the levels of P65 phosphorylation were observably down‐regulated at the expression of proteins in neonatal MI model rats after treatment with diosmetin. The research has exhibited 45 that activation of the p13/Akt pathway inhibits MIRI injury, inhibits cardiomyocyte apoptosis and inflammation, but inhibits NF‐κB‐P65 signalling, consistent with our results. Cardiomyocyte apoptosis and inflammation are associated with inhibition of pathway.…”

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

“…NF‐κB refers to a number of DNA binding proteins that specifically bind to the κB site of the promoters of various genes and promotes transcription, which plays an important role in cell growth regulation, inflammatory responses, and immune responses . Recently, there has been renewed interest in baicalin suppressed myocardial inflammation and apoptosis via inhibiting NF‐κB pathway . Huang et al hold the view that Arginase‐2 protected rats myocardial I/R injury by suppressing inflammatory response through inhibition of NF‐κB signaling .…”

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