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• W2893569388 abstract "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.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.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.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." @default.
• W2893569388 created "2018-10-05" @default.
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• W2893569388 date "2018-09-22" @default.
• W2893569388 modified "2023-09-26" @default.
• W2893569388 title "Baicalin attenuates myocardial ischemia‐reperfusion injury through Akt/NF‐κB pathway" @default.
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• W2893569388 doi "https://doi.org/10.1002/jcb.27587" @default.
• W2893569388 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30242878" @default.
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