Browsing by Subject "Myocardial ischemia"

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    Cardioprotective mechanisms of Jiangfu Decoction against myocardial ischemia may involve regulation of the AMPK/PINK1/ Parkin mitochondrial autophagy pathway
    (2026) Yiwei Hao; Chen Li; Haoying Li; Xue Han; Hefei Wang; Xi Chu; Zhiwei Su; Shijiang Sun; Yawei Zhao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
    Background. Jiangfu Decoction (JFD) is a classical traditional herbal medicine used to clinically treat ischemic heart disease (IHD). Nonetheless, the influence of JFD on myocardial ischemia (MI), along with its precise underlying mechanism, is still unclear. The objective of this research was to investigate the potential mechanisms by which JFD exerts cardio protective effects on MI induced by isoproterenol (ISO). Methods. An acute MI model was established by subcutaneous injection of ISO (85 mg/kg/d). To evaluate alterations in myocardial structure, electrocardiogram recordings and heart histology examinations were employed. The myocardial ultrastructure was observed by transmission electron microscopy (TEM). Using specific kits, the levels and activities of oxidative stress markers as well as inflammatory cytokines were separately assessed. Western blotting was employed to assess the expression levels of proteins related to adenosine monophosphate activated protein kinase (AMPK), PTEN-induced putative kinase 1 (PINK1), Parkin, Nod-like receptor protein 3 (NLRP3), and Caspase-1. Results. The findings show that JFD treatments markedly diminished heart rate, pathological alterations in cardiac tissue, chondriosome injury, and serum concentrations of creatine kinase, creatine kinasemyocardial band, lactate dehydrogenase, malon dialdehyde, interleukin-1β, and interleukin-18. Concurrently, these treatments augmented the activation of superoxide dismutase, catalase, and glutathione peroxidase in the serum of animals subjected to ISO treatment. Additionally, JFD also reversed the ISO induced changes in the levels of AMPK, PINK1, Parkin, NLRP3, and Caspase-1. Conclusion. JFD exhibits a notable safeguarding influence on MI via a mechanism that involves regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway, inhibition of pyroptosis, and reduction of oxidative stress and inflammation.
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    Immunohistochemistry of connexin43 and zonula occludens-1 in the myocardium as markers of early ischemia in autopsy material
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Kawamoto, Osamu; Michiue, Tomomi; Ishikawa, Takaki; Maeda, Hitoshi
    Immunohistochemistry of the terminal complement complex (C5b-9) and fibronectin (FN) is useful to detect myocardial ischemia preceding necrosis in the postmortem diagnosis of sudden cardiac death. The present immunohistochemical study examined connexin43 (Cx43) and zonula occludens-1 (ZO-1) as markers of early myocardial ischemia in addition to the above-mentioned markers, using forensic autopsy cases of acute deaths due to myocardial infarction (MI, n=15) and acute ischemic heart disease (AIHD) without apparent myocardial necrosis (n=8), compared with those of acute mechanical asphyxiation (As, n=24) and drowning (D, n=10) as controls. Immunopositivities of each marker in the myocardium were semi-quantitatively graded by scoring. ZO-1, C5b-9 and FN were detected in the myocardial cytoplasm, whereas Cx43 and nonphosphorylated (np) Cx43 showed varied localizations at the intercalated disc, in the cytoplasm and along the lateral cell border. ZO-1 and FN showed a tendency to be detected more intensely in MI and IHD than in As and D. C5b-9 showed specific staining at the site of ischemia in MI (n=10/15) and AIHD (n=6/8), while the distribution of npCx43 was different in most cases of MI (n=14/15) and AIHD (n=5/8), compared with As and D; npCx43 positivity score was higher in the cytoplasm than at the intercalated disc, indicating redistribution due to myocardial ischemia. Such findings were detected in a few cases of As (n=3/24). These findings suggest that the combination of npCx43 and C5b-9 immunohistochemistry is useful for detecting early lesions of myocardial ischemia in sudden cardiac death.
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    LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Fu, Dongliang; Gao, Tong; Liu, Mengru; Li, Chunyan; Li, Haiwei; Jiang, Hong; Li, Xianlun
    Cardiomyocyte apoptosis is a fundamental pathogenic factor leading to myocardial ischemia/ reperfusion (MI/R) injury. The long non-coding RNA (lncRNA) TUG1 regulates apoptosis in various cell types. We report here that TUG1 expression is induced in mouse heart following MI/R injury as well as in cardiomyocytes subjected to simulated ischemia/ reperfusion (SI/R) in vitro. Clinically, TUG1 expression is also elevated in plasma from patients with acute myocardial infarction (AMI), which implies its potential application as a disease biomarker. Functionally, TUG1 overexpression promotes, and its knockdown reduces SI/R-induced lactate dehydrogenase (LDH) release and caspase-3 activity in cardiomyocytes in vitro, illustrating that TUG1 exacerbates SI/R-induced apoptosis. Furthermore, in vivo, TUG1 aggravates MI/R injury in a mouse model, and subsequent observations show concurrent increased apoptosis of cardiomyocytes. Hence, this study unveils a clinical relevance and functional role of TUG1 in MI/R injury, and also implicates that targeting TUG1 m