Effect of electroacupuncture pretreatment on the protein expression of c-fos in fastigial nucleus and lateral hypothalamus area in rats with acute myocardial ischemia-reperfusion injury

2021 ◽  
Vol 19 (1) ◽  
pp. 10-18
Author(s):  
Cai Rong-lin ◽  
Shao Xue-fang ◽  
Yu Qing ◽  
Zhang Ya-ting ◽  
Wei Xiao-tong ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Lateral Hypothalamus ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Myocardial Ischemia ◽  
Fastigial Nucleus ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

scholarly journals Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

2020 ◽  
Author(s):  
Xiujing Zhang ◽  
Wei Wang ◽  
Jie Tang ◽  
Qin Xie ◽  
Di Ma
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Changes ◽  
Apoptosis Protein ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Trillium Tschonoskii

Abstract BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

scholarly journals Positive Inotropic Agents in Myocardial Ischemia–Reperfusion Injury

2013 ◽  
Vol 118 (6) ◽  
pp. 1460-1465 ◽  
Author(s):  
Jean-Luc Fellahi ◽  
Marc-Olivier Fischer ◽  
Georges Daccache ◽  
Jean-Louis Gerard ◽  
Jean-Luc Hanouz
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Myocardial Ischemia ◽  
Surgical Patients ◽  
Inotropic Agents ◽  
Positive Inotropic Agents ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Positive inotropic agents should be used judiciously when managing surgical patients with acute myocardial ischemia–reperfusion injury, as use of these inotropes is not without potential adverse effects.

Abstract 1000: Dichotomous Roles Of TNF-α Receptors p55 And p75 In Acute Ischemia/reperfusion Injury And Late Ischemic Preconditioning

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Michael P Flaherty ◽  
Yiru Guo ◽  
Xian-Liang Tang ◽  
Sumit Tiwari ◽  
Greg Hunt ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Coronary Occlusion ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Myocardial Ischemia ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

We have previously demonstrated that TNF-alpha signaling is critical for the development of protection afforded by the late phase of ischemic preconditioning (PC). In the current study, we investigated the roles of p55 (TNFR-I) and p75 (TNFR-II) in acute myocardial ischemia/reperfusion injury as well as late PC. Wild-type (WT, B6 and B6,129 strains), TNF-a−/−, p55−/−, p75−/−, and p55−/−/p75−/− double-knockout mice underwent a 30-min coronary occlusion followed by 4 h of reperfusion with or without six cycles of coronary occlusion/reperfusion (O/R) 24 h earlier. Six cycles of O/R reduced infarct size 24 h later in B6 as well as B6,129 WT mice, indicating a rob ust late PC effect (Figure ). This infarct-sparing effect of late PC was abolished in the absence of TNF-a, p55, p75, and both p55/p75, indicating that TNF-a signaling is critical for the development of late PC protection; and that signaling via both p55 and p75 is necessary for the development of protection. In nonpreconditioned TNF-a−/− and p75−/− mice, infarct size was similar to that observed in strain-matched WT mice (Figure ). However, infarct size in nonpreconditioned p55−/− mice was reduced compared with nonpreconditioned WT mice (46.8 ± 2.8% vs. 63.4 ± 3.2%, P < 0.05, Figure ). These observations were confirmed via linear regression analysis of myocardial risk region and infarct size. We conclude that nonredundant TNF-a signaling via both p55 and p75 is crucial for the development of late PC protection. However, the reduction in infarct size in naïve p55−/− mice indicates a deleterious role of this receptor during acute myocardial ischemia/reperfusion injury.

Sign in / Sign up

Export Citation Format

Share Document