scholarly journals Ginsenoside Re Attenuates Isoproterenol-Induced Myocardial Injury in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Quan-wei Wang ◽  
Xiao-feng Yu ◽  
Hua-li Xu ◽  
Yi-chuan Jiang ◽  
Xue-zhong Zhao ◽  
...  

Objective. Panax ginseng is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of Panax ginseng. This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats. Methods. Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathological examination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method. Results. Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re. Conclusion. These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes.

2021 ◽  
Vol 72 (2) ◽  
pp. 11-18
Author(s):  
Nina Gatarić ◽  
Ana Ilić ◽  
Dušan Todorović ◽  
Slavica Mutavdžin ◽  
Jovana Jakovljević-Uzelac ◽  
...  

Introduction: Isoprenaline or isoproterenol (1-(3,4-dihydroxyphenyl)-2-isopropylaminoethanolhydrochloride; ISO), a synthetic b-adrenergic agonist, can be used to establish myocardial ischemia, cardiotoxicity, necrosis and/or an experimental model of infarction in rats. Aim: Determination of the dynamics of myocardial injury biomarkers production of aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), and high-sensitive troponin T (hsTnT), with changes on electrocardiogram (ECG) parameters during the subcutaneous aplication of ISO in male Wistar rats. Material and methods: All animals (n = 23) were divided into two groups: control group (n = 11) treated with a saline solution, during two consecutive days (0,2 ml/kg b.m. daily, sc); and the ISO group (n = 12) treated with isoprenaline, during two consecutive days (85 mg/kg b.m. daily, sc). Blood was drawn from the rat tail vein in both groups, in order to determine serum activity levels of myocardial injury biomarkers, and an ECG (n = 6) was registered prior to the application, as well as 48h following the first dose of of saline solution or isoprenaline. Results: In comparison to the control group, in which no significant enzyme activities elevation (p > 0.05) nor ECG changes were registered, ISO group presented a significant rise of two clinically significant biomarkers of acute myocardial injury/myocardial infarction (AMI), CK (p = 0.05) and hsTnT (p < 0.01), as well as an ST segment elevation, with a patognomonic ECG change. Conclusion: Obtained results support previous studies, proving that isoprenaline represents an adequate experimental model for myocardial injury/AMI induction, and a "golden standard" for evaluating potential cardioprotective effects of pharmacological and non-pharmacological therapeutic modalities, with the ultimate goal of lowering the degree of lesions and improving post-infarction myocardium function.


2019 ◽  
Vol 27 (1) ◽  
pp. 94-104 ◽  
Author(s):  
Enver Tahir ◽  
Benedikt Scherz ◽  
Jitka Starekova ◽  
Kai Muellerleile ◽  
Roland Fischer ◽  
...  

Aims The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis. Methods and results Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE–). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE– triathletes (192 ± 30 mmHg, P < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms ( P = 0.797) and 989 ± 21 ms versus 989 ± 28 ms ( P = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE– triathletes (53 ± 6% vs. 59 ± 6%, P < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE –  triathletes (121 ± 30 ml/s/m2) compared to LGE + triathletes (161 ± 34 ml/s/m2, P < 0.01). Post-race atrial peak filling rates increased in LGE– triathletes to 163 ± 46 ml/s/m2, P < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m2, P = 0.747). Conclusion Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.


Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1122
Author(s):  
Li-You Chen ◽  
Chien-Ning Huang ◽  
Chih-Kai Liao ◽  
Hung-Ming Chang ◽  
Yu-Hsiang Kuan ◽  
...  

Long-term poor glycemic control negatively affects macrovascular and microvascular diseases, as well as wound restoration. Buckwheat is a good source of rutin (quercetin-3-O-rutoside) and has benefits in regulating blood sugar. This study was to evaluate the antioxidant and anti-inflammatory effects of rutin on wound healing in streptozotocin-induced hyperglycemic rats. Eighteen male Wistar rats were randomly divided into three groups: normal (NDM), hyperglycemic (DM), and hyperglycemic with rutin (DMR). After induction of hyperglycemia for 2 days, a 15 × 15 mm wound was induced on the back of each rat. Intraperitoneal injection of rutin significantly ameliorated diabetes-induced body weight loss and improved metabolic dysfunctions of hyperglycemic rats. Based on appearance and histopathological staining, rutin promotes wound healing and inhibits production of inflammatory cells. The immunoblotting data indicated that rutin promotes production of antioxidant enzymes induced by nuclear factor erythroid 2-related factor 2 (NRF2), inhibits the expression of matrix metalloproteinases (MMPs) regulated by NF-κB, and decreases the expression of vascular endothelial growth factor (VEGF). It also promotes the expression of neurogenic-related protein (UCH-L1). The aforementioned results indicated that rutin reduces oxidative stress and inflammatory response in hyperglycemic rats, promoting wound healing and subsequently reducing the risk of wound ulcers.


Open Heart ◽  
2019 ◽  
Vol 6 (1) ◽  
pp. e000949 ◽  
Author(s):  
Ivan Zeljkovic ◽  
Sven Knecht ◽  
Nikola Pavlovic ◽  
Umut Celikyrut ◽  
Florian Spies ◽  
...  

IntroductionMyocardial injury markers such as high-sensitive cardiac troponin T (hs-cTnT) and creatine kinase MB (CK-MB) reflects the amount of myocardial injury with ablation. The aim of the study was to identify the value of myocardial injury markers to predict outcomes after pulmonary vein isolation (PVI) using three different ablation technologies.MethodsConsecutive patients undergoing PVI using a standard 3.5 mm irrigated-tip radiofrequency catheter (RF-group), an irrigated multielectrode radiofrequency catheter (IMEA-group) and a second-generation cryoballoon (CB-group) were analysed. Blood samples to measure injury markers were taken before and 18–24 hours after the ablation. Procedural complications were collected and standardised follow-up was performed. Logistic regression was used to identify predictors of recurrence and complications.Results96 patients (RF group: n=40, IMEA-group: n=17, CB-group: n=39) undergoing PVI only were analysed (82% male, age 59±10 years). After a follow-up of 12 months, atrial fibrillation (AF) recurred in 45% in the RF-group, 29% in the IMEA-group and 36% in the CB-group (p=0.492). Symptomatic pericarditis was observed in 20% of patients in the RF-group, 15% in the IMEA-group and 5% in the CB-group (p=0.131). None of the injury markers was predictive of AF recurrence or PV reconnection after a single procedure. However, hs-cTnT was identified as a predictor of symptomatic pericarditis (OR: 1.003 [1.001 to 1.005], p=0.015).ConclusionHs-cTnT and CK-MB were significantly elevated after PVI, irrespective of the ablation technology used. None of the myocardial injury markers were predictive for AF recurrence or PV reconnection, but hs-cTnT release predicts the occurrence of symptomatic pericarditis after PVI.


2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Qing Zeng ◽  
XingSan Li ◽  
Ge Xu

Abstract Background: To evaluate myocardial injury in Atrial flutter (AFL) patients undergoing Radiofrequency ablation (RF) and cryoablation (CRYO) treatments. Methods: We conducted a systematic search on PubMed, Embase, Cochrane Library, and CBM databases. All relevant clinical trials (up to October 2018) on myocardial injury in AFL patients were retrieved and subsequent results analyzed with a random-effects model or a fixed-effects model. Results: A total of eight clinical trials with a sample size of 644 patients, were identified and incorporated in the present study. The results indicated no significant differences in creatine kinase (CK) levels (mean difference (MD) = 62.74, P=0.46; 4–6 h and MD = 30.73, P=0.49; 12–24 h after ablation), creatine kinase MB(CK-MB) levels (MD = 17.32, P=0.25; 12–24 h post-ablation), troponinI (TnI) levels (MD = 0.12, P=0.08; 6 h after ablation), and troponin T (TnT) levels (MD = 0.30, P=0.08; 4–6 h post-ablation) between the two treatment approaches. However, patients receiving CRYO xhibited higher levels of CK (MD = 179.54, P=0.04; tested immediately after the procedure), CK-MB (MD = 10.08, P=0.004) 4–6 h after ablation, and TnT (MD = 0.19, P=0.002) tested the next morning. Moreover, those patients had a significantly reduced pain perception (odds ratio (OR) = 0.05, P=0.04) compared with those in the RF group. Conclusion: These results indicate that CRYO in comparison with RF significantly increases myocardial injury in AFL patients. Additionally, it decreases pain perception during the procedure. Further large-sampled studies are needed to support these findings.


2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Orapin Gerdprasert ◽  
Nantana Choomchuay ◽  
Boonrat Chantong ◽  
Narueporn Sutanthavibul ◽  
Duangdeun Meksuriyen ◽  
...  

Phikud Navakot (PN) is nine major herbs in a famous traditional Thai recipe namely “Yahom Navakot” used to treat cardiovascular disorders. This study investigated the cardioprotective effects of PN formula on isoproterenol-induced myocardial infarction (IMI) in Sprague-Dawley rats. Forty-five rats were randomly divided into nine groups (n = 5 per group): the control, the IMI, the IMI + propranolol, the control or the IMI + PN formula (PN ethanolic extract at doses of 64, 127, or 255 mg/kg) by oroesophageal gavage for 28 days. The ST segment and serum troponin T levels were significantly increased in IMI rats. PN did not eliminate tissue necrosis, infiltration of inflammatory cells, or interstitial edema in IMI rats. All doses of PN decreased (p<0.001) serum TNF-α and IL-6 levels. PN (127 and 255 mg/kg) up-regulated (p<0.05) heme oxygenase (HO)-1 expression, whereas PN (255 mg/kg) significantly increased superoxide dismutase (SOD) 1 and 2 expression, compared with IMI rats. Nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 expression significantly increased in IMI rats and IMI rats that received PN. PN formula possesses potential anti-inflammatory and antioxidant properties by modulating the levels of TNF-α, IL-6 and antioxidant enzymes. Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling.


2013 ◽  
Vol 32 (5) ◽  
pp. 351-357 ◽  
Author(s):  
Victorita Sorodoc ◽  
Laurentiu Sorodoc ◽  
Didona Ungureanu ◽  
Anca Sava ◽  
Irina M. Jaba

The main objective of this study was to investigate whether cardiac troponin (cTn) and N-terminal, protein B-type natriuretic peptide (NT-proBNP) can be useful as indicators for amitriptyline cardiotoxicity which is a known drug having sublethal toxic cardiac effects. At the same time, this study looked at detecting potential histopathological changes specific to irreversible cardiac injuries in a rat model of amitriptyline cardiotoxicity. Male Wistar rats were randomly divided into 2 groups, control (saline) group and amitriptyline group (100 mg/kg body weight intraperitoneally, equivalent for lethal dose at 50%). Blood was collected 30 minutes after the administration. The cTn was measured using 3 different methods (2 methods designed for human use and a sandwich enzyme immunoassay specific for rat cTnT). The brain natriuretic peptide was measured by 2 different methods (1 for human and 1 specific for rats). Electrocardiography showed that the QRS complex ( P < .0001) and the QT interval ( P = .002) were significantly prolonged for amitriptyline-treated animals. Troponin T and NT-proBNP had significantly increased levels in all the rats but showed positive results only when using rat-specific quantitative measurement. In certain rats, the histopathological examination identified a few small foci of acute myocardial necrosis. In conclusion, elevation of cTnT and NT-proBNP are early indicators of cardiotoxicity, yet the significance of irreversible myocardial damage in amitriptyline cardiotoxicity needs to be further understood.


2021 ◽  
Vol 12 ◽  
Author(s):  
Linzi Long ◽  
Zikai Yu ◽  
ShengJun Chen ◽  
Jiarui Wu ◽  
Yingying Liu ◽  
...  

Background: Myocardial ischaemia/reperfusion (I/R) results in myocardial injury via excessive autophagy. Huoxue Jiedu Formula (HJF) has been widely applied in China for the treatment of ischaemic heart disease. However, the mechanisms of HJF are still poorly understood. Thus, the present experiment was designed to observe the effects of HJF on myocardial I/R injury and explore the possible mechanism.Methods: Myocardial injury in rats subjected to myocardial I/R was reflected by nitrotetrazolium blue chloride staining, thioflavin S staining, serum creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT). Autophagy was determined by electron microscopy, laser confocal microscopy, Q-PCR and western blot. The possible pathway was predicted by network pharmacology and validated in vivo and in vitro.Results: Pretreatment of HJF decreased the no-reflow area, infarcted area, serum CK-MB levels and serum cTnT levels in I/R rat model. In addition, pretreatment of HJF decreased autophagy in heart tissues (decrease in Beclin-1 and LC3-II, and increase in Bcl-2, p62 and ratio of LC3-I/LC3-II). In the vivo study, pretreatment of HJF significantly decreased hypoxia/reoxygenation (H/R)-induced autophagy in H9C2 cells. Network pharmacology was applied to predict the possible mechanism by which HJF affects cardiac autophagy, and the PI3K/AKT/mTOR signalling pathway was the most significantly enriched pathway. And experimental studies demonstrated that pretreatment of HJF increased the phosphorylation of AKT and mTOR, and the effects of HJF on autophagy would be offset by PI3K inhibitor LY294002.Conclusion: Pretreatment of HJF ameliorates myocardial I/R injury by decreasing autophagy through activating PI3K/AKT/mTOR pathway.


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