scholarly journals Protective Effects of Chinese Traditional Medicine Buyang Huanwu Decoction on Myocardial Injury

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Guangde Yang ◽  
Zhiyuan Fang ◽  
Yu Liu ◽  
Hui Zhang ◽  
Xiaolian Shi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Myocardial Injury ◽  
Control Group ◽  
Protective Effects ◽  
Buyang Huanwu Decoction ◽  
Pre Treatment ◽  
Cluster Of Differentiation ◽  
Electrocardiogram Ecg

Many clinical studies have reported that Buyang Huanwu Decoction (BYHWD) has a protective effect on ischemic heart disease (IHD). In the present study, the protective effect of BYHWD on myocardial ischemia was investigated. Different doses of BYHWD and Compound Danshen Dropping Pills (CDDP) were lavaged to rats, respectively, isoproterenol (ISO) was intraperitoneally injected in to all animals to induce myocardial ischemia except the control group. Electrocardiogram (ECG) of each animal was recorded; activities of lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in serum were detected. As the results of ECG showed, pre-treatment with BYHWD inhibited ischemic myocardial injury, and the activities of LDH, CK and AST were lower than those in the myocardial ischemia model group, which suggests that BYHWD rescues the myocardium from ischemia status. To research the potential mechanism, the level of nitric oxide (NO), nitric oxide syntheses (NOS) and inducible nitric oxide syntheses (iNOS), the expression of iNOS and ligand of cluster of differentiation 40 (CD40L) were detected. The results revealed that BYHWD significantly decreased the level of NO, NOS and iNOS in serum. Moreover, BYHWD decreased the expression of iNOS and CD40L in myocardial tissues. These results indicate that the protective effect of BYHWD on myocardial ischemia and mechanism are associated with inhibition of iNOS and CD40L expression.

scholarly journals Protective Effects of Millettia Pulchra Flavonoids on Myocardial Ischemia In Vitro and In Vivo

2015 ◽  
Vol 35 (2) ◽  
pp. 516-528 ◽  
Author(s):  
Jianchun Huang ◽  
Xudong Zhang ◽  
Feizhang Qin ◽  
Yingxin Li ◽  
Xiaoqun Duan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Protective Effects ◽  
Bax Protein ◽  
Oxide Synthase

Background: Previous studies have demonstrated that Millettia pulchra flavonoids (MPF) exhibit protective effects on myocardial ischemia reperfusion injury (MI/RI) in isolated rat hearts and show anti-oxidative, anti-hypoxic and anti-stress properties. Methods: In this study, the cardioprotective effects of MPF on myocardial ischemia and its underlying mechanisms were investigated by a hypoxia/ reoxygenation (H/R) injury model in vitro and a rat MI/RI model in vivo. Results: We found that the lactate dehydrogenase (LDH) and inducible nitric oxide synthase (iNOS) activities were decreased in the MPF pretreatment group, whereas the activities of constructional nitric oxide synthase (cNOS), total nitric oxide synthase (tNOS), Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased. In addition, the cardiocytes were denser in the MPF groups than in the control group. The mortality rate and apoptosis rate of cardiocytes were significantly decreased. Furthermore, pretreatment with MPF in vivo significantly improved the hemodynamics, decreased malondialdehyde (MDA) abundance, increased the activities of plasma superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the expression of the Bax protein and ratio Bax/Bc1-2 ration. Conclusions: These results suggest that MPF is an attractive protective substance in myocardial ischemia due to its negative effects on heart rate and ionotropy, reduction of myocardial oxidative damage and modulation of gene expression associated with apoptosis.

Protective Effect of Total Flavones of Rhododendra on Ischemic Myocardial Injury in Rabbits

2006 ◽  
Vol 34 (03) ◽  
pp. 483-492 ◽  
Author(s):  
Li-Ping Yuan ◽  
Zhi-Wu Chen ◽  
Fan Li ◽  
Liu-Yi Dong ◽  
Fei-Hu Chen
Keyword(s):  
Nitric Oxide ◽  
Protective Effect ◽  
Myocardial Injury ◽  
Ginkgo Biloba Extract ◽  
Control Group ◽  
Infarction Size ◽  
Plasma Effects ◽  
Myocardial Ischemic Injury ◽  
Plasma Creatine Kinase ◽  
Dual Staining

This study was to investigate the effect of total flavones of rhododendra (TFR) on ischemic myocardial injury in rabbits. Rabbit ischemic myocardial injury was induced by occluding the anterior descent of the left artery (LAD). The ECG was recorded; the plasma creatine kinase (CK), nitric oxide (NO) and endothelin-1 (ET-1) levels were measured using spectrophotometry, Griess method and radioimmunoassay, respectively. The myocardial ischemic size and infarction size were determined by dual staining with Evan's blue and Nitroblue tetrazolium reductionest (N-BT). A typical ECG S-T segment elevation and an increase of plasma CK activity were observed 6 and 24 hours after the induction of ischemia. These changes were inhibited in rabbits treated with either TFR (30, 60 mg/kg) or ginkgo biloba extract (EGB) for 7 days, indicating a protective effect of TFR on ischemic myocardial injury. The myocardial ischemic size and infarction size were 40.7 ± 3.6% and 36.8 ± 3.6% respectively in the control group, while TFR (60 mg/kg) pretreatment for 7 days significantly reduced both myocardial ischemic size (32.40 ± 5.38%, p < 0.05) and infarction size (28.7 ± 5.8%, p < 0.05). In addition, the occlusion of LAD resulted in an increase of ET-1 and a decrease of NO levels in the plasma, effects that were inhibited by TFR treatment, suggesting a possible mechanism for the protective effect of TFR against myocardial ischemic injury.

Empagliflozin significantly attenuates QTc prolongation in rats due to sotalol

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V.O Baris ◽  
B Dincsoy ◽  
E Gedikli ◽  
A Erdem
Keyword(s):  
Qt Prolongation ◽  
Control Group ◽  
Diabetic Patients ◽  
Protective Effects ◽  
Qtc Prolongation ◽  
Positive Effects ◽  
T Wave ◽  
Qt Intervals ◽  
Electrocardiogram Ecg

Abstract Introduction Sotalol (SOT) is a Class 3 antiarrhythmic drug and commonly used for various arrhythmia treatments. However; it can prolong QT interval and lead to malignant arrhythmias. Empagliflozin is a selective SGLT-2 inhibitor used in the treatment of Type 2 diabetes and has been shown to have positive effects on cardiovascular outcomes. Since the effect of empagliflozin (EMPA) on potassium channel activation is not yet known, there is no recommendation for the concomitant use of these drugs. Purpose In this study, we aimed to evaluate possible protective effects of empagliflozin in sotalol induced QT prolongation. Materials and methods Twenty-four male Wistar Alba rats were randomized into four groups. The first (control) group (n: 6) received only serum physiologic (1ml) via orogastric gavage (OG). The second (EMPA) group (n: 6) received EMPA (10 mg/kg) via OG. The third (SOT) group (n: 6) received SOT (80 mg/kg) via OG. The fourth (EMPA+SOT) group (n: 6) received EMPA (10 mg/kg) and SOT (80 mg/kg) via OG. Under anesthesia; PR, QT intervals and heart rate (HR) were measured and QTc value was also calculated at second hour on lead II using electrocardiogram (ECG). Results In the SOT group; QT intervals, T wave durations and QTc values were found to be statistically longer than the control group, whereas HR was found to be lower than the control group (p&lt;0.01). In the EMPA+SOT group; QT intervals, T wave durations and QTc values were significantly lower and HR was significantly higher compared to the SOT group (p&lt;0.001, p&lt;0.01, p&lt;0.001, p&lt;0.001 respectively) (Table) Conclusion In the present study, we detected that EMPA significantly ameliorates SOT induced QT prolongation. In addition to this, we have also shown that EMPA can be used safely with SOT in clinical practice. With more clinical trials, the routine use of EMPA may be suggested to prevent QTc prolongation in diabetic patients receiving SOT. Finally; our study indicates that EMPA can effect on potassium channels. Funding Acknowledgement Type of funding source: None

Abstract 309: Role of Hemeoxygenase in the Reno-Protective Effects of Soluble Epoxide Hydrolase Inhibition In Diabetic Spontaneously Hypertensive Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Jessica Faulkner ◽  
Chelsey Pye ◽  
Babak Baban ◽  
Katelyn Rouch ◽  
...  
Keyword(s):  
Protective Effect ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Spontaneously Hypertensive Rats ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Control Group ◽  
Protective Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We previously showed that inhibition of soluble epoxide hydrolase (sEH) increased epoxyeicosatrienoic acids (EETs) levels and reduced renal injury in diabetic mice and these changes were associated with induction of hemeoxygenase-1 (HO-1). The present study determines whether the inhibition of HO negates the reno-protective effect of sEH inhibition in diabetic spontaneously hypertensive rats as a model of diabetic nephropathy in which hypertension coexists with diabetes. After six weeks of induction of diabetes with streptozotocin, SHR were divided into the following groups: untreated, treated with the sEH inhibitor, trans -4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (AUCB), treated with the HO inhibitor, stannous mesoporphyrin (SnMP), and treated with both inhibitors for four more weeks; non diabetic SHR served as a control group. Although inhibition of sEH increased renal EETs/DHETEs ratio and HO-1 activity in diabetic SHR, it did not significantly alter blood pressure (plasma EETs/DHETEs ratio was 0.5± 0.1 in AUCB-treated vs. 0.1± 0.01 in untreated diabetic SHR, P<0.05). Treatment of diabetic SHR with AUCB reduced the elevation in urinary albumin and nephrin excretion (albuminuria was 6.5± 0.5 in AUCB-treated diabetic SHR vs. 9± 1.7 mg/day in untreated diabetic SHR and nephrinuria was 70±11 in AUCB-treated diabetic SHR vs. 111± 9 μg/day in untreated diabetic SHR, P<0.05) whereas co-administration of SnMP with AUCB prevented these changes (albuminuria was 10.6± 0.6 mg/day and nephrinuria was 91±11 μg/day). Immunohistochemical analysis revealed elevations in renal fibrosis and apoptosis as evidenced by increased renal TGF-β, fibronectin and annexin V expression in diabetic SHR and these changes were reduced with sEH inhibition. Co-administration of SnMP with AUCB prevented its ability to reduce renal fibrosis and apoptosis in diabetic SHR. In addition, SnMP treatment also prevented AUCB-induced decreases in renal macrophage infiltration and renal TGF-β, NFκB and MCP-1 levels in diabetic SHR. These data suggest that HO-1 induction is involved in the protective effect of sEH inhibition against diabetic renal injury.

Protective effect of vanillin against carbon tetrachloride (CCl4)-induced oxidative brain injury in rats

2011 ◽  
Vol 28 (7) ◽  
pp. 655-662 ◽  
Author(s):  
Mohamed Makni ◽  
Yassine Chtourou ◽  
Mohamed Barkallah ◽  
Hamadi Fetoui
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Brain Damage ◽  
Glutathione Transferase ◽  
Single Injection ◽  
Male Rats ◽  
Control Group ◽  
Protective Effects ◽  
Degree Of Protection ◽  
Oxidative Brain Injury

This study investigated the protective effects of vanillin against acute brain damage induced by carbon tetrachloride (CCl4) in rats. The study was performed on 32 male rats divided into four groups: a control group, vanillin group ([Va] 150 mg/kg/day, intraperitoneally [i.p.]) and CCl4 toxication groups received a single injection of CCl4 (1 ml/kg, i.p.; CCl4 and Va + CCl4 groups). The degree of protection in brain tissue was evaluated by the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase, glutathione transferase, glutathione peroxidase and nitric oxide (NO). Vanillin showed a significant brain-protective effect by decreasing the level of lipid peroxidation and NO2 and elevated the activities of antioxidative enzymes and level of GSH. Consequently vanillin blocked oxidative brain damage induced by CCl4 in rats.

scholarly journals Protective Effects and Mechanisms of Rosuvastatin on Acute Kidney Injury Induced by Contrast Media in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Zehui Jiang ◽  
Jun Zhang ◽  
Yuanan Lu
Keyword(s):  
Protective Effect ◽  
Contrast Medium ◽  
Renal Injury ◽  
Intervention Group ◽  
Inflammatory Factors ◽  
Control Group ◽  
Renal Tubules ◽  
Protective Effects ◽  
Sod Activity ◽  
Biochemical Indicators

Objective. To explore the protective effect and mechanism of rosuvastatin on acute renal injury induced by a nonionic hypotonic contrast medium in rats. Methods. Forty-eight healthy adult SD rats were randomly divided into three groups: normal control group (NC); contrast medium control group (CM); and rosuvastatin intervention group (RI). The RI group was intragastrically administered with a 10 mg/kg of rosuvastatin 12 h prior to the contrast exposure. All rats in CM and RI groups were inoculated with 10 mL/kg of chemical (IV) while the same volume of saline for the NC group. At 24 h and 72 h posttreatments, pathomorphological changes of renal tubules were documented, respectively, and several biochemical indicators were tested to assess renal injury of experimental rats. Results. Compared with the CM group, rats in the RI group showed significantly reduced injury of kidneys and decreased levels of biochemical indicators such as blood Scr, blood Cys-C, urine NAG, urine α1-MG, and urine mALB. The serum Hs-CRP in the CM group increased significantly from 24 h to 72 h (p<0.05), but this was not observed in the rats of the RI group. In addition, SOD activity in the RI group was significantly increased (p<0.01) while SOD activity in renal tissue decreased significantly with time in the CM group (p<0.05). Conclusion. Short-term intervention with rosuvastatin can lead to reduced kidney damage associated with the contrast agent by reducing the levels of inflammatory factors and oxidative stress. Thus, rosuvastatin intervention has a protective effect on rats from contrast-induced nephropathy.

TGF-β1 attenuates myocardial ischemia-reperfusion injury via inhibition of upregulation of MMP-1

2003 ◽  
Vol 284 (5) ◽  
pp. H1612-H1617 ◽  
Author(s):  
Hongjiang Chen ◽  
Dayuan Li ◽  
Tom Saldeen ◽  
Jawahar L. Mehta
Keyword(s):  
Myocardial Ischemia ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Necrosis ◽  
Left Ventricular ◽  
Blue Staining ◽  
Control Group ◽  
Dependent Manner ◽  
Arterial Blood ◽  
Group I

Ischemia-reperfusion (I/R) is thought to upregulate the expression and activity of matrix metalloproteinases (MMPs), which regulate myocardial and vascular remodeling. Previous studies have shown that transforming growth factor-β1 (TGF-β1) can attenuate myocardial injury induced by I/R. TGF-β1 is also reported to suppress the release of MMPs. To study the modulation of MMP-1 by TGF-β1 in I/R myocardium, Sprague-Dawley rats were given saline and subjected to 1 h of myocardial ischemia [total left coronary artery (LCA) ligation] followed by 1 h of reperfusion ( n = 9). Parallel groups of rats were pretreated with recombinant TGF-β1(rTGF-β1, 1 mg/rat, n = 9) before reperfusion or exposure to sham I/R (control group). I/R caused myocardial necrosis and dysfunction, indicated by decreased first derivative of left ventricular pressure, mean arterial blood pressure, and heart rate (all P < 0.01 vs. sham-operated control group). Simultaneously, I/R upregulated MMP-1 ( P < 0.01). Treatment of rats with rTGF-β1 reduced the extent of myocardial necrosis and dysfunction despite I/R (all P < 0.01). rTGF-β1 treatment also inhibited the upregulation of MMP-1 in the I/R myocardium ( P < 0.05). To determine the direct effect of MMP-1 on the myocardium, isolated adult rat myocytes were treated with active MMP-1, which caused injury and death of cultured myocytes, measured as lactate dehydrogenase release and trypan blue staining, in a dose- and time-dependent manner ( P < 0.05). Pretreatment with PD-166793, a specific MMP inhibitor, attenuated myocardial injury and death induced by active MMP-1. The present study for the first time shows that MMP-1 can directly cause myocyte injury or death and that attenuation of myocardial I/R injury by TGF-β1 may, at least partly, be mediated by the inhibition of upregulation of MMP-1.

scholarly journals Modulatory Effect of Guinep (Melicoccus bijugatus Jacq) Fruit Pulp Extract on Isoproterenol-Induced Myocardial Damage in Rats. Identification of Major Metabolites Using High Resolution UHPLC Q-Orbitrap Mass Spectrometry

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 235 ◽  
Author(s):  
Chukwuemeka Nwokocha ◽  
Isheba Warren ◽  
Javier Palacios ◽  
Mario Simirgiotis ◽  
Magdalene Nwokocha ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
High Resolution ◽  
Myocardial Injury ◽  
Weight Ratio ◽  
Mass Spectrometry Analysis ◽  
Control Group ◽  
Qtc Interval ◽  
Protective Effects ◽  
Orbitrap Mass Spectrometry ◽  
Hematological Analysis

Guinep is traditionally used in the management of cardiovascular ailments. This study aims to evaluate its medicinal constituents and effects in the management of myocardial injury in an experimental isoproterenol (ISO) rat model. Sprague-Dawley rats were randomly assigned to four groups: Group 1 was the control group; Group 2 received M. bijugatus extract (100 mg/Kg; MB) for six weeks; Group 3 was given ISO (85 mg/Kg) i.p. twice during a 24-hour period; and Group 4 was given ISO (85 mg/Kg) i.p. and MB extract (100 mg/Kg) for six weeks. The MB was administered orally by gavage, daily. The blood pressure of conscious animals was measured, while ECG was performed under anesthesia. Blood and serum were collected for biochemical and hematological analysis. The ISO group treated with MB showed a significant decrease (p < 0.001) in (SBP), diastolic (DBP), mean arterial (MAP) and heart rate (HR) compared to the ISO only group. Conversely, MB treated rats that were not induced with ISO displayed a significant decreases (p < 0.001) in SBP, DBP, MAP, and HR. ISO significantly elevated the ST segment (p < 0.001) and shortened the QTc interval (p < 0.05), which were recovered after treatment with 100 mg/Kg of MB. In addition, the results showed a significant decrease (p < 0.001) in the heart to body weight ratio of the ISO group treated with MB compared to the ISO only group. Furthermore, the extract normalized the hematological values depressed by the ISO while significantly elevating the platelet count. UHPLC high-resolution orbitrap mass spectrometry analysis results revealed the presence of several antioxidants like vitamin C and related compounds, phenolic acids, flavonoid, fatty acids (oxylipins), and terpene derivatives. The results of this study indicated that Melicoccus bijugatus did display some cardio-protective effects in relation to myocardial injury.

Dynamic Analysis of Myocardial Enzymes and Electrocardiogram in Pediatric Pneumonia

2019 ◽  
Vol 9 (8) ◽  
pp. 1596-1599
Author(s):  
Yanling Wang ◽  
Li Sheng ◽  
Xuan Zhou
Keyword(s):  
Creatine Kinase ◽  
Myocardial Injury ◽  
Myocardial Damage ◽  
Control Group ◽  
Healthy Children ◽  
Dynamic Changes ◽  
Non Invasive ◽  
Pediatric Pneumonia ◽  
Electrocardiogram Ecg ◽  
Myocardial Enzymes

Objective: The condition of pediatric pneumonia changes rapidly. Non-invasive myocardial enzymes and electrocardiogram (ECG) can reflect the myocardial damage of patients noninvasively. The purpose of this study was to investigate the dynamic changes of myocardial enzymes and ECG in the pediatric pneumonia. Method: A total of 18 pediatric pneumonia cases in our hospital from April 2018 to February 2019 were chosen. Another 18 healthy children were chosen as control group. The activity of creatine kinase (CK), creatine kinase isoenzymes (CK-MB), lactate dehydrogenase (LDH), and Glutamic oxaloacetic transaminase (GOT) was collected, and the ECG were recorded in all subjects. Result: Before treatment, the CK, CK-MB, LDH and GOT in pneumonia group was higher than the data in control group. After treatment, the level decreased significantly, but still slight higher than the data in control group. Compare with control groups, the incidence of abnormal ECG increased significantly. There was no statistical difference of incidence between control group and the patients after treatment. Conclusion: The serum myocardial enzymes such as CK, CK-MB, LDH and GOT and ECG changes are useful markers for monitoring the myocardial injury in pediatric pneumonia.

scholarly journals Gastro-protective Effects of Honey in Male Wistar Rats

2021 ◽  
pp. 4114-4125
Author(s):  
Owoyele B.V. ◽  
Ayinla M.T. ◽  
Esan A.A. ◽  
Bayo-Olugbami A.
Keyword(s):  
Gastric Acidity ◽  
Wistar Rats ◽  
Control Group ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Water Control ◽  
Significant Difference ◽  
Male Wistar Rats ◽  
Pre Treatment ◽  
Laboratory Models

Honey is consumed as food and also used in the treatments of ailment. However, honey of various types exhibit varying properties. Their therapeutic effects are determined by whether the honey is multifloral or monofloral, and also on the variety of nectars the honey is derived from. Manuka and Tualang types of honey were observed to possess anti-ulcer effects. However, no such report is available for University of Ilorin honey. This study therefore aimed to determine the gastroprotective effects of University of Ilorin honey in Wistar rats using two laboratory models for inducing ulcer (HCl/Ethanol and Indomethacin). Twenty rats each were assigned to four groups for each model of ulcer. The rats were treated for 12 days with the administration of distilled water (control), cimetidine (100 mg/kg b.w.) and University of Ilorin honey (250 mg/kg b.w. in one group and 1000 mg/kg b.w in another group). The rats were fasted for 24 hours after the last treatment. Then, the ulcerogens were given orally. After four hours, the rats were sacrificed, gastric juice was collected and the stomachs were examined for ulceration. The results revealed that pre-treatment with University of Ilorin honey reduced gastric index from 6.80±0.20 (1000 mg/kg b.w. to 2.40±0.24 (control) P<0.05 and 7.20±0.37 (1000 mg/kg b.w.) to 3.20±0.37 (control) P<0.05 in HCl/Ethanol and indomethacin induced ulcer models respectively. There was no significant difference in ulcer index between the cimetidine administered rats and the honey administered group (1000 mg/kg bw.), but the honey group (250 mg/kg bw.) was less effective than the cimetidine group in the models used. Also, there were no changes in gastric acidity in all the groups compared with the control group. In conclusion, the results showed that University of Ilorin honey has protective effect on the gastrointestinal tract which is not due to alteration of gastric acidity.

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