Cardiac Marker Enzymes Research Articles

Synergistic Effects of Cinnamomum verum and Stingless Bee Honey on Isoproterenol-induced Cardiac Hypertrophic Murine Model

Abstract Objectives: This study aimed to validate the synergistic effects of Cinnamomum verum (C. verum) barks and stingless bee honey (SBH) against cardiac hypertrophy (CH). Materials and Methods: Isoproterenol (ISO-group II-30 mg/kg)-induced cardiac hypertrophic Wistar rats were used in this study. Hypertrophic rats were treated using the reference drug losartan (LOS Group III: 50 mg/kg) and aqueous extracts of C. verum barks and SBH (ACH Group IV: 250 mg/kg and 250 mg/kg). CH was characterized by electrocardiography, hypertrophic indices, and biochemical estimations such as total glucose, protein, albumin, lipid profiles, cardiac marker enzymes, and histopathological studies. Results: Rats received ISO had increased levels of glucose, protein, cholesterol, triglycerides, very low-density lipoprotein, and low-density lipoprotein, coupled with decreased levels of albumin and high-density lipoprotein. These levels were restored to near normal when treated with ACH extracts of the standard drugs. Contrary to the ISO-induced myocardial damaged hearts, ACH extracts had a profound effect compared to LOS, which was also reflected in histopathological studies. Conclusion: These data explicitly reveal that the ACH have a synergistic cardioprotective (antihypertrophic) effect.

Gynostemma pentaphyllum Makino exerts cardioprotective effects by improving hemodynamic, biochemical and histopathological changes through activation of PI3K signalling in isoproterenol-induced myocardial infarction in rats.

To evaluate the cardioprotective effects of Gynostemma pentaphyllum Makino in isoproterenol-induced myocardial infarction in rats and to evaluate the role of phosphatidylinositol 3-kinases (PI3K) in cardioprotection. The protective effect of the hydroalcoholic leaf extract of Gynostemma pentaphyllum (LEGP) on the heart was investigated against isoproterenol (ISO)-induced MI in rats. Preliminary phytochemical screening was performed followed by molecular docking. For the in vivo studies Wistar albino rats (Male) were divided among different groups. Different parameters were evaluated such as heart weight index, Electrocardiogram (ECG) analysis, triphenyl tetrazolium chloride assay, cardiac enzyme markers, oxidative stress, antioxidant enzymes, PI3K levels, and histopathology of cardiac tissue. Results showed that LEGP improved the electrocardiogram, reduced infarct size, and decreased the levels of cardiac enzyme markers and oxidative stress, while antioxidant enzymes and PI3K levels were increased. LEGP protected the heart against ISO-induced MI in rats by improving hemodynamic, biochemical and histological attributes. These protective effects were produced by the phytoconstituents of the LEGP through modulation of the PI3K signalling pathway.

Pleiotropic attenuating effect of Ginkgo biloba against isoprenaline-induced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na+, K+-ATPase activities

ObjectiveMyocardial infarction (MI) is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles. Beta-blockers and calcium antagonists are just two of the common medications used to treat MI. However, these have reportedly been shown to be either ineffective or to have undesirable side effects. Extract of Ginkgo biloba leaves (GBE), a Chinese herbal product offers special compatibility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress. In order to better understand how GBE affects MI in rats insulted by isoprenaline (ISO), the current study was designed. MethodsThe heart weight index, serum lipid profile, cardiac marker enzymes, endogenous antioxidants [catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), nitrites and malondialdehyde (MDA)], inflammatory mediators [tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6)], immunohistochemical expressions of B-cell lymphoma factor-2 (Bcl-2), extracellular signal-regulated kinase (ERK1/2), and mammalian target of rapamycin (mTOR) and histopathological analysis were used to assess the cardioprotective properties of GBE. ResultsThe findings showed that GBE effectively attenuated myocardial infarction by boosting the body’s natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes. The expression of Bcl-2, ERK1/2 and mTOR was increased while the histomorphological alterations were reversed. ConclusionThe cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na+, K+-ATPase activity.

Antidiabetic and Cardioprotective effect of Terminalia phillyreifolia (Van Heurck and Mull. Arg.) Gere and Boatwr. bark extract in Experimental animals

Objective: Objective of the current study was to evaluate the effect of methanolic extract of Terminalia phillyreifolia (Van Heurck and Müll. Arg.) Gere and Boatwr. (TP) bark in Type 2 diabetes mellitus and cardiovascular complications. Methods: Diabetes mellitus was induced in Wistar rats by administration of fructose and streptozotocin (40mg/kg, i.p.). TP bark extract was administered to diabetic animals at doses of 100mg/kg and 300mg/kg for 12 weeks. Glibenclamide (5mg/kg/day, p.o.) was administered as standard treatment. Various biochemical and functional parameters were evaluated at appropriate time intervals. Results: Methanolic extract of TP bark produced statistically significant (p< 0.05) hypoglycemic and antioxidant effect. Treatment with extract resulted in significant reduction in plasma glucose, HbA1C, lipid levels and oxidative stress parameters. TP treated rats demonstrated significantly lower insulin resistance and improved β cell function as compared to untreated diabetic rats. TP treatment resulted in improvement in cardiac and left ventricular hypertrophy as reflected by lower cardiac and left ventricular hypertrophy index. It could successfully improve the levels of cardiac enzyme markers such as LDH and CK-MB levels in a dose dependent manner. TP treatment could also efficiently prevent abnormalities of haemodynamic parameters such as mean blood pressure and heart rate. Conclusion: The results suggest that methanolic extract of TP bark exerted hypoglycemic effect in diabetic rats, comparable to that of standard. TP bark extract treatment was also able to inhibit development of cardiomyopathy in diabetic animals.

Cadmium exposure disturbs myocardial lipid signature and induces inflammation in C57BL/6J mice

Cadmium is a highly ubiquitous environmental pollutant that poses a serious threat to human health. In this study, we assessed the cardiotoxicity of Cd exposure and explored the possible mechanisms by which Cd exerts its toxic effects. The results demonstrated that exposure to Cd via drinking water containing CdCl2 10 mg/dL for eight consecutive weeks induced cardiac injury in C57BL/6J mice. The histopathological changes of myocardial hemolysis, widening of myocardial space, and fracture of myocardial fiber were observed. Meanwhile, elevated levels of cardiac enzyme markers and up-regulation of pro-apoptotic genes also indicated cardiac injury after Cd exposure. Non-targeted lipidomic analysis demonstrated that Cd exposure altered cardiac lipid metabolism, resulted in an increase in pro-inflammatory lipids, and changed lipid distribution abundance. In addition, Cd exposure affected the secretion of inflammatory cytokines by activating the NF-κB signaling pathway, leading to cardiac inflammation in mice. Taken together, results of our present study expand our understanding of Cd cardiotoxicity at the lipidomic level and provide new experimental evidence for uncovering the association of Cd exposure with cardiovascular diseases.

Effects of Taraxerol on Oxidative and Inflammatory Mediators in Isoproterenol-Induced Cardiotoxicity in an Animal Model.

Myocardial infarction (MI) continues to be an important issue in healthcare systems worldwide, leading to high rates of morbidity and mortality. Despite ongoing efforts towards the development of preventive measures and treatments, addressing the challenges posed by MI remains difficult both in developed and developing countries. However, researchers recently investigated the potential cardioprotective effects of taraxerol utilizing an isoproterenol (ISO)-induced cardiotoxicity model among Sprague Dawley rats. Specifically, subcutaneous tissue injections consisting of 5.25 mg/kg or 8.5 mg/kg ISO were administered over two consecutive days as stimuli to induce cardiac injury. To investigate the possibility of preventing damage caused by ISO-induced cardiotoxicity by taraxerol treatment, five groups were formed: a normal control group (1% Tween 80), an ISO control group, an amlodipine group administered 5 mg/kg/day, and various doses of taraxerol. The study results showed that treatment significantly reduced cardiac marker enzymes. Additionally, pretreatment with taraxerol increased myocardial activity in SOD and GPx, leading to significant reductions in serum CK-MB levels along with MDA, TNF-α, and IL-6. Further histopathological analysis supported these observations, as treated animals had less cellular infiltration compared to untreated ones. These multifaceted findings suggest that oral administration of taraxerol could potentially protect hearts from ISO-caused damage by increasing endogenous antioxidant concentrations while decreasing pro-inflammatory cytokines.

Impact on cardioprotective effect of Psidium guajava leaves extract in streptozotocin-induced Wistar mice with molecular in silico analysis

Cardiovascular disease (CVD) and its complications have been regarded as the leading cause of morbidity and mortality. The drugs available in the market are effective to treat CVD, but with many adverse reactions. Nowadays, herbal products are the attention of researchers because of their less adverse effects. In this study, the cardioprotective effects of ethanolic leaves extract of Psidium guajava Linn. (Guava) (P. guajava) were evaluated in streptozotocin (STZ)-treated animal models. Mice acquired for the study were divided into five groups, each consisting of six mice. The toxin-induced mice were treated with the ethanolic leaves extract of P. guajava (300 mg/kg body weight [b.w.]). The results were compared to the standard drug (glibenclamide)-treated mice (3 mg/kg b.w.). The following parameters were considered for further investigations: creatine kinase-muscle brain (CK-MB), creatine kinase (CK), troponin, lysosomal, and mitochondrial enzymes. Then the docking study was accomplished. The levels of cardiac marker enzymes and lysosomal enzymes increased significantly in the toxin-induced mice, while the level of mitochondrial enzyme decreased significantly. During treatment with the ethanolic leaves extract of P. guajava, the levels of all parameters were notably reversed to normal range (P < 0.05). Further, in docking analysis, the interaction of compounds, such as alpha-terpineol, cyclopentanecarboxamide, guaiol (a sesquiterpenoid alcohol), 1H-cyclopropanaphthalene, tetracyclotridecan-9-ol, dormin/abscisic acid, and epiglobulol, with the respective protein molecules, evidenced the cardioprotective effect of P. guajava leaves. Hence, it was concluded that the ethanolic leaves extract of P. guajava leaves have a cardioprotective effect.

Cardioprotective effects of Pinus eldarica bark extract on adrenaline-induced myocardial infarction in rats

Objective: To investigate the effect of Pinus eldarica bark extract on adrenaline-induced myocardial infarction. Methods: Hydroalcoholic extract was prepared using maceration method and its total phenolic content was determined using the Folin-ciocalteu method. Pretreatment was done by oral administration of 100, 200, and 400 mg/kg Pinus eldarica bark extract for 16 days in male Wistar rats. Injection of adrenaline (2 mg/kg, s.c.) was performed on the 15th and 16th days for induction of myocardial infarction. Lead II EEG was recorded. Serum cardiac marker enzymes and antioxidative parameters were evaluated and a histopathological examination of heart tissues was performed. Results: Pretreatment with Pinus eldarica bark extract especially at its high doses significantly lowered the ST-segment elevation, improved heart rate, and decreased RR interval in ECG pattern of rats with adrenaline-induced myocardial infarction. It declined serum markers of heart damage including aspartate aminotransferase, lactate dehydrogenase, and creatine phosphokinase-MB, and also decreased lipid peroxidation marker, and heart weight while raising total antioxidant capacity and considerably improved histopathological alterations of the heart induced by adrenaline. Conclusions: Pinus eldarica bark extract shows beneficial cardioprotective and antioxidant effects against adrenaline-induced myocardial infarction. It can be further explored as a potential treatment for myocardial infarction.

Protective effect of Pueraria lobata leaves on doxorubicin-induced myocardial infarction in experimental Wistar rats.

The present study intended to explore the preventive effects of Pueraria lobata leaves against doxorubicin (DOX)-induced myocardial infarction (MI) in Wistar rats. The rats were separated into four groups, with each group containing six rats. Group I control rats; group II received DOX-alone in six equivalent injections for 2 weeks; group III received DOX as abovementioned with P. lobata oral administration for 2 weeks; group IV received P. lobata alone for 2 weeks. At the end of the experiment, postcervical dislocation and MI induced by DOX were determined on the basis of the variations in the animal body and heart weight and further instabilities in cardiac marker enzymes aspartate transaminase, lactate dehydrogenase, creatine kinase, creatine kinase-myoglobin binding, and cardiac troponin I in the serum. At the same time, for group III animals, which were exposed to P. lobata, all the above-denoted marker levels were maintained. Levels of some crucial heart-binding proteins like heart fatty acid binding protein, monocyte chemoattractant protein-1, and transforming growth factor beta were elevated in DOX-alone treated rats. Additionally, group III animals treated with P. lobata showed some preventive downregulated expressions of these binding proteins. Histopathological observations also revealed the preventive effect of P. lobata. Ultimately proteins tangled in the phosphoinositide 3-kinase/protein kinase B pathway were studied by Western blot. P. lobata treatment downregulated the inflammatory markers. The findings suggest that P. lobata exhibits cardioprotective effect on MI.

Protective effects of gallic acid and SGK1 inhibitor on oxidative stress and cardiac damage in an isolated heart model of ischemia/reperfusion injury in rats.

Oxidative stress and serum and glucocorticoid-induced Kinase 1 gene (SGK1) perform a central role in the consequences of ischemia in the heart. This research aimed to investigate the effect of coadministration of gallic acid and the GSK650394 (as SGK1 gene inhibitor) on the ischemic complications of a rat model of cardiac ischemia/reperfusion (I/R) injury. Sixty male Wistar rats were divided into 6 groups with or without pretreatment with gallic acid for 10 days. After that, the heart was isolated and perfused with Krebs-Henseleit solution. A 30 min of ischemia was performed followed by a 60 min reperfusion. In 2 groups, GSK650394 was infused 5 min before ischemia induction. Ten minutes after reperfusion commencement, cardiac marker enzyme (CK-MB, LDH, and cTn-I) activities were measured in the cardiac perfusate. At the end of reperfusion, the activity of anti-oxidant enzymes (Catalase, Superoxide dismutase, and Glutathione peroxidase), lipid peroxidation (MDA), total anti-oxidant capacity (TAC), intracellular reactive oxygen species (ROS), infarct size, and SGK1 gene expression were measured in the heart tissue. The results indicated that dual therapy with both drugs significantly improved endogenous anti-oxidant enzyme activity and TAC more than each drug alone. However, the heart marker enzymes (CK-MB, LDH, and cTn-I), MDA, ROS, infarct size, and SGK1 gene expression were reduced significantly compared with the ischemic group. The results of this study suggest that concomitant administration of both drugs in the case of cardiac I/R injury may have a more beneficial effect than each one alone.

Ameliorative Effects of Ponicidin Against the Isoproterenol-induced Acute Myocardial Infarction in Rats

Background Cardiovascular disease (CVD) is a group of heart disorders, which is a major cause of non-communicable disease-related mortalities worldwide. Myocardial infarction (MI) is an acute disorder due to the poor supply of oxygen and blood to the myocardium. MI is the foremost form of CVD, which is the primary cause of mortality worldwide. Objectives Here, we intended to discover the ameliorative properties of the ponicidin against the isoproterenol (ISO)-stimulated MI in rats. Materials and Methods About 85 mg/kg of ISO was administered to the rats to trigger the MI and then treated with 25 and 50 mg/kg of ponicidin. The body weight and heart weight of all rats were determined. The total protein, c-reactive protein (CRP), and uric acid levels were examined. The activities of cardiac function markers such as creatine kinase (CK), ALT, AST, and gamma-glutamyl transferase (GGT) were examined. The antioxidants such as glutathione (GSH), GST, and GPx were examined by the previous methods. The status of Na+/K+, Mg2+, and Ca2+ ATPase activities was assessed using kits. The status of Na+, K+, and Ca2+ ions and inflammatory makers such as TNF-α and IL-6 were investigated using respective kits. The histopathological analysis was performed on the heart tissues to detect the histological changes. Results The results revealed that ponicidin increased body weight and decreased heart weight in MI rats. The status of CRP and uric acid was decreased and total protein was augmented in the ponicidin-treated MI rats. The AST, ALT, CK, and GGT activities were appreciably decreased in serum and elevated in the cardiac tissues of the ponicidin-administered MI rats. Furthermore, the ponicidin improved the antioxidant levels, decreased the TNF-α and IL-6, and regulated the Na+, K+, and Ca2+ ion transports in the MI rats. The activities of Na+/K+, Mg2+, and Ca2+ ATPase enzymes were remarkably increased in the heart tissues by the ponicidin-treated MI rats. Ponicidin treatment also ameliorated the ISO-stimulated histological alterations in the heart tissue of the MI rats. Conclusion Ponicidin treatment appreciably improved the antioxidants, Na+/K+, Mg2+, and Ca2+ ATPase enzyme activities, decreased the inflammatory markers, and regulated the cardiac marker enzyme activities in the MI rats. Hence, it can be a talented therapeutic candidate in the future to treat MI.

Okluzija u dominantnom levom koronarnom sistemu - EKG dilema u radu lekara hitne pomoći

Introduction/Objective Acute chest pain is the main clinical manifestation of acute coronary syndrome. A posterior myocardial infarction (MI) most commonly occurs as a complication or extension of an inferior MI because of the overlapping coronary vascularization. We are presenting a case in which the patient exhibited mild anginal symptoms and an ECG pattern which did not correlate with a devastating infarction. Case report: The Emergency Medical Team (EMT) was dispatched at 5 am to help a 62-year-old patient, who had been woken from his sleep by a feeling of tightness in his chest and weakness in both arms. Upon examination, the patient was hypertensive (160/90 mmHg) and moderately bradycardic (58-62/min), with normal oxygen saturation on room air (SaO2 98%). His prehospital ECG findings were as follows: sinus rhythm, horizontal ST depression in V1-V3 1 to 2mm, ST elevation ≤1mm in lead V6, subtle ST depression in D1 and aVL <1mm, ST elevation in D3 and aVF <1mm. After attaching additional posterior leads, the modified ECG recording showed an ST elevation of 1 to 2 mm in V7-V9. Continuous laboratory monitoring of cardiac enzyme markers showed elevated and increasing values: Troponin T -2377, 3756 ng/l; CK -1572, 1564 U/l. Coronary angiography: The LCA system was dominant. The RCA was nondominant with a 70-80% stenosis, and a complete Occlusion Myocardial Infarction (OMI) distally. Using the most accurate LCxc/RCA occlusion algorithms, the ECG finding suggested an occlusion in the right dominant coronary system, which does not correlate with the coronary angiography report. Conclusion: Excellent knowledge of recording, analysis, and interpretation of ECG tracings, facilitates adequate pre-hospital care and precise planning for further processing of patients with chest pain. It is recommended to record posterior and right unipolar leads in all patients with inferior and suspicion of posterior myocardial infarctions and to include the ST-elevation myocardial infarction equivalent into the STEMI network. Given the physiological differences in left ventricular vascularization and the possible predominance of the left coronary system over the right, future studies must focus on establishing more precise algorithms for assessing RCA/LCx occlusion.

Decalepis hamiltonii and its bioactive constituents mitigate isoproterenol-induced cardiotoxicity in aged rats

Aging is associated with functional decline and structural deteriorations of the myocardium and plays a crucial role in cardiovascular ailments. Decalepis hamiltonii ( Dh ) is well known medicinal plant used in traditional medicine and exhibits potent antioxidant properties. Therefore, the current study was proposed to assess the cardioprotective potential of Dh extract and its bioactive constituents [Ellagic acid (EA) and 4‑hydroxyisophthalic acid (4-HIA)] against isoproterenol (ISO)-induced region-specific myocardial damage in aging rats. Male albino Wistar rats aged 22 months were administered orally with Dh extract (100mg/kg BW), EA (50 mg/kg BW), and 4‑HIA (30 mg/kg BW) for one month before inducing MI using ISO (150 mg/kg BW) for the consecutive last two days. The ISO group exhibited a significant increase in hemodynamic parameters, cardiac marker enzymes, serum lipids, and oxidative stress markers. A significant reduction in region-specific antioxidant enzymes levels and histopathological alterations were observed in ISO-treated rats. Whereas, pretreatment of EA, 4-HIA, and Dh extract reduced the cardiac dysfunction biomarkers and mitigated oxidative stress by enhancing antioxidant enzymes and restoring histopathological changes in ISO-treated rats. The Overall findings give insights into the therapeutic applications of Dh extract and its compounds in ameliorating cardiovascular disorders through its antioxidant potential.

In Vivo and In Silico Assessment of the Cardioprotective Effect of Thymus linearis Extract against Ischemic Myocardial Injury.

Myocardial infarction is irreversible cardiac tissue necrosis due to the blockage of one of the arteries. It leads to an insufficient supply of oxygen and nutrients, creating muscular damage in the affected regions. In the present study, aqueous methanolic extract of Thymus linearis was prepared to evaluate its activity against ischemic stress due to free radical production. GC-MS analysis was performed to evaluate the phytochemicals present in the plant extract. A chemical database of 30 compounds was virtually screened against NF-κB, COX2, and MCL, where γ-cadinene, β-bisabolene, and β-caryophyllene were found to be the best interacting ligands. To systematically assess cardioprotective activity against ischemia, isoproterenol and doxorubicin were used to induce cardiotoxicity in rats. The prepared extract of T. linearis (100 mg/kg) was given daily to animals for 21 days before injecting isoproterenol (85 mg/kg of animal weight) subcutaneously in two doses on the 20th and 21st days. In the case of doxorubicin, cardiotoxicity was induced in rats by a single injection (15 mg/kg) on the seventh day, and the extract was given to animals for 10 consecutive days. Animals' blood samples were used to monitor cardiac, liver, and other marker enzymes, including LDH, CPK, and AST. Superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were also assayed in blood plasma to determine the degree of oxidative stress. H&E staining was performed to evaluate cardioprotection by plant extract, showing significant preventive effects in reducing cardiac injury induced by isoproterenol and doxorubicin.

Ophiopogon japonicas Alleviates Myocardial Ischemia/Reperfusion Injury in Rats Through Regulation of TLR4/Myd88/NF-κB, PI3K/AKT/mTOR, and Nrf2/HO-1 Signaling Pathway

Ophiopogon japonicas has a protective effect on myocardial ischemia/reperfusion injury-related diseases. Using network pharmacology and molecular docking approaches, we aimed to investigate the potential role of OJPs in myocardial damage. Also, the effects of OJPs and verapamil on cardiac function, cardiac marker enzymes, oxidative stress, inflammation, histopathological changes, apoptosis, TLR4/Myd88/NF-κB, PI3K/AKT/mTOR, as well Nrf2/HO-1 pathways were determined by echocardiography, hematoxylin-eosin and staining, Enzyme-Linked Immunosorbnent Assay, TdT-mediated dUTP nick end labeling, IHC and Western blot assays in MI/RI rats, respectively. A total of 28 absorbable compounds of OJPs and 65 OJPs-MI/RI-related targets were screened. Regulation of inflammatory response and apoptotic signaling pathway might contribute to OJPs against MI/RI. Besides, molecular docking presented that there are 6 core targets including AKT1, IL6, TNF, VEGFA, EGFR, and Caspase 3 with a certain binding affinity on the absorbable components of OJPs. The in vivo experiments illustrated that OJPs ameliorated cardiac function, oxidative stress, inflammation, and histopathological injury in I/R rats. Moreover, OJPs also could repress levels of apoptosis and TLR4/Myd88/NF-κB-related targets, as well as activate PI3K/AKT/mTOR and Nrf2/HO-1 pathways. Collectively, our findings suggest OJPs could attenuate MI/RI by weakening the TLR4/Myd88/NF-κB signaling, as well as activating PI3K/AKT/mTOR and Nrf2/HO-1 pathways.

Astragaloside IV ameliorates sepsis-induced myocardial dysfunction by regulating NOX4/JNK/BAX pathway

AimsSepsis can induce multiple organ dysfunction, and sepsis-induced myocardial dysfunction (SIMD) is relatively common. The current dilemma might ascribe partly to SIMD's lack of unified molecular mechanisms. Our study aims to assess the function of Astragaloside IV (ASI) in cecal ligation and puncture (CLP)-induced cardiac dysfunction and explore its underlying mechanisms. Main methodsIn vivo, ASI (30 mg/kg/day), NADPH oxidase 4 (NOX4) inhibitor 4-hydroxy-3-methoxyacetophenone (APO, 30 mg/kg/day), reactive oxygen species (ROS) inhibitor N-Acetylcysteine (NAC, 150 mg/kg/day) and c-Jun NH2-terminal kinase (JNK) inhibitor (SP600125, 15 mg/kg/day) were severally administered to Sprague Dawley rats following the CLP surgery. The cardiac function, cardiac enzyme markers, proinflammatory cytokine, and cell apoptosis-associated proteins were detected. In vitro, cardiomyocyte H9C2 cells were treated with lipopolysaccharide (LPS, 40 μg/ml) after the presence of ASI (100 μmol/ml), SP600125 (10 μmol/ml), APO (10 μmol/ml). A series of experiments verified the relationship among NOX4, JNK, and BAX. Key findingsThe results indicated that CLP-induced sepsis increased the secretion of creatine kinase isoenzymes (CKMB), brain natriuretic peptide (BNP), cardiac troponin T (c-TnI), interleukin-1β (IL-1β) and interleukin-18 (IL-18), as well as the protein expression of NOX4 and Caspase-3 in vivo. LPS increased the protein level of NOX4 and Caspase-3, upregulated the rate of p-JNK/JNK, and downregulated the rate of Bcl2/BAX in vitro. ASI can reverse these changes in vivo and has a synergistic effect with APO and SP600125 in vitro. SignificanceThis study suggested that ASI may ameliorate SIMD, through regulating NOX4/JNK/BAX signaling pathway, which may be a feasible therapeutic strategy.

Crassocephalum rubens extract and fractions: Hypolipidemic and cardioprotective activities

Globally, cardiovascular diseases are becoming the major cause of death. Crassocephalum rubens is an indigenous vegetable used traditionally in the treatment of several disease conditions including stomach upset, wounds, and high blood pressure. However, there are limited literature reports on its hypolipidemic and cardioprotective activities, hence this study investigated the effects of leaf methanol extract and fractions of C. rubens on lipid profile, liver, cardiac marker enzymes; alanine (ALT), and aspartate (AST) aminotransferases, and cardiac tissue integrity in Isoproterenol-induced myocardial infarction (MI) in rats. Forty-five male Wistar rats were randomly divided into nine groups and administered different doses (100 & 150 mg/kg) of the plant extract and fractions for 14 days while normal control and MI control received phosphate buffer saline. C. rubens leaf methanol extract and fractions significantly (p<0.05) reduced TC (75.45 ± 2.44 - 96.09 ± 1.65 mg/dL), TG (84.04 ± 1.79 - 127.00 ± 0.47 mg/dL), VLDL-C (16.81 ± 0.36 - 25.42 ± 0.10 mg/dL), LDL-Cholesterol (03.49 ± 1.03 - 26.04 ± 1.64 mg/dL), and AST of the pretreated myocardial infarcted rats versus MI control (168.70 ± 9.85 mg/dL, 146.60 ± 1.74 mg/dL, 29.31 ± 0.34 mg/dL, 77.73 ± 9.67 mg/dL, respectively), while plasma HDL-C was increased. The crude extract and fractions of C. rubens showed significant cardioprotective activities on the integrity of the heart tissues of the experimental rats. The findings reveal antihyperlipidemic and cardioprotective potentials and provide a possible lead for isolation of bioactive compounds from C. rubens in the management of hyperlipidemia and its associated ailments.

Rare Causes of Acute Coronary Syndrome: Carbon Monoxide Poisoning.

Acute coronary syndrome (ACS) is a spectrum of clinical and paraclinical disorders arising from an imbalance of oxygen demand and supply to the myocardium. The most common cause is atherosclerosis; however, other rare causes such as carbon monoxide (CO) poisoning should be considered. Through tissue hypoxia and direct cell injury, CO poisoning can lead to a broad spectrum of cardiac disorders, especially ACS. Materials and Methods. We have conducted a retrospective study in the Toxicology Department of Saint Spiridon Emergency University Hospital, including all patients admitted through the emergency department with CO poisoning. We divided the cohort into event group (myocardial injury) and non-event group (patients without myocardial injury) and performed a subset analysis of the former. Results. A total of 65 patients were included, 22 in the event and 43 in the non-event group. The severity of poisoning did not correlate with myocardial injury; however, 50% of the event group had severe poisoning with carboxyhaemoglobin ≥ 20%. Cardiac enzyme markers (troponin and creatin-kinase MB) had a statistically significant increase in the event group compared to the non-event group (p < 0.05). Most of the patients in the STEMI (50%) and NSTEMI (66.7%) groups had severe CO intoxication. The STEMI group had a mean age of 27.7 years old and no comorbidities. Conclusions. Myocardial injury can develop in CO poisoning irrespective of the severity of poisoning, and it can be transient, reversible, or permanent. Our study introduces new information on adverse cardiac events in patients with CO poisoning, focusing on the ACS. We found that the severity of CO poisoning plays an important role in developing myocardial injury, as 50% of patients in the event group were severely intoxicated. While in-hospital mortality in our study was low, further prospective studies should investigate the long-term mortality in these patients.

Bergenin from Bergenia Species Produces a Protective Response against Myocardial Infarction in Rats

Bergenin is a phenolic glycoside that has been reported to occur naturally in several plant species, reported as a cardioprotective. However, bergenin, one of the important phytochemicals in these plants, is still not reported as a cardioprotective. The present study was designed to investigate the cardioprotective effects of bergenin on isoproterenol-induced myocardial infarction in rats. Bergenin and atenolol were administered through intraperitoneal (i.p.) injection to Sprague Dawley (SD) rats in separate experiments for five (5) days. At the end of this period, rats were administered isoproterenol (80 mg/kg s.c.) to induce myocardial injury. After induction, rats were anaesthetized to record lead II ECG, then sacrificed, blood was collected to analyze cardiac marker enzymes, and a histopathological study of the heart tissues was also performed. Pretreatment with bergenin showed a significant decrease in ST-segment elevation, deep Q-wave, infarct size, and also normalized cardiac marker enzymes (cTnI, CPK, CK-MB, LDH, ALT, and AST), particularly at 3 mg/kg, as compared to isoproterenol treated group. Our findings revealed, for the first time, the use of glycoside bergenin as a potential cardioprotective agent against the isoproterenol-induced MI in rats.

Cardioprotective effects of Ferulic acid in Streptozotocin- induced diabetic rats

Background: Diabetes mellitus causes changes in the structural or functional anatomy of the heart. A high blood glucose level and oxidative stress are key factors in diabetic cardiac damage. Ferulic acid (4-hydroxy-3-methoxy cinnamic acid) is a biologically active compound in many functional foods like fruits, vegetables, and medicinal herbs. It belongs to the group of cinnamic acid derivatives.Objective: In the present study, we investigated the effects of Ferulic acid (FA) on Streptozotocin-induced diabetic cardiac damage in male Sprague Dawley rats.Materials and methods: A total of 30 male Sprague-Dawley rats were divided into five groups of six each. Diabetes was induced by a single intraperitoneal injection of Streptozotocin (STZ) (40 mg/kg body weight). Group I consisted of normal rats (N); group II consisted of normal rats treated with FA (N+FA); group III consisted of STZ-induced diabetic rats (D), and groups IV and V consisted of STZ-induced diabetic rats treated with FA at a dose of 50 mg/kg body weight and glibenclamide at a dose of 5 mg/kg body weight respectively (N+FA and N+G) for 60 days. Rats were sacrificed after the treatment period, and blood and heart tissue were collected for analysis.Results: STZ injection significantly increased blood glucose, HbA1c, cardiac marker enzymes LDH, CK-MB, and oxidative stress in heart tissue. The oral administration of FA to diabetic rats for 60 days significantly improved diabetic markers, oxidative stress, and cardiac markers.Conclusion: The present study indicated that FA affords cardioprotective effect in diabetic rats, and this protection may be due in part to the attenuation of oxidative stress.Keywords: ferulic acid, streptozotocin, diabetes, cardiac damage, oxidative stress