Isoprenaline-induced Myocardial Infarction Research Articles

Cardioprotective effect of Tofisopam against isoprenaline-induced myocardial infarction in rats via modulation of NLRP3\\IL-1β\\caspase-1 pathway

Purpose Cardiovascular diseases (CVDs) are a leading cause of morbidity and mortality worldwide. Ischemic heart diseases, particularly acute myocardial infarction (MI), represent the most common cause of death. MI is influenced by multiple factors, including the release of inflammatory mediators. A significant percentage of individuals with CVD experience psychological effects, such as anxiety and depression, which are linked to an increased risk of coronary heart disease. Certain anti-anxiety medications have demonstrated immunomodulatory and anti-inflammatory effects. Tofisopam, a 2,3-benzodiazepine with anxiolytic properties, has been shown to exert in vitro anti-inflammatory and immunomodulatory effects. The present study investigates the potential of tofisopam as a protective adjuvant against isoprenaline-induced MI in rats and explores the possible underlying mechanisms. Methods: The study included four groups: a control group, a group pretreated with tofisopam, an isoprenaline toxic group, and an isoprenaline toxic group pretreated with tofisopam. Results: The findings demonstrated that isoprenaline significantly increased cardiac enzyme levels, as well as elevated oxidative and inflammatory stress parameters, along with evident apoptosis in cardiac cells. In contrast, the tofisopam-pretreated group showed a significant reversal of the cardiac damage induced by isoprenaline. Conclusions: Tofisopam protects against isoprenaline-induced MI through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Metformin's cardioprotective role in isoprenaline-induced myocardial infarction: Unveiling insights into the AMPK, NF-κB, JAK2/STAT3 pathways, and cholinergic regulation

AimDespite advancements in treatment modalities, myocardial infarction (MI) remains a significant global cause of mortality and morbidity. Metformin (MET), a commonly used antidiabetic medication, has demonstrated potential in various cardioprotective mechanisms. This study investigated whether MET could alleviate the histopathological, electrocardiographic, and molecular consequences of MI in rats. Materials and methodsThe study hypothesis was tested using an isoprenaline (ISOP)-induced MI model, where male Wistar rats were injected with ISOP (85 mg/kg/day, s.c., for 2 days) and treated with MET at the doses of 500 and 1000 mg/kg/day for 18 days or left untreated. Key findingsISOP-treated rats exhibited several indicators of MI, including significant ST-segment depression and prolonged QT-intervals on ECGs, worsened left ventricular histopathology with increased inflammatory cell infiltration, reduced expression of cardiac CHRM2, a cardioprotective cholinergic receptor, adaptive increases in AMPK and α7nAchR levels, and elevated levels of iNOS, NO, STAT3, JAK2, IL-6, TNF-α, and NF-κB. These effects were attenuated in rats treated with either low or high doses of MET. MET administration restored normal ECG recordings, diminished oxidative stress and inflammatory mediators, and downregulated NF-κB expression. Moreover, MET improved CHRM2 expression and normalized α7nAchR levels. Additionally, MET influenced the expression of key signaling molecules such as Akt, STAT3, and JAK2. SignificanceThese findings might suggest that MET exerts cardioprotective effects in ISOP-induced MI in rats by mitigating critical inflammatory signaling pathways and regulating protective cholinergic mechanisms in the heart.

Protective effect of Galectin-3 inhibitor against cardiac remodelling in an isoprenaline-induced myocardial infarction in type 2 diabetes

Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor; modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups; groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.

CARDIOPROTECTIVE AND ANTIOXIDANT PROPERTIES OF THE ARILS OF THE FRUIT OF BLIGHIA SAPIDA KD KOENIG (SAPINDACEAE) IN ISOPRENALINE-INDUCED MYOCARDIAL INFARCTION IN WISTAR RATS

Coronary artery disease and myocardial infarction are major global health issues, with myocardial infarction becoming more common. In the current study, the cardioprotective effects of methanol extract from the aril of the Blighia sapida fruit were assessed in relation to certain cardiac function biomarkers, endogenous antioxidant activity, and the pathology of the heart in Wistar rats that had undergone isoprenaline-induced myocardial infarction. Phytochemical screening was according to methods described by Trease and Evans. The LD50 of the extract was calculated using Lorke’s approach. The LD50 was calculated using nine (9) Wistar rats. For cardioprotective and antioxidant activities, six groups of seven Wistar rats each were formed from forty-two (42), which were divided at random. Group 1 were administered 1ml of normal saline daily, group 2 through 4 were pretreated with 250 mg/kg, 500 mg/kg, and 750 mg/kg of the extract, respectively, for 28 days. Group 5 were administered 85 mg/kg of isoprenaline on days 26 and 27, 24 hours apart to cause myocardial infarction. Group 6 served as the positive control (pretreated with 2 mg/kg carvedilol for 28 days). The plant contains bioactive substances like alkaloids, flavonoids, polyphenols, cardiac glycosides, cyanogenic glycosides, steroid glycosides, cardenolides, terpenes, and tannins. No mortality even at a dose of 5000mg/kg. Glutathione peroxidase, reduced glutathione, catalase, and superoxide dismutase all show considerable increases. Total troponin, troponin c, troponin I, creatine kinase, creatine kinase-MB, and myoglobin, significantly decreased when compared to the isoprenaline group. Additionally, there was a significant drop in the levels of some biochemical markers in the extract treated groups compared to the isoprenaline control. Total cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides, and ALT, AST, and ALP significantly decreased. Histological analysis revealed some degree of cardiac modification and a notable improvement. According to the data, the extract contains modest antioxidant and cardioprotective characteristics

Cardioprotective effect of Sanguisorba minor against isoprenaline-induced myocardial infarction in rats.

Introduction: Oxidative stress is a major instigator of various cardiovascular diseases, including myocardial infarction (MI). Despite available drugs, there is still an increased need to look for alternative therapies or identify new bioactive compounds. Sanguisorba minor (S. minor) is a native herb characterized by its potent antioxidant activity. This study was designed to evaluate the effect of S. minor against isoprenaline-induced MI. Methods: Rats were treated with the hydro-ethanolic extract of the aerial parts of S. minor at doses of 100 or 300mg/kg orally for 9 days. Isoprenaline was injected subcutaneously at the dose of 85mg/kg on days 8 and 9. Then, the activities of various cardiac injury markers including cardiac troponin (cTnT), lactate dehydrogenase (LDH), creatinine kinase muscle brain (CK-MB), creatinine phosphokinase (CPK), and antioxidant enzymes in serum were determined. Malondialdehyde (MDA) and thiol content were measured in cardiac tissue, and histopathological analysis was conducted. Results: Our results show that isoprenaline increased the serum levels of cTnT, LDH, CK-MB, and CPK (p < 0.001) and elevated MDA levels (p < 0.001) in cardiac tissue. Isoprenaline also reduced superoxide dismutase (SOD), catalase, and thiol content (p < 0.001). Importantly, the extract abolished isoprenaline-induced MI by elevating SOD and catalase (p < 0.001), reducing levels of MDA, and diminishing levels of cTnT, LDH, CK-MB, and CPK cardiac markers (p < 0.001). Histopathological studies of the cardiac tissue showed isoprenaline-induced injury that was significantly attenuated by the extract. Conclusion: Our results suggest that S. minor could abrogate isoprenaline-induced cardiac toxicity due to its ability to mitigate oxidative stress.

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.

Cardioprotective potential of Lavandula stoechas against isoprenaline-induced myocardial necrosis in rats

This study assessed Lavandula stoechas flower extract's impact on Isoprenaline-induced myocardial necrosis in rats. Five groups of five rats each were used. Group I received 1 ​ml/kg normal saline orally for 13 days, Group II received 10 ​ml/kg normal saline orally, Group III received 200 ​mg/kg Lavandula stoechas extract orally, Group IV received 400 ​mg/kg Lavandula stoechas extract orally, and Group V received 10 ​mg/kg Metoprolol orally. On days 14 and 15, Group I received 0.5 ​ml/kg subcutaneous normal saline, and Groups II to V received 85 ​mg/kg Isoprenaline subcutaneously. On day 16, rats were weighed, and cardiac blood samples were collected. Serum was analyzed for total protein, triglycerides, and cardiac enzymes (cardiac injury markers). Rats were sacrificed, and heart tissues were histologically examined.Results showed significant serum marker enzyme reductions (p ​< ​0.01) in Lavandula stoechas-treated rats. Total protein and triglyceride levels (p ​< ​0.01) decreased, and heart weight-to-body weight ratio (p ​< ​0.05) decreased in Lavandula stoechas-treated rats. Histopathology confirmed the extract's protective effect.In conclusion, Lavandula stoechas flower extract offers protection against Isoprenaline-induced myocardial infarction in rats.

Curdione inhibits ferroptosis in isoprenaline-induced myocardial infarction via regulating Keap1/Trx1/GPX4 signaling pathway.

Myocardial infarction (MI) is a common disease with high morbidity and mortality. Curdione is a sesquiterpenoid from Radix Curcumae. The current study is aimed to investigate the protective effect and mechanism of curdione on ferroptosis in MI. Isoproterenol (ISO) was used to induce MI injury in mice and H9c2 cells. Curdione was orally given to mice once daily for 7 days. Echocardiography, biochemical kits, and western blotting were performed on the markers of cardiac ferroptosis. Curdione at 50 and 100 mg/kg significantly alleviated ISO-induced myocardial injury. Curdione and ferrostatin-1 significantly attenuated ISO-induced H9c2 cell injury. Curdione effectively suppressed cardiac ferroptosis, evidenced by decreasing malondialdehyde and iron contents, and increasing glutathione (GSH) level, GSH peroxidase 4 (GPX4), and ferritin heavy chain 1 expression. Importantly, drug affinity responsive target stability, molecular docking, and surface plasmon resonance technologies elucidated the direct target Keap1 of curdione. Curdione disrupted the interaction between Keap1 and thioredoxin1 (Trx1) but enhanced the Trx1/GPX4 complex. In addition, curdione-derived protection against ISO-induced myocardial ferroptosis was blocked after overexpression of Keap1, while enhanced after Keap1 silence in H9c2 cells. These findings demonstrate that curdione inhibited ferroptosis in ISO-induced MI via regulating Keap1/Trx1/GPX4 signaling pathway.

Enhancements of Bcl-2/mTOR/ERK1/2 activities by antioxidant mechanisms confer cardioprotection on Ginkgo biloba supplement against isoprenaline-induced myocardial infarction in rats

BackgroundMyocyte necrosis and apoptosis can be severely induced by acute adrenergic stimulation due to the activation of several cell signalling pathways. However, uncertainty exists regarding the potential cardioprotective effects of Ginkgo biloba (GBS), a Chinese herbal supplement rich with antioxidants, on isoprenaline (ISO)-induced myocardial infarction. Therefore, this work was designed to investigate the cardioprotective mechanisms of GBS on ISO-induced myocardial infarction. MethodsAnimals were selected into four groups. Groups 1 and 2 were pre-treated with normal saline (10 mL/kg i.p) for 28 days. Groups 3 and 4 received GBS (50 mg/kg, i.p) for 28 days. However, groups 2 and 4 were administered ISO (150 mg/kg, s.c) on days 27 and 28 respectively. Following the end of 28-day experiment, animals were euthanised and serum as well as heart tissue were harvested and processed for biochemical and histological examinations. ResultsOur results showed that ISO induced cardiac necrosis, evidenced by increased levels of cardiac injury enzymes (LDH, GGT, CK-MB and cT-1), oxidative stress markers such as GSH, SOD, and CAT levels were significantly reduced while MDA and nitrite concntration were significantly increased. Inflammatory cytokines (IL-6 and TNF-α) were significantly increased while decreasing Bcl-2, mTOR and ERK1/2 cardiac immuno-expressions. Moreso, histological investigation revealed degeneration of cardiomyofibres together with patchy necrosis. However, pre-treatment with GBS significantly inhibited apoptotic processes evidenced by increased antioxidant-mediated activation of Bcl-2, mTOR and ERK1/2. GBS also suppressed the release of cardiac injury enzymes and histological changes were significantly improved. ConclusionGBS protects myocardium against ISO-induced infarction by mechanisms related to antioxidant-mediated by enhancement of Bcl-2/mTOR/ERK1/2 activities.

Metformin and Carvedilol ameliorate isoprenaline-induced myocardial infarction in non-diabetic rats through AMPK activation and suppression of apoptosis

Metformin and Carvedilol ameliorate isoprenaline-induced myocardial infarction in non-diabetic rats through AMPK activation and suppression of apoptosis

The myokine decorin improves the cardiac function in a rat model of isoprenaline-induced myocardial infarction.

Myocardial infarction is a common cause of disability. Decorin is a myokine that has anti-inflammatory, anti-apoptotic effects. Some studies stated that decorin protects myocardium from ischemia. Other studies stated that decorin levels are associated with acute coronary syndrome. The study aimed to investigate the therapeutic role of decorin on cardiac function in a rat model of myocardial infarction. Thirty adult male Wistar rats were divided into control group-rats were subcutaneously injected with normal saline, isoprenaline-injected group-rats were subcutaneously injected with isoprenaline (85 mg/kg) once daily for 2 days to induce myocardial infarction, and decorin ± isoprenaline-injected group-rats were injected as the previous group, followed by decorin injection (0.1 mg/kg) once daily for 7 days. Cardiac hemodynamics, serum lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), oxidative stress markers, gene expression for myocardial-transforming growth factor beta 1 (TGF-β1), interleukin 1 b (IL-1β), tumor necrosis factor alpha (TNF-α), and cardiac caspase-3 immunohistochemical analysis were done. Isoprenaline + decorin group had significant improvement in cardiac hemodynamics and oxidative stress markers; significant decrease in serum CK-MB, LDH, and myocardial gene expression for TNF-α, IL-1β, and TGF-β1; and decreased cardiac caspase-3 immunoreactivity was present. Therefore, decorin can be used as a therapeutic agent after myocardial infarction as it improved the cardiac function.

New Approaches on the Anti-Inflammatory and Cardioprotective Properties of Taraxacum officinale Tincture

The present research investigated the in vivo anti-inflammatory and cardioprotective activities, as well as the antioxidant potential of Taraxacum officinale tincture (TOT), in relation to the polyphenolic composition. Chromatographic and spectrophotometric techniques were used to determine the polyphenolic profile of TOT and the antioxidant activity was preliminarily assessed in vitro by DPPH• and FRAP spectrophotometric methods. The in vivo anti-inflammatory and cardioprotective activities were studied in rat turpentine-induced inflammation and in rat isoprenaline-induced myocardial infarction (MI) models. The main polyphenolic compound identified in TOT was cichoric acid. The oxidative stress determinations showed the capacity of the dandelion tincture not only to decrease the total oxidative stress (TOS), the oxidative stress index (OSI), and the total antioxidant capacity (TAC), but also the malondialdehide (MDA), thiols (SH), and nitrites/nitrates (NOx) levels both in inflammation and MI models. In addition, aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatin kinase-MB (CK-MB), and nuclear factor kappa B (NF-κB) parameters were decreased by the administration of the tincture. The results show that T. officinale could be considered a valuable source of natural compounds with important benefits in pathologies linked to oxidative stress.

Protective effects ofLacticaseibacillus rhamnosuson isoprenaline-induced myocardial infarction in rats

Myocardial infarction (MI) is among the main public health problems in the world. This atherosclerotic cardiovascular disease (ASCVD), which seriously endangers human health, progresses to cause heart failure and myocardial fibrosis with a poor prognosis. The gut microbiota plays an important role in health and disease, including obesity and ASCVD. In this study, the protective effect of Lacticaseibacillus rhamnosus GG, known for its anti-inflammatory and antioxidant effects, on isoprenaline (ISO)-induced MI in rats was investigated. Rats were divided into four groups of seven rats in each group as control, ISO, L. rhamnosus, and ISO+L. rhamnosus.The ISO application was made by subcutaneous injection to the rats on the last two days (days 27th and 28th) of the 28-day substance administration. The rats were anesthetized 24 hours after the application of ISO, and blood samples were collected after electrocardiogram (ECG) recordings. To determine myocardial damage and protective effects of L. rhamnosus, serum creatine kinase-MB, cardiac troponin-I, tumor necrosis factor-alpha, interleukin-10, and C-reactive protein (CRP) levels were examined. In addition, ECG recordings were evaluated. While L. rhamnosus had a decreasing effect on cardiac troponin-I, creatine kinase-MB, CRP, and tumor necrosis factor-alpha levels, which increased due to ISO, it had an increasing effect on interleukin-10 levels. Similarly, it decreased the ST-segment elevation caused by ISO while increasing the reduced R wave amplitude.

Attenuation of isoprenaline-induced myocardial infarction by Rheum turkestanicum

BackgroundOxidative stress plays a major role in the pathogenesis of myocardial infarction. This study evaluated the cardioprotective effects of the hydroalcoholic extract of Rheum turkestanicum on isoprenaline-induced myocardial infarction (MI) in Wistar rats. MethodsIn this study, we used liquid chromatography-mass spectrometry to determine the active compounds present in the extract. Thirty rats were divided to 5 groups (6 rats in each group). The extract was administered orally at the doses of 100 and 300 mg/kg body weight and then a subcutaneous injection of isoprenaline (85 mg/kg) was administered on the 8th and 9th days. Serum levels of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and creatinine kinase (CPK) were measured using standard commercial kits. Serum activities of superoxide dismutase, catalase, and cardiac levels of thiol and lipid peroxidation were also determined. Hematoxylin and eosin were used for histopathological staining. ResultsPhytochemical analysis revealed the presence of 24 compounds in the hydro-ethanolic extract of R. turkestanicum. Isoprenaline increased malondialdehyde (4.002 ± 0178, P < 0.001) while decreased thiol content (101.7 ± 6.186, P < 0.001). Moreover, reduced activities of superoxide dismutase (139 ± 10.88, P < 0.001) and catalase (2.812 ± 0.215, P < 0.001), and elevated levels of LDH (1245 ± 62.28, P < 0.001), CPK (898 ± 23.06, P < 0.001) and CK-MB (697 ± 50.22, P < 0.001) were observed. Pretreatment with the R. turkestanicum extract significantly reduced cardiac markers and increased thiol content as well as the activity of antioxidant enzymes. The extract attenuated the histopathological changes induced by isoprenaline. ConclusionAccording to the obtained results, R. turkestanicum may be an appropriate candidate to reduce isoprenaline-induced MI through modulation of oxidative stress. Administration of the extract attenuated cardiac enzymes following isoprenaline administration. The cardioprotective action of the extract can be attributed to the bioactive antioxidant ingredients of R. turkestanicum. To identify the precise mechanisms, further investigations are required. [Display omitted]

Mesenchymal stem cells seeded onto nanofiber scaffold for myocardial regeneration

ABSTRACT Cardiac disease is the leading cause of mortality and disability worldwide. We investigated the role of undifferentiated adipose tissue-derived mesenchymal stem cells (ADMSC) alone and ADMSC seeded onto the electro-spun nanofibers (NF) for reconstructing damaged cardiac tissue in isoprenaline-induced myocardial infarction (MI) in rats. ADMSC were sorted by morphological appearance and by detection of cluster of differentiation (CD) surface antigens. The therapeutic potential of ADMSC for treating MI was evaluated by electrocardiogram (ECG), biochemical analysis, molecular genetic analysis and histological examination. Treatment of MI-challenged rats with ADMSC improved ECG findings, which were corroborated by significant decreases in serum lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) enzyme activities together with reduced serum troponin T (cTnT) and connexin 43 (Cx43) levels. MI model rats treated with ADMSC exhibited a significant increase in serum alpha sarcomeric actin (Actn) and GATA binding protein 4 (GATA4), and NK2 homeobox 5 (NKX2.5) gene expression was decreased following treatment with ADMSC. ADMSC also ameliorated damage to cardiac tissue. The effects of ADMSC seeded onto NF were superior to those of ADMSC alone. ADMSC may be useful for mitigation of MI.

The cardioprotective effect of microRNA-103 inhibitor against isoprenaline-induced myocardial infarction in mice through targeting FADD/RIPK pathway.

The current study investigates the effect of the innovative phosphorothioate modified backbone locked nucleic acid (LNA) of microRNA-103 (miR-103) specifically designed for systemic delivery in the silencing of miR-103 in experimentally induced myocardial infarction (MI). MicroRNA-103 is a small non-coding RNA which regulates Fas-associated protein with death domain (FADD) gene expression, which is a negative regulator for necroptosis occurs during the progression of MI. Experimental male mice were allocated into three groups; the first group received normal saline, the second group was injected with isoprenaline and served as the infarcted control, while the third group was treated with LNA miR-103 power inhibitor before isoprenaline injection. Blood and heart samples were used for biochemical analysis of miR-103, FADD, receptor-interacting protein kinase (RIPK), nuclear factor-κβ, tumor necrosis factor-α, interleukin-6, troponin-I and creatine kinase-MB (CK-MB) as well as the histological examination of heart tissue. The treated mice showed marked improvement in the troponin-I and CK-MB levels with almost normal histological structure of heart tissue. Significant inhibition of miR-103 accompanied by increased FADD expression and markedly decreased expression of the other biomarkers were observed in the hearts of the treated mice. LNA miR-103 inhibitor is a potent cardioprotective agent and can be a promising treatment against MI through targeting FADD/RIPK pathway.

Cardioprotective Effect of Ethanolic Extract of Leaves of Amaranthus cruentus in Isoprenaline-Induced Myocardial Infarction in Rats

Objectives: The present study is focused to evaluate cardioprotective activity of ethanolic extract of Amaranthus cruentus. Methods: Amaranthus cruentus extract (Dose 200mg/kg and 400mg/kg) in isoprenaline induced myocardial infarction in rats. The ethanolic extract of Amaranthus cruentus was prepared and subjected to acute toxicity in albino rats. The extract was given orallyat two different doses 200mg/kg and 400mg/. Isoprenaline was administered subcutaneously (85mg/kg s.c.). Results: The histopathological examination revealed mild infarction and inflammation in isoprenaline treated rats. The ethanolic extract of Amaranthus cruentus showed significant cardio protective effect by decreasing the serum level of LDL and VLDL cholesterol levels. The biochemical parameters (AST, ALT and ALP) and HDL cholesterol levels were restored. Conclusion: The outcome of the present study suggested cardioprotective activity of Amaranthus cruentus extract.

Alterations of medial prefrontal cortex bioelectrical activity in experimental model of isoprenaline-induced myocardial infarction.

BackgroundClinical and animal studies have found that anxiety and depression are significantly more common after acute myocardial infarction (AMI). The medial prefrontal cortex (PFC) has a dual role: in higher brain functions and in cardiovascular control, making it a logical candidate for explaining the perceived bidirectional heart-brain connection. We used parallel Electrocardiography (ECG) and Electrocorticography (ECoG) registration to investigate AMI-induced changes in medial PFC bioelectrical activity in a rat model of AMI.Materials and methodsAdult male Wistar albino rats were used in the study. Gold-plated recording electrodes were implanted over the frontal cortex for ECoG recording. ECG was recorded via two holter electrodes attached on the skin of the back fixed in place by a jacket. Induction of AMI was performed by isoprenaline (150 mg/kg, i.p.). ECoG and ECG signals were registered at baseline, during 3 hours after isoprenaline administration and at 24 hours after isoprenaline administration.ResultsSignificant increases of theta, alpha, and beta electroencephalographic (EEG) band power were observed in different time intervals after isoprenaline administration. Significant increase of theta band peak frequency was also observed during the first hour after isoprenaline administration. No statistically significant differences in band-power activity were found between the pre-isoprenaline measurements and 24 hours after administration.ConclusionOur results demonstrate significant increases in EEG band power of alpha beta and theta bands during isoprenaline-induced AMI model. These are the first findings to connect heart damage during isoprenaline- induced AMI to disturbances in the cortical bioelectrical activity.

EFFECT OF MYOCARDIAL INFARCTION ON SPLEEN AND KIDNEY OF ISOPRENALINE-INDUCED MYOCARDIAL INJURY RAT MODEL

Myocardial infarction (MI)-associated inflammation is crucial for post-infarct healing. However, unregulated inflammation may lead to unnecessary systemic inflammation, and affect other organs. This study investigated the effects of MI on spleen and kidneys over early time-points (2 and 7 days) in isoprenaline-induced MI rat model. MI was evident by elevated levels of cardiac injury marker, troponin T, and lactate dehydrogenase (LDH). MI rats showed significant upregulation of myeloperoxidase (MPO) activity at day-2 post infarct while kidney MPO activity remained unaffected. Kidney function test revealed only slightly increased plasma urea at day-2 post MI with no changes in plasma creatine at both time-points. Histological observation on the spleen showed disorganization of spleen structure at day-2 post MI while the kidney structures were preserved at both time-points. In conclusion, although MI-associated damages in the spleen were seen at day-2 post infarct, it had no impact on the kidney structures at both time-points.

Anti-fibrotic Actions of Roselle Extract in Rat Model of Myocardial Infarction.

Heart failure-associated morbidity and mortality is largely attributable to extensive and unregulated cardiac remodelling. Roselle (Hibiscus sabdariffa) calyces are enriched with natural polyphenols known for antioxidant and anti-hypertensive effects, yet its effects on early cardiac remodelling in post myocardial infarction (MI) setting are still unclear. Thus, the aim of this study was to investigate the actions of roselle extract on cardiac remodelling in rat model of MI. Male Wistar rats (200-300g) were randomly allotted into three groups: Control, MI, and MI + Roselle. MI was induced with isoprenaline (ISO) (85mg/kg, s.c) for two consecutive days followed by roselle treatment (100mg/kg, orally) for 7days. Isoprenaline administration showed changes in heart weight to body weight (HW/BW) ratio. MI was especially evident by the elevated cardiac injury marker, troponin-T, and histological observation. Upregulation of plasma levels and cardiac gene expression levels of inflammatory cytokines such as interleukin (IL)-6 and IL-10 was seen in MI rats. A relatively high percentage of fibrosis was observed in rat heart tissues with over-expression of collagen (Col)-1 and Col-3 genes following isoprenaline-induced MI. On top of that, cardiomyocyte areas were larger in heart tissues of MI rats with upregulation of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) gene expression, indicating cardiac hypertrophy. Interestingly, roselle supplementation attenuated elevation of plasma troponin-T, IL-6, IL10, and gene expression level of IL-10. Furthermore, reduction of cardiac fibrosis and hypertrophy were observed. In conclusion, roselle treatment was able to limit early cardiac remodelling in MI rat model by alleviating inflammation, fibrosis, and hypertrophy; hence, the potential application of roselle in early adjunctive treatment to prevent heart failure.