Amelioration of intestinal ischemia reperfusion injury by carvedilol via regulation of eNOS/VEGF-A and inflammasome/ IL1β/ TNFα pathways.

Intestinal ischemia reperfusion (IIR) is a life threating clinical disorder and a serious emergency case with high mortality rate. Finding ameliorative agents is a critical requisite to safeguard the tissue against its harmful effect not only on the intestine, but also on other organs especially the heart. Therefore, we tried in the current study to evaluate the role of carvedilol (CAR); an effective beta and alpha blocker with anti-oxidant, anti-apoptotic, anti-inflammatory properties and a metabolic regulator, on both cardiac and intestinal tissue in a model of IIR.

Immune regulation of TLR4/MYD88/ NF-κB/AP1/IL-6 pathway and modulation of aldosterone/PPARα receptors by eplerenone and fenofibrate in ovarian ischemia reperfusion induced injury.

Background: The immune system is deeply involved in the pathogenesis of different gynecological disorders including ovarian torsion that commonly occurs during surgical manipulation or within ovarian masses, affecting not only the ovaries, but it has remote effect on different organs particularly cardiac tissue. Early intervention and proper medical treatment are so important to preserve the ovaries and prevent distant organ damage. Accordingly, the aim of this work was to evaluate the possible ameliorative role of eplerenone (EPL) or fenofibrate (FEN) on ovarian and cardiac affection in an experimental model of ovarian ischemia/reperfusion (OIR).

Role of sacubitril/valsartan in testicular ischaemia reperfusion injury via modulation of AngII/ASK/NF-κB and JAK/STAT pathways in juvenile rats.

Background And Purpose: Testicular torsion is a common urological emergency that affects children and young males and requires immediate surgical intervention and adequate management, or it may lead to male subfertility and infertility with remote effects on vital organs including the heart. To date, there has been no sufficient treatment for these cases, and further studies are highly recommended. Thus, our study aimed to evaluate the effect of sacubitril/valsartan (SV) on testicular ischaemia/reperfusion (TIR)-induced testicular damage and remote cardiac effect in juvenile rats.

Serum midkine level and its association with subclinical coronary artery calcification and carotid atherosclerosis in chronic kidney disease.

Background: There are no studies investigating the role of midkine (MK) in vascular calcification (VC) or vascular disease associated with chronic kidney disease (CKD). This study assessed serum MK level and investigated its relationship with carotid atherosclerosis and coronary artery calcification (CAC) in non-dialysis CKD.

Methods: The study comprised 80 controls and 185 adult patients with CKD at stages 3-5 who were free of cardiovascular diseases.

Predictors of renal outcomes and mortality in patients with renal vein thrombosis: a retrospective multicenter study.

Background: Studies on renal vein thrombosis have been conducted as case reports or case series. The renal outcomes and mortality risk of renal vein thrombosis have not been fully established. We aimed to investigate the clinical characteristics, treatment modalities, and predictors of renal outcomes and mortality in patients with renal vein thrombosis in a large multicenter cohort.

Sacubitril/valsartan alleviates sepsis-induced myocardial injury in rats via dual angiotensin receptor-neprilysin inhibition and modulation of inflammasome/caspase 1/IL1β pathway.

Sepsis is a life-threatening situation that ultimately affects cardiac function, leading to cardiomyopathy and myocardial injury as a result of uncontrolled response to infection.Till now, there is limited effective treatment to rescue those cases. Thus, novel therapeutic strategies should be identified to achieve better outcomes for septic patients.

Cardioprotective role of diacerein in diabetic cardiomyopathy via modulation of inflammasome/caspase1/interleukin1β pathway in juvenile rats.

Diabetes mellitus is a common metabolic disorder affecting different body organs; one of its serious complications is diabetic cardiomyopathy (DCM). Thus, finding more cardiopreserving agents to protect the heart against such illness is a critical task. For the first time, we planned to study the suspected role of diacerein (DIA) in ameliorating DCM in juvenile rats and explore different mechanisms mediating its effect including inflammasome/caspase1/interleukin1β pathway.

Molecular mechanism of empagliflozin cardioprotection in 5-fluorouracil (5-FU)-induced cardiotoxicity via modulation of SGLT2 and TNFα/TLR/NF-κB signaling pathway in rats.

Unlabelled: One of the commoly used chemotherapeutic agents is 5-Fluorouracil (5-FU). Unfortunately, the clinical administration of 5-FU is complicated with serious cardiotoxic effects and the safe use becomes an urgent task in cardio-oncology. Till now, there are no studies discussed the role of empagliflozin (EMP) against 5-FU cardiotoxicity.

Role of hypoxia inducible factor/vascular endothelial growth factor/endothelial nitric oxide synthase signaling pathway in mediating the cardioprotective effect of dapagliflozin in cyclophosphamide-induced cardiotoxicity.

Background: Cyclophosphamide (CP) is a commonly used chemotherapeutic and immunosuppressive alkylating agent. However, cardiac adverse effects of CP interfere with its clinical benefit. Cardio-oncology research is currently an important issue and finding effective cardiopreserving agents is a critical need.

Molecular mechanisms mediate roflumilast protective effect against isoprenaline-induced myocardial injury.

Background: Myocardial necrosis is one of the most common cardiac and pathological diseases. Unfortunately, using the available medical treatment is not sufficient to rescue the myocardium. So that, we aimed in our model to study the possible cardioprotective effect of roflumilast (ROF) in an experimental model of induced myocardial injury using a toxic dose of isoprenaline (ISO) and detecting the role of vascular endothelial growth factor/endothelial nitric oxide synthase (VEGF/eNOS) and cyclic guanosine monophosphate/cyclic adenosine monophosphate/ sirtuin1 (cGMP/cAMP/SIRT1) signaling cascade.

Sacubitril/valsartan cardioprotective effect against cisplatin-induced cardiotoxicity via modulation of VEGF/eNOS and TLR4/TNFα/IL6 signalling pathways.

Objectives: Drug-induced cardiac injury is a potentially preventable cause of heart failure. Cisplatin (CIS) is a widely used chemotherapeutic agent complicated with cardiotoxicity that limits its clinical application so we aimed to evaluate the suspected cardioprotective effect of sacubitril/valsartan (Sac/Val) against CIS cardiotoxic injury.

Methods: Forty male rats of Wistar albino species were divided into four groups.

Exploring the role of ATP-sensitive potassium channel, eNOS, and P-glycoprotein in mediating the hepatoprotective activity of nicorandil in methotrexate-induced liver injury in rats.

Background: Methotrexate (MTX) is a commonly used chemotherapeutic agent; however, its clinical use is challenged by various types of injuries, including hepatotoxic side effects. Therefore, finding new protective drugs against MTX-induced toxicities is a critical need. Moreover, the different mechanisms mediating such effects are still not clear.

Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways.

Methods: 50 male Wistar albino rats were subjected to DOX toxicity via administration of single Dose (15 mg/kg) on the 4th day with or without co-administration of VIN (10, 20, 30 mg/kg/day) orally for 5 days.

Results: Our data revealed that VIN succeeded in protecting the heart against DOX induced damage as manifested by significant decrease of cardiac enzymes, hypoxia inducible factor alpha (HIF-1α), vascular endothelial growth factor-A (VEGF-A), tissue malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α) and caspase3 levels. Furthermore, VIN given group showed marked improvement of the histopathological changes of cardiac injury, total antioxidant capacity (TAC), elevation of reduced glutathione (GSH), cyclic guanosine monophosphate (cGMP), cyclic adenosine monophosphate (cAMP) and sirtuin-1 (SIRT-1).

Dapagliflozin Guards Against Cadmium-Induced Cardiotoxicity via Modulation of IL6/STAT3 and TLR2/TNFα Signaling Pathways.

Cadmium (Cd) is a common environmental pollutant that leads to severe cardiotoxic hazards. Several studies were carried out to protect the myocardium against Cd-induced cardiotoxicity. Up till now, no researches evaluated the protective effect of dapagliflozin (DAP) against Cd induced cardiotoxicity.

Simvastatin cardioprotection in cyclophosphamide-induced toxicity via the modulation of inflammasome/caspase1/interleukin1β pathway.

Drug-induced cardiotoxicity is a serious adverse effect that occurs during the administration of chemotherapeutic agents such as cyclophosphamide (CYC). Therefore, there is a critical need to find cardioprotective agents to keep the heart healthy. The current study aimed to investigate the protective effect of simvastatin (SIM) against CYC-induced heart damage and evaluate different mechanisms involved in mediating this effect, including the inflammasome/caspase1/interleukin1β (IL1β) pathway and endothelial nitric oxide synthase (eNOS).

TLR4/NF-κB/TNFα and cAMP/SIRT1 signaling cascade involved in mediating the dose-dependent effect of cilostazol in ovarian ischemia reperfusion-induced injury.

Background: One of the most dangerous gynecological emergencies is ovarian ischemia that commonly occurs during surgical manipulation or presence of ovarian masses.

Objectives: finding new therapies to prevent the associated harmful effects of ischemia/reperfusion-induced damage is still a critical need. For the first time, we aimed to evaluate the possible role of phosphodiesterase (PDE) 3 A inhibitor (PDEI), cilostazol (CLZ) in the treatment of ovarian ischemia reperfusion induced damage (OIR).

Dose dependent effect of cilostazol in induced testicular ischemia reperfusion via modulation of HIF/VEGF and cAMP/SIRT1 pathways.

Twisting of the spermatic cord is a common dangerous health problem that may be accompanied with testicular necrosis and infertility. Cilostazol (CLZ) is a selective phosphodiesterase (PDE) 3A inhibitor used for treatment of intermittent claudication. It has a great role in myocardial, spinal cord and hepatic ischaemia/reperfusion.

Dose-Dependent Cardioprotective Effect of Hemin in Doxorubicin-Induced Cardiotoxicity Via Nrf-2/HO-1 and TLR-5/NF-κB/TNF-α Signaling Pathways.

Doxorubicin (DOX) is one of the most widely used chemotherapeutic drugs, but its cardiotoxicity has been shown to be a dose-restricting factor during therapy. Finding new agents for reducing these complications is still in critical need. The current study aimed to evaluate the possible cardioprotective effect of hemin (HEM) in DOX-induced cardiotoxicity and exploring the role of toll like receptor-5/nuclear factor kappa-B/tumor necrosis factor-alpha (TLR-5/NF-κB/TNF-α) and nuclear factor erythroid 2-related factor-2/hemeoxygenase-1 (Nrf-2/HO-1) signaling pathways in mediating such effect.

The IL-6/STAT Signaling Pathway and PPARα Are Involved in Mediating the Dose-Dependent Cardioprotective Effects of Fenofibrate in 5-Fluorouracil-Induced Cardiotoxicity.

Purpose: The cardiotoxicity of anticancer drugs such as 5-fluorouracil (5FU) is a major complication that challenges their clinical usefulness. Thus there is a critical need to find new protective drugs to defend against these harmful side effects. Up to now, there have been no studies evaluating the possible cardioprotective effects of fenofibrate (FEN) in 5FU-induced cardiotoxicity.

Role of ATP-Sensitive Potassium Channel (K) and eNOS in Mediating the Protective Effect of Nicorandil in Cyclophosphamide-Induced Cardiotoxicity.

Cyclophosphamide (CP) is a widely used chemotherapeutic agent but its clinical usefulness is challenged with different forms of toxicities. No studies have evaluated the possible protective effect of nicorandil (NIC) in CP-induced cardiotoxicity. Our study aimed to investigate this effect by using NIC (3 mg/kg/day) orally for 5 days, in the presence or absence of cardiotoxicity induced by intraperitoneal (i.

Mechanisms mediating the cardioprotective effect of carvedilol in cadmium induced cardiotoxicity. Role of eNOS and HO1/Nrf2 pathway.

Cadmium (Cd) is a highly toxic heavy metal with several harmful effects including cardiotoxicity. For the first time, we aimed to evaluate the possible cardioprotective effect of carvedilol (CAR) in Cd induced cardiotoxicity and study the mechanisms involved in such protection including endothelial nitric oxide synthase (eNOS) and HO1/Nrf2 pathway. CAR (1,10 mg/kg/d) was administered orally for 4 weeks with Cd induced cardiac injury (3 mg/kg/d) orally for 4 weeks.

Clinical and procedural predictors of suboptimal myocardial reperfusion in primary percutaneous coronary intervention.

Background: Suboptimal myocardial perfusion in primary PCI is associated with increased infarct size, left ventricular (LV) dysfunction and higher mortality rates as compared as those with optimal myocardial perfusion. We identified clinical and procedural predictors of suboptimal myocardial reperfusion as judged by myocardial plush grade (MBG) in primary PCI.

Methods And Results: 100 patients with acute STEMI who underwent primary PCI were prospectively subjected to clinical, ECG, laboratory and angiographic evaluation.