The Overexpression of NUSAP1 and GTSE1 Could Predict An Unfavourable Prognosis and Shorter Disease Free Survival in ccRenal Cell Carcinoma.

Background: Although it has been reported that NUSAP1 and GTSE1 are highly expressed in different types of tumors and associated with malignant progression and poor clinical prognosis, their significances with clinicopathological data and correlations with patients' survival in ccRCC are still poorly understood. Therefore, in our study we attempted to evaluate the link between NUSAP1 and GTSE1 in ccRCC and to correlate their immunoexpression with clinico-pathological parameters and the patients' survival to identify their significance as potential therapeutic targets, indicators for tumor progression, and patients' prognosis.

Method: NUSAP1 and GTSE1 were examined in 100 ccRCC patients by immunohistochemistry.

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.

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.

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).

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).

Diacerein ameliorates induced polycystic ovary in female rats via modulation of inflammasome/caspase1/IL1β and Bax/Bcl2 pathways.

Polycystic ovary syndrome (PCOS) is a very common gynecological disease during childbearing period and markedly affects female fertility. Until now, there are no studies evaluating the possible curative effect of diacerein (DIA) in induced PCOS. For the first time, we aimed in current model to study the effect of DIA (50 mg/kg/day) orally for 3 weeks on experimentally induced PCOS by letrozole (1 mg/kg/day) for 3 weeks.

Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway.

Endometrial hyperplasia (EH) is a common gynecological problem and may progress to carcinoma. Early detection and management of EH are mandatory for the prevention of endometrial cancer. Activation of the renin-angiotensin system and angiotensin II signaling are involved in the progression of precancerous and cancerous lesions.

Possible Role of TGF-1, MMP-2, E-CAD, -Catenin and Antioxidants in Pathogenesis of Placenta Accreta.

Placenta accreta (PA) can be life-threatening due to postpartum hemorrhage and may lead to cesarean hysterectomy. We investigated the expression of Matrix metalloproteinase-2 (MMP-2), β-catenin, E-cadherin (E-CAD), transforming growth factor β1 (TGF-β1), glutathione peroxidase 1 (GPx-1), reduced glutathione (GSH) and superoxide dismutase (SOD) in PA compared to controls to determine if alterations may contribute to PA. Materials and methods: Twenty six PA and 31 controls were evaluated immunohistochemically for expression of MMP-2, β-catenin and E-CAD on villous and extravillous trophoblasts.

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.

Protective effect of pioglitazone on ovarian ischemia reperfusion injury of female rats via modulation of peroxisome proliferator activated receptor gamma and heme-oxygenase 1.

Ovarian torsion is a dangerous gynecological emergency condition. Early diagnosis of this case is necessary to preserve the function of the ovaries and fallopian tubes and prevent further damage. Ovarian torsion means complete or partial rotation of the adnexa with ischemia followed by reperfusion period.

Protective role of nebivolol in cadmium-induced hepatotoxicity via downregulation of oxidative stress, apoptosis and inflammatory pathways.

Cadmium (Cd) intoxication in human occurs through inhalation of cigarette smoke and ingestion of contaminated water and food. We investigated the role of nebivolol (NEB) in Cd induced hepatotoxicity. In our study; NEB was given as (10 mg/kg/d) orally to rats for 6 weeks, in the presence or absence of hepatotoxicity induced by oral administration of Cd (7 mg/kg/d) for 6 weeks.

Diacerein inhibits Estradiol-benzoate induced cervical hyperkeratosis in female rats.

Cervical hyperkeratosis is a common gynecological lesion and usually caused by inflammation or trauma. We investigated the effect of Diacerein on Estradiol benzoate-induced cervical hyperkeratosis. Diacerein (50mg/kg/day) was given orally to rats for 4 weeks in the presence or absence of cervical hyperkeratosis induced by intramuscular injection of Estradiol benzoate (60μg/100g) 3 times per week for 4 weeks.

The role of interleukin-1b and its antagonist (diacerein) in estradiol benzoate-induced endometrial hyperplasia and atypia in female rats.

Endometrial hyperplasia (EH) is a common gynecological condition and may progress to carcinoma. We investigated the effect of diacerein (DIA) on estradiol benzoate (EB)-induced EH and atypia. DIA (50 mg/kg/day) was administered orally to rats for 4 weeks, in the presence or absence of EH induced by intramuscular injection of EB (60 μg/100 g) three times per week for 4 weeks.