Correction: Cardiac angiogenesis enhances by activating Mir-126 and related target proteins in type 2 diabetic rats: rescue combination effect of sodium butyrate and voluntary exercise therapy.

[This corrects the article DOI: 10.1007/s40200-023-01198-1.].

Silibinin, Synergistically Enhances Vinblastine-Mediated Apoptosis in Triple Negative Breast Cancer Cell Line: Involvement of Bcl2/Bax and Caspase-3 Pathway.

Triple-negative breast cancer (TNBC) with a poor prognosis and survival is the most invasive subtype of breast cancer. Usually, TNBC requires a chemotherapy regimen at all stages, but chemotherapy drugs have shown many side effects. We assumed that combination therapy of vinblastine and silibinin might reduce the vinblastine toxicity and dose of vinblastine.

Cardiac angiogenesis enhances by activating Mir-126 and related target proteins in type 2 diabetic rats: Rescue combination effect of Sodium butyrate and voluntary exercise therapy.

Objective: type 2 diabetes, metabolic disorder, is one of the main risk factors for cardiovascular disease, leading to angiogenesis injury. The present study wanted to discover the effect of sodium butyrate (NaB) and voluntary exercise, alone or together, on miR-126 and related proteins in rats with type 2 diabetes.

Methods: thirty-five male Wistar rats (200-250 g) were randomly divided into five groups: control, diabetes, diabetes-NaB, diabetes-exercise, and diabetes-NaB-exercise.

Sodium butyrate and voluntary exercise through activating VEGF-A downstream signaling pathway improve heart angiogenesis in type 2 diabetes.

Background: Inadequate angiogenesis in patients with type 2 diabetic heart could result in deprived collateral formation. Herein, we aimed to investigate the effects of sodium butyrate (NaB) along with voluntary exercise simultaneously on the mechanisms acting on cardiac angiogenesis.

Materials And Methods: Animals were divided into the following five groups: control (Con), diabetic rats (Dia), diabetic rats treated with NaB (200 mg/kg, i.

5-FU and the dietary flavonoid carvacrol: a synergistic combination that induces apoptosis in MCF-7 breast cancer cells.

Along with the benefits of chemotherapy in the treatment of breast cancer, the side effects of these drugs along with drug resistance make their use complicated. One of the solutions to overcome this problem is the use of herbal products and combination therapy. In this research, we try to investigate the effects of carvacrol, a monoterpene flavonoid, in combination with the chemotherapy drug 5-FU.

Carvacrol Enhance Apoptotic Effect of 5-FU on MCF-7 Cell Line via inhibiting P-glycoprotein: An In-silco and In-vitro Study.

Background: P-glycoprotein (P-gp), is an ATP-dependent efflux transporter and overexpressed in cancer cells which is responsible for drug resistance and transportation of anticancer agents out of cells. Hence, P-gp inhibition is a promising way to reverse multi-drug resistance, finding a suitable inhibitor is essential. Carvacrol, an active compound of thyme, has been shown anticancer properties in several types of cancers but the mechanisms underlying this effect remain unclear.

Cytochrome P450-derived fatty acid epoxides and diols in angiogenesis and stem cell biology.

Cytochrome P450 (CYP) enzymes are frequently referred to as the third pathway for the metabolism of arachidonic acid. While it is true that these enzymes generate arachidonic acid epoxides i.e.

Pretreatment with vildagliptin boosts ischemic-postconditioning effects on cardioprotection and expression profile of genes regulating autophagy and mitochondrial fission/fusion in diabetic heart with reperfusion injury.

The burden of myocardial ischemia/reperfusion (IR) injury is 2-3-folds higher in diabetic patients, so protecting diabetic hearts is clinically important. Here, we investigated the effect of combinational therapy with vildagliptin and ischemic postconditioning (IPostC) on cardioprotection and the expression of genes regulating autophagy and mitochondrial function in diabetic hearts with IR injury. Type 2 diabetes was induced through high-fat diet and streptozotocin protocol in Wistar rats.