Low concentration of Bisphenol a induces proliferation of gastric cancer cells, HGC-27

Bisphenol A, an endocrine disrupting compound that affects human homeostasis. Studies on BPA are focusing on the impact of BPA in reproductive function and brain development. However, the effect of BPA on gut especially gastric cells is not well explored. Gut is directly in contact with ingested BPA; therefore, we aimed to determine the effect of BPA exposure on gastric cells proliferation at safe recommended concentration. Human gastric cancer cells (HGC-27) were treated with BPA at different concentration (low: 10-9M, 10-7M; high10-5M, 10-4M) and time point (24 hr, 48 hr, 72 hr). Cell viability assays were determined using MTS assay. Cells were further stained with Alexa Fluor-635 (F-actin) and Fluorescein (Hif-1α) protein for immunocytofluorescence. Data were analysed using ANOVA (p<0.05, n≥3). Cells treated with 10-9M BPA showed significance increase of cell viability after 48 hr (Mean ±SEM; 146%±0.03, p=0.01) and 72 hr (113%±0.03, p=0.00) compared to 24 hr treatment (77%±0.11, p=0.002). Similarly, cell treated with 10-7M BPA showed a significance increase after 48 hr (141%±0.03, p=0.03) and 72 hr (190%±0.03, p=0.02) compared to 24 hr cells treated with 10-7M (88%±0.05, p=0.01) and untreated (100%±0.07). Lower concentration of BPA increases the condensation of F-actin in all HGC-27 cells. Meanwhile, translocation of Hif-1α protein were observed in all BPA-exposed cells. Findings of this study revealed that BPA induced proliferation and condensation of F-actin structure of gastric cancer cells at low concentration

Review: Ischemic heart disease and the potential role of Fenugreek (Trigonella foenum graecum linn.) in cardioprotection

Ischemic heart disease, often known as coronary heart disease (CHD), is a term for heart disorders caused by narrowing heart arteries (coronary arteries) that provide blood to the heart's muscles. The body is prone to heart attacks when there is less oxygen supply (hypoxia) to the heart resulting a major cell death in the heart tissues. Cardiovascular disease (CVD) is the leading cause of death worldwide. Over the last few decades, the potential therapeutic effects of herbs and other types of complementary medicines for managing risk factors for CVD have gotten a lot of attention. Fenugreek (Trigonella foenum graecumLinn.) is a very important spice in most Asian dishes. In Malaysia, fenugreek, locally known as ‘halba’, is used in the preparation of popular dishes; ‘nasi dagang’ for breakfast, and ‘putu halba’ as snacks for hi-tea and sometimes applied in drinks. Although, to date, the effect of fenugreek against diabetes and heart diseases is well investigated, most studies do not focus on its the effects at molecular levels. This review gives an insight on the ischemic heart disease and the nutritional values of fenugreek as functional food in protecting the heart

Effects of bisphenol a on neonatal cardiomyocytes beating rate and morphology

Bisphenol A (BPA) has been utilised excessively at a global capacity of 2.9 billion kg/year. It is widely used in manufacturing polycarbonate polymers and epoxy resins. Hence, humans are potentially exposed to this chemical substance in their daily life. As a typical endocrine disruptor, BPA exhibits detectable hormone-like properties. Many studies have been linking BPA exposure in humans with the risk of developing cardiovascular disease, however the direct exposure of BPA on cardiomyocytes beating rates and morphology have not been entirely explored. Therefore, in this study, we aimed to investigate the effects of BPA on cells structure and function of neonatal rat cardiomyocytes culture. Cardiomyocytes were isolated from 0 to 2 days old newborn rats and treated with 0.001 to 100 µM concentration of BPA. All cardiomyocytes were subjected to immunostaining, beating frequency assessment assay, MTS assay and Scanning Electron microscopy (SEM). In immunostaining, cardiomyocytes showed positive staining for F-actin. This staining allows identification of the cells thus differentiate cardiomyocytes from other cell types. Significance effects of BPA on cardiomyocytes were observed in MTS assay (p<0.05) and beating rates (p<0.01). Significant reduction (48%-64%, ± 1.5280) was observed in beating rate of cardiomyocytes exposed to 0.1 to 100 µM of BPA. Meanwhile in MTS assay, significant reduction (54%, 0.067 ± 0.0026) in cell viability was observed in cells exposed to 0.1 µM of BPA only. Interestingly, under SEM, cardiomyocytes showed altered cell surface homogeneity after BPA exposure. Exposure of 0.1 to 100 µM BPA lead to flatten of cardiomyocytes cell surface and blurring of the cell borders. This study offers an in vitro evidence of BPA effects on cardiomyocytes morphology and beating rates, thus suggest the potential adverse effect of BPA exposure. However, further investigation would be required to understand how BPA effects normal cells morphology and beating rates of heart cells

Overview of Bile Acids Signaling and Perspective on the Signal of Ursodeoxycholic Acid, the Most Hydrophilic Bile Acid, in the Heart

Bile acids (BA) are classically known as an important agent in lipid absorption and cholesterol metabolism. Nowadays, their role in glucose regulation and energy homeostasis are widely reported. BAs are involved in various cellular signaling pathways, such as protein kinase cascades, cyclic AMP (cAMP) synthesis, and calcium mobilization. They are ligands for several nuclear hormone receptors, including farnesoid X-receptor (FXR). Recently, BAs have been shown to bind to muscarinic receptor and Takeda G-protein-coupled receptor 5 (TGR5), both G-protein-coupled receptor (GPCR), independent of the nuclear hormone receptors. Moreover, BA signals have also been elucidated in other nonclassical BA pathways, such as sphingosine-1-posphate and BK (large conductance calcium- and voltage activated potassium) channels. Hydrophobic BAs have been proven to affect heart rate and its contraction. Elevated BAs are associated with arrhythmias in adults and fetal heart, and altered ratios of primary and secondary bile acid are reported in chronic heart failure patients. Meanwhile, in patients with liver cirrhosis, cardiac dysfunction has been strongly linked to the increase in serum bile acid concentrations. In contrast, the most hydrophilic BA, known as ursodeoxycholic acid (UDCA), has been found to be beneficial in improving peripheral blood flow in chronic heart failure patients and in protecting the heart against reperfusion injury. This review provides an overview of BA signaling, with the main emphasis on past and present perspectives on UDCA signals in the heart

Promoting cardioprotection with fenugreek: Insights from CoCl2 -induced hypoxia in neonatal rat cardiomyocytes

Objective(s): This study aimed to investigate the protective effects of fenugreek on CoCl2 -induced hypoxia in neonatal rat cardiomyocytes. Materials and Methods: Primary cardiomyocytes were isolated from Sprague Dawley rats aged 0–2 days and incubated with various concentrations of fenugreek (10-320 µg/ml) and CoCl2 -induced hypoxia for different durations (24, 48, and 72 hr). Cell viability, calcium signaling, beating rate, and gene expression were evaluated. Results: Fenugreek treatments did not cause any toxicity in cardiomyocytes. At a concentration of 160 µg/ml for 24 hr, fenugreek protected the heart against CoCl2 -induced hypoxia, as evidenced by reduced expression of caspases (-3, -6, -8, and -9) and other functional genes markers, such as HIF-1α, Bcl-2, IP3R, ERK5, and GLP-1r. Calcium signaling and beating rate were also improved in fenugreektreated cardiomyocytes. In contrast, CoCl2 treatment resulted in up-regulation of the hypoxia gene HIF-1α and apoptotic caspases gene (-3, -9, -8, -12), and down-regulation of Bcl-2 activity. Conclusion: Fenugreek treatment at a concentration of 160 µg/ml was not toxic to neonatal rat cardiomyocytes and protected against CoCl2 -induced hypoxia. Furthermore, fenugreek improved calcium signaling and beating rate and altered gene expression. Fenugreek may be a potential therapeutic agent for promoting cardioprotection against hypoxia-induced injurie