Publications by authors named "Maysa Ahmed Mobasher"

<b>Background and Objective:</b> Despite advancements in modern therapeutic strategies, breast cancer still the most common cause of the high death rate among women worldwide. Wild plants and their extracts have been used in traditional medicine because of their efficient anti-cancer properties. This study aims to investigate <i>in vitro</i> the anti-cancer, anti-proliferative and potential therapeutic effects of <i>Convolvulus spicatus </i>(<i>C.

View Article and Find Full Text PDF

Background: Several studies have found an association between Diabetes mellitus (DM) and an increased risk for hepatocellular carcinoma (HCC). Evidence suggests that Metformin (Met) may have a therapeutic and protective effect against both DM and HCC. Therefore, the aim of this study was to evaluate the antioxidant effect of Met against DM and HCC-induced oxidative stress in rat model.

View Article and Find Full Text PDF

Introduction: Hepatitis C virus (HCV) is the main cause of chronic liver disease, with calamitous complications. Its highest rate is recorded in Egypt. This study investigated whether oxidative stress, immunological chaos and cellular hypoxia are implicated in the pathophysiology of the disease.

View Article and Find Full Text PDF

Many drugs are associated with the development of glucose intolerance or deterioration in glycemic control in patients with pre-existing diabetes. We have evaluated the cross-talk between signaling pathways activated by acetaminophen (APAP) and insulin signaling in hepatocytes with or without expression of the protein-tyrosine phosphatase 1B (PTP1B) and in wild-type and PTP1B-deficient mice chronically treated with APAP. Human primary hepatocytes, Huh7 hepatoma cells with silenced PTP1B, mouse hepatocytes from wild-type and PTP1B-deficient mice, and a mouse model of chronic APAP treatment were used to examine the mechanisms involving PTP1B in the effects of APAP on glucose homeostasis and hepatic insulin signaling.

View Article and Find Full Text PDF

Acute hepatic failure secondary to paracetamol poisoning is associated with high mortality. Paracetamol-induced hepatotoxicity causes oxidative stress that triggers signalling pathways and ultimately leads to lethal hepatocyte injury. We will review the signalling pathways activated by paracetamol in the liver emphasizing the role of protein tyrosine phosphatase 1B (PTP1B) in the balance between cell death and survival in hepatocytes.

View Article and Find Full Text PDF