The significance of serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) in early screening of hepatocellular carcinoma in cirrhotic patients was evaluated. The effect of diabetes on GAGs and IGF-1 levels was also estimated. Fifty cirrhotic patients with early stage Hepatocellular carcinoma (HCC) (22 were diabetic), thirty control cirrhotic patients without HCC (11 were diabetic) and twenty normal control subjects, were enrolled to the study. Serum α-fetoprotein (AFP), the commonly used marker for HCC, was measured in all HCC patients. Serum GAGs increased significantly, while IGF-1 was reduced in patients with cirrhosis and early stage HCC compared to normal control (P < 0.001). There was a significant reduction in GAGs and IGF-1 levels in control cirrhotic group compared to HCC group (P < 0.05). HCC patients who had normal AFP showed significantly increased GAGs and reduced IGF-1 levels compared to normal control. In comparison with corresponding non-diabetic patients, diabetic patients showed a significant increase in serum GAGs in both cirrhotic control and HCC (P < 0.01), while a significant decrease was observed in serum IGF-1 only in HCC (P < 0.05). Concomitant determination and monitoring of serum GAGs and IGF-1 could be used as a simple, low cost and non-invasive marker for HCC in cirrhotic patients.
Introduction: Diabetes mellitus possesses severe adverse effects on the urinary bladder. Urinary bladder dysfunction is a common health problem affecting diabetic patients causing recurrent infections and urinary incontinence. Objective: To evaluate the histopathological changes in the tissue of urinary bladder in Streptozotocin (STZ) diabetic rats and the protective role of insulin. Methods: Thirty rats were classified into three groups: a control group which received no treatment (Group A), STZ diabetic group (Group B) and Insulin diabetic group (Group C). Animals were sacrificed after six weeks and urinary bladders were harvested and processed for light and electron microscopy. Results: Several histopathological changes were observed in the urinary bladder of the diabetic group including an increase in the thickness of the urothelium, epithelial cells with dark nuclei and large lenticular vesicles, and wide intercellular spaces with numerous collagen fibers. Treatment with insulin reduced the pathological changes induced by STZ. Conclusion: Diabetes mellitus caused significant pathological changes in the urinary bladder of experimental rats. For instance, treating diabetic animals with insulin prevented the development of damaging effects of diabetes on the urinary bladder.
The use of antioxidants to protect against a wide range of human disease, including ischemic heart disease, has moved to the forefront in cardiovascular research. Gallic acid has shown promising effects against oxidative stress-induced disease; however, its effect in ischemic heart disease has not been well-studied. We designed the current work to investigate the potential protective effect of gallic acid against isoprenaline (ISO)-induced myocardial infarction (MI). Rats were injected subcutaneously with ISO, 100 mg/kg for 2 days, to induce MI. Gallic acid treated rats received 15 mg/kg gallic acid orally for 10 days prior to ISO injection. The histopathological examination of the Hematoxylin and Eosin-stained heart sections from the ISO treated rats shows karyopyknosis, hypereosinophilia, loss of striation, infiltration of macrophage in the interstitium, and thrombosis of the blood vessels, all of which indicate the induction of MI. In addition, ISO treatment significantly increased the plasma level of malondialdehyde and troponin-I, as well as the activity of alanine aminotransferase, lactate dehydrogenase, and creatine kinase, compared to untreated controls. Pretreatment with gallic acid significantly attenuated the ISO-induced biochemical and histopathological changes, compared to untreated controls. Our results show that ISO induced oxidative stress-mediated MI, and that gallic acid protects the rat heart from MI, at least in part, through antioxidant mechanisms.
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