94 research outputs found
In vivo and in vitro effects of epigallocatechin gallate on intestinal motility of spontaneously hypertensive rats
No full textIN VIVO AND IN VITRO EFFECTS OF EPIGALLOCATECHIN GALLATE (EGCG) ON INTESTINAL MOTILITY OF SPONTANEOUSLY HYPERTENSIVE RATS (SHR)
POTENZA Maria Assunta, NACCI Carmela, MONTAGNANI Monica and DE SALVIA Maria Antonietta.
Dept. Biomedical Sciences and Human Oncology, Medical School, University of Bari, Piazza G. Cesare, 70124 Bari, Italy
Anti-hypertensive effects of green tea drinking are mediated by its most abundant catechin, EGCG. EGCG reaches the highest concentrations in the intestine, where it reduces lipids absorption, inhibits angiogenesis and decreases cancer cell proliferation. Whether EGCG may interfere with gastrointestinal motility is not known. The present study investigates the effects of EGCG on intestinal motility of SHR and WKY rats. For in vivo studies, 9-wk old male SHR were administered with EGCG (200 mg/kg/day) or vehicle (n = 5/group) by gavage for 3 weeks. The contractile dose-response to carbachol (0.05 – 5 μM) and the inhibitory response to electrical field stimulation (EFS, 1- 10 Hz, 13 V, 1 msec, 10-sec train duration) from colon and duodenum specimens were measured before and after L-NNA (100 μM), and compared between EGCG- and vehicle-treated SHR. Colonic response to carbachol and duodenal response to L-NNA were respectively reduced and increased (p < 0.05) in EGCG-treated SHR (vs. vehicle). For in vitro studies, the contractile response to carbachol (1.5 μM) and the inhibitory response to EFS (5 Hz) were measured in colonic and duodenal specimens before and after EGCG (100 μM), and results in SHR compared to those obtained in WKY. EGCG significantly reduced colonic response to carbachol only in SHR, whereas a decreased duodenal inhibitory response to EFS (5 Hz) after EGCG was observed in both SHR and WKY. These data suggest that EGCG may influence intestinal motility, and that gastrointestinal side effects might be associated with drinking of green tea, particularly in hypertensive patients
Adiponectin stimulates production of endothelin-1 (ET-1) and nitric oxide (NO) from vascular endothelium using signaling pathways both overlapping and distinct from those used by insulin RID B-1970-2008
No full textMolecular and clinical aspects of endothelial dysfunction in diabetes
No full textAbstract
Diabetic patients have an increased risk for cardiovascular complications with respect to the general population. Micro- and macrovascular complications such as nephropathy, retinopathy, atherosclerosis, and coronary artery disease are usually preceded by endothelial dysfunction, a condition characterized by impaired vasorelaxation resulting from reduced bioavailability of the endothelial mediator nitric oxide (NO). Nitric oxide is among endothelial mediators released by endothelial cells in response to insulin stimulation. Therefore, metabolic abnormalities such as insulin resistance, dyslipidemia, compensatory hyperinsulinemia and overt hyperglycemia may all contribute to impaired NO bioavailability and abnormal vasodilatation in diabetic patients. Each of these alterations may trigger endothelial dysfunction by multiple intracellular mechanisms including accelerated formation of advanced glycolysis end products, activation of protein kinase C, increased pro-inflammatory signaling, and impaired sensitivity of the PI 3-kinase signaling pathways. This review outlines the most important mechanisms by which insulin takes part in physiological regulation of endothelial function. Abnormal insulin signaling in endothelium under diabetic conditions and patho-physiological consequences on cardiovascular homeostasis will also be discussed
HYPERGLYCEMIA-MEDIATED OVEREXPRESSION OF CYCLOOXYGENASE-2 (COX-2) PARTICIPATES IN VASCULAR HYPOREACTIVITY OF STREPTOZOTOCIN-INDUCED TYPE 1 DIABETES
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Immunoregulatory effects of L-arginine and therapeutical implications
No full textArginine, initially classified as a non-essential amino acid, participates to multiple biological processes including release of several hormones, collagen synthesis during wound healing, antitumor and antibacterial activities and non-specific immunity. Nitric oxide synthase and arginase competes for L-arginine as a substrate and this event appears to play a key role in the regulation of the inflammatory process. In this framework recent studies have identified complex patterns of interactions among these enzymes. This review will emphasizes some effects of L-arginine on immune cell functions, including triggering of L-arginine-nitric oxide and arginase pathways, its biological properties and therapeutical applications
Cardiovascular Complications in Diabetes: Lessons from Animal Models
No full textMicro- and macro-vascular complications are the leading causes of morbidity and mortality in type 1 and type 2 diabetic patients. Despite the vast clinical experience linking diabetic metabolic abnormalities to cardiovascular lesions, the molecular basis of individual susceptibility to diabetic cardiovascular injury is still largely unknown. Significant advances in this area may come from studies on suitable animal models. Although no animal model can accurately reproduce the human disease, experimental studies in animals have the great advantage to eliminate factors such as ethnicity, economic and geographic variables, drug interactions, diet, gender and age differences that importantly limit clinical studies. Indeed, appropriate animal models have provided important information on genetic and environmental risks of diabetes, and helped to dissect molecular mechanisms underlying the development, progression and therapeutic control of this disease. Unfortunately, none of the diabetic models presently available fully mimics the human syndrome. Therefore, the current knowledge on the pathogenesis of cardiovascular complications relies on the evaluation of distinct phenotypes from various diabetic models. In addition to strains prone to diabetes, this disease can be induced by surgical, pharmacological or genetic manipulation in several animal species. Rodents are the most used, although some studies are still performed in larger animals as rabbits, cats, pigs or monkeys. Far from being exhaustive, this work should serve as a general overview of the most relevant clues provided by major species and models for the overall comprehension of cardiovascular complications in type 1 and type 2 diabetes
Overexpression of cyclo-oxygenase 2 (COX-2) in endothelium may contribute to vascular protective effects of adiponectin
No full textReduction in adiponectin levels may contribute to endothelial dysfunction in an experimental model of type I diabetes
No full textAlzheimer's disease murine models: focus on late-onset disease
No full textAlzheimer's disease (AD) is a progressive neurodegenerative disorder clinically characterized by impairment of cognitive functions and memory loss. The two core neuropathological hallmarks of AD are deposits of beta-amyloid (A beta) fibrils in senile plaques and accumulation of hyperphosphorylated tau protein filaments in neurofibrillary tangles. An increasing number of murine models of AD have been generated. Animal models have been valuable tools for reproducing aspects of the neuropathological characteristics of AD strongly supporting the amyloid cascade hypothesis. However, we need to learn much more about the link between the pathological cascade of AD and the emergence of clinical symptoms to identify the factors which best predict the risk of progression from normal cognition to mild cognitive impairment and AD dementia. The few therapeutic agents currently available, such as galantamine, memantine, rivastigmine and donepezil are useful for symptomatic management and none of them is able to modify the disease progression. Studies with transgenic mouse models and data from clinical trials suggest that A beta-modifying therapies have no or limited effect after neuronal degeneration has begun, and stress the need of validated biomarkers for stratification of patients more responsive to immunotherapeutic agents. It is hoped that further efforts will move toward defining the preclinical stage of AD when intervention with anti-A beta immunotherapy may be most efficacious. The present paper reports a brief overview of AD and some murine models focusing on what we have learned from AD modelin
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