22 research outputs found
Cinnamomum burmannii improves insulin serum level in the normal obese subjects : preliminary study
Obesity is characterized with excessive accumulation of the body fat which occurs when
the energy intake exceeds the expenditure. It is routinely associated with insulin resistance
and hyperinsulinemia. Additionally, suppressing insulin level protects female mice from
weight gaining. Cinnamon [Cinnamomum burmannii (Ness) Bl. Cortex] suppresses
hyperinsulinemia condition in the type 2 diabetic rat suggesting the possible beneficial its
role in the obesity. We aimed to investigate the effect of Cinnamon extract in the normal
obese subjects. In this preliminary cross-over clinical trial, 24 normal obese subjects
were recruited and divided randomly into two groups i.e. treatment and placebo. Two
grams of the cinnamon extract were given twice daily for 56 days in the treatment group.
Normal obese subjects given placebo were allocated as the placebo group. After the
treatment, each of the group ran a one month run-in period, then the groups were crossovered
for the next 56 days. Body mass index (BMI), insulin serum level, cholesterol and
triglyceride plasma levels were measured at the beginning and at the end of the study.
No diet restriction nor exercise intervention was given during the study. At the end of the
study, BMI in the treatment group (58%) were slightly reduced when compared to the
placebo group (33%), however, it was not significantly different (p>0.05). Moreover,
significantly reduction in the insulin serum level was observed in 63% subject in the
treatment group compared to 33% subject in the placebo group (p < 0.05). Additionally,
there were no significant differences of cholesterol and triglyceride plasma level observed
in the both group. In conclusion, cinnamon extract may give beneficial role in the normal
obese subjects by suppressing the serum insulin level. Further studies are required to
elucidate the specific role of cinnamon in preventing weight gain
Curcumin ameliorates macrophage infiltration by inhibiting NF-κB activation and proinflammatory cytokines in streptozotocin induced-diabetic nephropathy
<p>Abstract</p> <p>Background</p> <p>Chronic inflammation plays an important role in the progression of diabetic nephropathy (DN) and that the infiltration of macrophages in glomerulus has been implicated in the development of glomerular injury. We hypothesized that the plant polyphenolic compound curcumin, which is known to exert potent anti-inflammatory effect, would ameliorate macrophage infiltration in streptozotocin (STZ)-induced diabetic rats.</p> <p>Methods</p> <p>Diabetes was induced with STZ (55 mg/kg) by intraperitoneal injection in rats. Three weeks after STZ injection, rats were divided into three groups, namely, control, diabetic, and diabetic treated with curcumin at 100 mg/kg/day, p.o., for 8 weeks. The rats were sacrificed 11 weeks after induction of diabetes. The excised kidney was used to assess macrophage infiltration and expression of various inflammatory markers.</p> <p>Results</p> <p>At 11 weeks after STZ injection, diabetic rats exhibited renal dysfunction, as evidenced by reduced creatinine clearance, increased blood glucose, blood urea nitrogen and proteinuria, along with marked reduction in the body weight. All of these abnormalities were significantly reversed by curcumin. Hyperglycemia induced the degradation of IκBα and NF-κB activation and as a result increased infiltration of macrophages (52%) as well as increased proinflammatory cytokines: TNF-α and IL-1β. Curcumin treatment significantly reduced macrophage infiltration in the kidneys of diabetic rats, suppressed the expression of above proinflammatory cytokines and degradation of IκBα. In addition, curcumin treatment also markedly decreased ICAM-1, MCP-1 and TGF-β<sub>1 </sub>protein expression. Moreover, at nuclear level curcumin inhibited the NF-κB activity.</p> <p>Conclusion</p> <p>Our results suggested that curcumin treatment protect against the development of DN in rats by reducing macrophage infiltration through the inhibition of NF-κB activation in STZ-induced diabetic rats.</p
Modulation of endoplasmic reticulum stress and cardiomyocyte apoptosis by mulberry leaf diet in experimental autoimmune myocarditis rats
Mulberry is commonly used as silkworm diet and an alternative medicine in Japan and China, has recently reported to contain many antioxidative flavanoid compounds and having the free radical scavenging effects. Antioxidants reduce cardiac oxidative stress and attenuate cardiac dysfunction in animals with pacing-induced congestive heart failure. Hence we investigated the cardioprotective effect of mulberry leaf powder in rats with experimental autoimmune myocarditis. Eight-week-old Lewis rats immunized with cardiac myosin were fed with either normal chow or a diet containing 5% mulberry leaf powder and were examined on day 21. ML significantly decreased oxidative stress, myocyte apoptosis, cellular infiltration, cardiac fibrosis, mast cell density, myocardial levels of sarco/endo-plasmic reticulum Ca2+ ATPase2, p22phox, receptor for advanced glycation end products, phospho-p38 mitogen activated protein kinase, phospho-c-Jun NH2-terminal protein kinase, glucose regulated protein78, caspase12 and osteopontin levels in EAM rats. These results may suggest that mulberry diet can preserve the cardiac function in experimental autoimmune myocarditis by modulating oxidative stress induced MAPK activation and further afford protection against endoplasmic reticulum stress mediated apoptosis
Carvedilol-Afforded Protection against Daunorubicin-Induced Cardiomyopathic Rats In Vivo: Effects on Cardiac Fibrosis and Hypertrophy
Anthracyclines, most powerful anticancer agents, suffer from their cardiotoxic effects, which may be due to the induction of oxidative stress. Carvedilol, a third-generation, nonselective β-adrenoreceptor antagonist, possesses both reactive oxygen species (ROS) scavenging and ROS suppressive effects. It showed protective effects against daunorubicin- (DNR-) induced cardiac toxicity by reducing oxidative stress and apoptosis. This study therefore was designed to examine the effects of carvedilol on DNR-induced cardiomyopathic rats, focused on the changes of left ventricular function, cardiac fibrosis, and hypertrophy. Carvedilol increased survival rate, prevented systolic and diastolic dysfunction, and attenuated myocardial fibrosis and hypertrophy. DNR alone treated rats showed upregulated myocardial expression of ANP, PKC-α, OPN, and TGF-β1 and downregulation of GATA-4 in comparison with control, and treatment with carvedilol significantly reversed these changes. The results of the present study add the available evidences on the cardioprotection by carvedilol when associated with anthracyclines and explain the mechanisms underlying the benefits of their coadministration
Role of Differential Signaling Pathways and Oxidative Stress in Diabetic Cardiomyopathy
Diabetes mellitus increases the risk of heart failure independently of underlying coronary artery disease, and many believe that diabetes leads to cardiomyopathy. The underlying pathogenesis is partially understood. Several factors may contribute to the development of cardiac dysfunction in the absence of coronary artery disease in diabetes mellitus. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Hyperglycemia-induced oxidative stress is a major risk factor for the development of micro-vascular pathogenesis in the diabetic myocardium, which results in myocardial cell death, hypertrophy, fibrosis, abnormalities of calcium homeostasis and endothelial dysfunction. Diabetes-mediated biochemical changes show cross-interaction and complex interplay culminating in the activation of several intracellular signaling molecules. Diabetic cardiomyopathy is characterized by morphologic and structural changes in the myocardium and coronary vasculature mediated by the activation of various signaling pathways. This review focuses on the oxidative stress and signaling pathways in the pathogenesis of the cardiovascular complications of diabetes, which underlie the development and progression of diabetic cardiomyopathy
Detection of the SARS-CoV-2 Omicron Variant in COVID-19 Patients from South Tangerang Using SNP-Probes S371L and K417N
The COVID-19 pandemic caused by the SARS-CoV-2 virus has posed a global challenge. Experts from various branches of science have endeavoured to find solutions to control its spread, one of which has been the quick and precise detection of the virus and its variants in patients. This study aimed to detect the presence of SARS-CoV-2, notably the rapidly spreading Omicron variant, using the spike (S)-gene target failure (SGTF) and S-gene target positive (SGTP) with the principle of the single nucleotide polymorphism (SNP)-probe test. Our descriptive experimental approach detected Omicron variants with the SNP-probe technique using samples of SARS-CoV-2 patients and controls. The probes were designed to recognize the nucleotide code of the amino acids in positions 371 and 417 of SARS-CoV-2. The existence of variants was monitored by the presence or absence of a fluorescence signal, which was translated into a sigmoidal graph using a real-time (RT)-PCR machine. One hundred and twelve samples that had tested positive for SARS-CoV-2 and the Omicron variant using a registered commercial kit showed a similar result to our in-house-developed SNP-probe 371 and 417 assays. The results of this study indicate that the SNP-probe we designed can be used in the detection of the SARS-CoV-2 Omicron variant
The Potential Effect of Honey-derived D-Allulose in Counteracting Hyperglycemia by Time and Dose Dependent Manner in Diabetes Mellitus
Diabetes mellitus has become a worldwide burden due to its persistent, chronic hyperglycemia. D-allulose, a monosaccharide sugar with a 180.16 molecular weight, is widely used as a low-calorie sweetener, is not involved in glucose-related metabolism, and thus does not alter insulin and pancreatic function. This study aimed to evaluate the potential role of honey-derived D-allulose in acute and sub-chronic diabetes mellitus. Diabetic Sprague-Dawley rats were divided into 9 groups and treated with 0.1, 0.2, and 0.4 g/kg BW honey-derived D-allulose for 28, 56, and 84 days. Post-prandial blood glucose levels and body weight were measured every 4 weeks. Significant reductions in post-prandial blood glucose levels were observed on days 56 and 84 treatment with 0.1 g/kg BW D-allulose. More significant reductions were observed on days 28, 56, and 84 of treatment with 0.2 or 0.4 g/kg BW D-allulose. Eighty-four days of treatment with 0.4 g/kg BW D-allulose significantly reduced post-prandial blood glucose levels compared to all groups. We identified that honey-derived D-allulose reduced post-prandial blood glucose levels in a dose- and time-dependent manner. Thus, honey-derived D-allulose may provide beneficial support for diabetic conditions not only as a sweetener but also as a pharmacological treatment
The Role of Carvedilol in the Treatment of Dilated and Anthracyclines-Induced Cardiomyopathy
Although chronic sympathetic activation provides inotropic and chronotropic support to the failing heart, such activation may also have deleterious effects, including the direct cardiotoxic effects of catecholamines, activation of the renin-angiotensin-aldosterone system and an increase in myocardial oxygen demand. These observations indicate that β-blockade might be beneficial in the treatment of heart failure resulting from dilated cardiomyopathy or ischaemic heart disease. Carvedilol is a non-selective β-blocker acting on β1-, β2-, and α1-adrenoceptors. It possesses potent anti-oxidant and anti-apoptotic properties, along with neuroprotective, vasculoprotective, cardioprotective effects, and it has reduced overall mortality in patients with heart failure in controlled clinical trials. Its role in treating cardiomyopathy requires focus. The fact that anthracyclines are cardiotoxic seriously narrows their therapeutic index in cancer therapy. The cardiotoxic risk increases with the cumulative dose and may lead to congestive heart failure and dilated cardiomyopathy in adults and in children. This review focuses on recent research regarding the beneficial effects of carvedilol in the treatment of dilated cardiomyopathy and to revisit the available evidence on the cardioprotection of carvedilol when associated with anthracycline and to explain the mechanisms underlying the benefits of their co-administration
The Role of Carvedilol in the Treatment of Dilated and Anthracyclines-Induced Cardiomyopathy
Although chronic sympathetic activation provides inotropic and chronotropic support to the failing heart, such activation may also have deleterious effects, including the direct cardiotoxic effects of catecholamines, activation of the renin-angiotensin-aldosterone system and an increase in myocardial oxygen demand. These observations indicate that β-blockade might be beneficial in the treatment of heart failure resulting from dilated cardiomyopathy or ischaemic heart disease. Carvedilol is a non-selective β-blocker acting on β1-, β2-, and α1-adrenoceptors. It possesses potent anti-oxidant and anti-apoptotic properties, along with neuroprotective, vasculoprotective, cardioprotective effects, and it has reduced overall mortality in patients with heart failure in controlled clinical trials. Its role in treating cardiomyopathy requires focus. The fact that anthracyclines are cardiotoxic seriously narrows their therapeutic index in cancer therapy. The cardiotoxic risk increases with the cumulative dose and may lead to congestive heart failure and dilated cardiomyopathy in adults and in children. This review focuses on recent research regarding the beneficial effects of carvedilol in the treatment of dilated cardiomyopathy and to revisit the available evidence on the cardioprotection of carvedilol when associated with anthracycline and to explain the mechanisms underlying the benefits of their co-administration