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Dunnione protects against experimental cisplatin-induced nephrotoxicity by modulating NQO1 and NAD+ levels

Posted by N Rashtchizadeh, H Argani, L Roshangar, et al. on 2018-06-24 18:59:58


Despite being an efficacious anticancer agent, the clinical utility of cisplatin is hindered by its cardinal side effects. This investigation aimed to appraise potential protective impact of dunnione, a natural naphthoquinone pigment with established NQO1 stimulatory effects, on cisplatin nephrotoxicity of rats. Dunnione was administered orally at 10 and 20 mg/kg doses for 4 d and a single injection of cisplatin was delivered at the second day. Renal histopathology, inflammatory/oxidative stress/apoptotic markers, kidney function, and urinary markers of renal injury were assessed. Dunnione repressed cisplatin-induced inflammation in the kidneys as indicated by decreased TNF-alpha/IL-1beta levels, and reduced nuclear phosphorylated NF-kB p65. This agent also obviated cisplatin-invoked oxidative stress as elucidated by decreased MDA/GSH levels and increased SOD/CAT activities. Dunnione, furthermore, improved renal histological deteriorations as well as caspase-3 activities and terminal deoxynucleotidyl transferase (TUNEL) positive cells, the indicators of apoptosis. Moreover, it up-regulated nuclear Nrf2 and cytosolic haeme-oxygenase-1 (HO-1) and NQO1 levels; meanwhile, promoted NAD+/NADH ratios followed by enhancing the activities of Sirt1 and PARP1; and further attenuated nuclear acetylated NF-kB p65. Dunnione additionally declined cisplatin-evoked retrogression in renal function and upraise in urinary markers of glomerular and tubular injury as demonstrated by decreased serum urea and creatinine with simultaneous reductions in urinary excretions of collagen type IV, podocin, cystatin C, and retinol-binding protein (RBP). Altogether, these findings offer dunnione as a potential protective agent against cisplatin-induced nephrotoxicity in rats.


OBJECTIVES: Bipolar disorder (BD) is a chronic psychiatric disorder with a high prevalence of obesity. There are a number of hypotheses regarding the association between obesity and BD. One involves common neurobiological abnormalities, such as dysfunction in the hypothalamic pituitary adrenal axis and changes in secretions of orexigenic and anorectic peptides. The purpose of this study was to evaluate the blood levels of agouti-related peptide (AgRP), obestatin cortisol, and corticosteroid-binding globulin (CBG) and metabolic parameters in patients with euthymic BD, and to compare these to those of healthy controls.

METHODS: Twenty-nine outpatients with BD type I admitted to the psychiatric clinic were consecutively enrolled and compared with 25 sex- and body mass index (BMI)-matched controls.

RESULTS: There was a significant difference in AgRP, cortisol, and CBG levels between patients and the controls (p = .005, .021, and .034, respectively). AgRP and CBG did not correlate with any parameter in BD patients, but cortisol correlated with BMI.

CONCLUSIONS: We conclude that BD patients have higher levels of AgRP, cortisol, and CBG than healthy controls with similar BMIs. This may represent a new insight into the neurobiology of BD.


Angiopoietin-like 8 (ANGPTL8) a hepatic protein, implicated by several studies with a role in promoting pancreatic beta-cell proliferation and improving glucose tolerance. Although a matter of controversy, a growing number of reports support ANGPTL8 potential, yet unclear role in type 2 diabetes mellitus (T2D).


To examine changes in fasting ANGPTL8 level in people with morbid obesity, with or without diabetes following laparoscopic sleeve gastrectomy (LSG) in 1-year prospective study.


Fasting serum ANGPTL8 was measured by ELISA at baseline in participants with morbid obesity, 17 with diabetes and 23 without diabetes, and in normal weight participants, 19 with and 15 without diabetes, and during 1-year post-LSG in participants with morbid obesity.


At baseline, people with T2D had higher ANGPTL8 level, (morbid obese, Mean ±SEM; 1415 ±196.4 pg/ml, and normal-weight, 2231 ±328.1 pg/ml), compared with individuals without T2D (morbid obese, 876 ±155.0 pg/ml, and normal weight controls 868.9 ±218.7 pg/ml). In participants with diabetes and morbid obesity, T2D remission occurred 15 days post-LSG, defined by a sustained reduced fasting blood glucose levels <6.9 mmol/L. In this group, the 1-year post-LSG measurement of ANGPTL8 showed unique biphasic changes, first a prominent elevation (day 60, 3336 ±916.5 pg/ml, P <0.01), followed by a gradual decrease to reach almost the baseline level (day 360, 1184 ±119.3 pg/ml).


Elevated baseline ANGPTL8 in participants with diabetes at baseline reflected a link to T2D. Interestingly, the unique biphasic pattern of change in fasting ANGPTL8 post-LSG, occurred only in people with diabetes, suggesting ANGPTL8 potential role in T2D remission.


Angiopoietin-like 8; Betatrophin; Type 2 diabetes mellitus; Bariatric surgery; Laparoscopic sleeve gastrectomy; Morbid obesity


Many inconsistent findings are reported on the correlation between circulating betatrophin and insulin resistance in the different population. The aim of this analysis was to explore the correlation between the level of betatrophin and insulin resistance in the general population. The databases of PubMed, EMBASE, and the Cochrane Library (inception to October 26, 2016) were searched without language restrictions for publications that reported studies on associations between betatrophin and insulin resistance in adults. Subgroup analyses were performed to investigate potential sources of heterogeneity. The pooled effect size was calculated using a random-effects model. Twenty-five studies were included in this meta-analysis. Meta-analysis showed that betatrophin was positively and significantly correlated with insulin resistance (r=0.16, 95% CI: 0.08–0.25). When all participants were divided into DM, GDM, and Non-DM groups, this association was also significant in T2DM, GDM, and Non-DM participants (T2DM: r=0.09, 95% CI: 0.01–0.17; I 2=45.1%; GDM: r=0.39, 95% CI: 0.24–0.55; I 2=0.0%; non-DM: r=0.15, 95% CI: 0.04–0.26; I 2=89.3%), and it was obvious that heterogeneity existed in Non-DM group (I 2=89.3%, p<0.001). Subgroup analysis revealed that gender, serum sample and ELISA kits for full-length betatrophin had significant influence on the association between betatrophin and insulin resistance. In conclusion, the level of circulating betatrophin is positively associated with insulin resistance in the general population, especially in T2DM and GDM patients. Gender, serum sample, and ELISA kits for full-length betatrophin may affect this association. More large-scale studies are needed to determine whether improving insulin resistance concomitantly declines betatrophin levels in different diseases.


Hyperlipidemia is often associated with obesity and diabetes, and can lead to serious complications like atherosclerosis and fatty liver disease. Coagonist of GLP-1 and glucagon receptors is a therapy under clinical investigation for treatment of obesity and diabetes. In this study, we have characterized the mechanism of hypolipidemic effect of a balanced coagonist using high cholesterol-fed hamsters. Tyloxapol-induced hypertriglyceridemia, lipolysis in adipose tissue, and bile homeostasis were assessed after repeated dose treatment of the coagonist of GLP-1 and glucagon receptors (Aib2 C24 chimera 2, SC). Antagonists of GLP-1, glucagon, and FGF21 receptors were coadministered, and FGF21 sensitivity was determined in liver and adipose tissue. Repeated dose treatment of coagonist reduced cholesterol and increased FGF21 in blood and liver. Coagonist treatment reduced hepatic triglyceride secretion, increased lipolysis and reduced body weight. Antagonism of GLP-1 and glucagon receptors partially blocked the effect of the coagonist on lipid metabolism in circulation and liver, while FGF21 receptor antagonist completely abolished it. Glucagon and GLP-1 receptors antagonists blocked the action of coagonist on cholesterol excretion and bile flow in liver, but FGF21 antagonist was not effective. Treatment with the coagonist increased expression of FGF21, FGF21R and cofactor ßKlotho in liver and adipose. In conclusion, coagonist of GLP-1 and glucagon receptors improved lipid metabolism in liver of dyslipidemic hamsters. This effect is partially mediated by GLP-1 and glucagon receptors, and the improved FGF21 sensitivity could be the mechanism of hypolipidemic action of the coagonist of GLP-1/glucagon receptors.

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