Background: Diabetes mellitus is the leading cause of diabetic nephropathy and a major public health issue worldwide. Approximately 20-30% of patients with type 2 diabetes mellitus (T2DM) have renal impairment. Fatty acid-binding protein 1 (FABP1) is expressed in renal proximal tubule cells and released into urine in response to hypoxia caused by decreased peritubular capillary blood flow, and FABP2 is responsible for the transport of free fatty acids in the intestinal endothelium cells. There is increasing evidence that FABP1 and FABP 2 play a role in the development and progression of chronic kidney disease. The aim of this study was to investigate the relation of circulating FABP1 and FABP2 levels to nephropathy in patients with T2DM. Methods: For this study, 268 subjects with T2DM who were enrolled in a disease management program were stratified according to urinary microalbumin and serum creatinine measurements. The plasma FABP1 and FABP2 concentrations were examined by enzyme-linked immunosorbent assay. Demographic and potential metabolic confounding factors were analyzed with logistic regression to calculate the effects of FABP1 and FABP2 levels on diabetic nephropathy. Results: The FABP1 and FABP2 levels increased in parallel with the advancement of diabetic nephropathy. Increasing concentrations of FABP1 and FABP2 were independently and significantly associated with diabetic nephropathy. Multiple logistic regression analysis revealed FABP1 and FABP2 as an independent association factor for diabetic nephropathy, even after full adjustment of known biomarkers. Furthermore, receiver operating characteristic curve analysis showed that a FABP1 level of >33.8 ng/mL and a FABP2 level of >2.8 ng/mL were associated with diabetic nephropathy. Conclusion: Our results suggest that FABP1 and FABP2 may be novel biomarkers of diabetic nephropathy.
Chronic inflammation plays a pivotal role in the development of atherosclerosis, where the pro-inflammatory cytokine-induced expression of endothelial adhesion molecules and the recruitment of monocytes are the crucial events leading to its pathogenesis. Glossogyne tenuifolia ethanol extract (GTE) is shown to have potent anti-inflammatory and antioxidant activities. We evaluated the effects of GTE and its major components, luteolin (lut), luteolin-7-glucoside (lut-7-g), and oleanolic acid (OA) on TNF-α-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs). The results demonstrated that GTE, lut, and lut-7-g attenuated the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-activated HUVECs, and inhibited the adhesion of monocytes to TNF-α-activated HUVECs. The OPEN ACCESSMolecules 2015, 20 16909 TNF-α-induced mRNA expression of ICAM-1 and VCAM-1 was also suppressed, revealing their inhibitory effects at the transcriptional level. Furthermore, GTE, lut, and lut-7-g blocked the TNF-α-induced degradation of nuclear factor-κB inhibitor (IκB), an indicator of the activation of nuclear factor-κB (NF-κB). In summary, GTE and its bioactive components were effective in preventing the adhesion of monocytes to cytokine-activated endothelium by the inhibition of expression of adhesion molecules, which in turn is mediated through blocking the activation and nuclear translocation of NF-κB. The current results reveal the therapeutic potential of GTE in atherosclerosis.
Background and Aim: The occurrence of peri-procedural myocardial ischemia with endoscopic retrograde cholangiopancreatography (ERCP) has been documented, but its significance remains controversial. This study aimed to investigate the incidence and risk factors of myocardial ischemia during ERCP procedures and to analyze the potential association between myocardial ischemia and post-ERCP complications. Results: Cardiac ischemia occurred in 13 patients (18.3%) during ERCP and one patient developed myocardial infarction. More patients in the ischemic group (38.5%) than in the non-ischemic group (5.2%) had ST-T changes in pre-ERCP resting electrocardiography (P < 0.01). Hypotension during ERCP was found only in the ischemic group (15.4% vs 0%; P = 0.03). Patients with cardiac ischemia during ERCP had a significantly higher rate of elevated serum amylase and lipase levels (53.8% vs 15.5%; P < 0.01) and post-ERCP pancreatitis (30.8% vs 6.9%; P = 0.03). Multivariable logistic regression analysis revealed that cardiac ischemia during ERCP (OR: 5.21, P = 0.050) and pancreatic duct cannulation (OR: 5.7, P = 0.036) were independent predictors for post-ERCP pancreatitis. Conclusions: ST-T changes on resting electrocardiography and intra-procedural hypotension are risk factors of myocardial ischemia during ERCP. Post-ERCP hyperamylasemia, hyperlipasemia, and pancreatitis were associated with myocardial ischemia during ERCP.
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