Naringin Ameliorates Skeletal Muscle Atrophy and Improves Insulin Resistance in High-Fat-Diet-Induced Insulin Resistance in Obese Rats

Obesity causes progressive lipid accumulation and insulin resistance within muscle cells and affects skeletal muscle fibres and muscle mass that demonstrates atrophy and dysfunction. This study investigated the effects of naringin on the metabolic processes of skeletal muscle in obese rats. Male Sprague Dawley rats were divided into five groups: the control group with normal diet and the obese groups, which were induced with a high-fat diet (HFD) for the first 4 weeks and then treated with 40 mg/kg of simvastatin and 50 and 100 mg/kg of naringin from week 4 to 8. The naringin-treated group showed reduced body weight, biochemical parameters, and the mRNA expressions of protein degradation. Moreover, increased levels of antioxidant enzymes, glycogen, glucose uptake, the expression of the insulin receptor substrate 1 (IRS-1), the glucose transporter type 4 (GLUT4), and the mRNA expressions of protein synthesis led to improved muscle mass in the naringin-treated groups. The in vitro part showed the inhibitory effects of naringin on digestive enzymes related to lipid and glucose homeostasis. This study demonstrates the potential benefits of naringin as a supplement for treating muscle abnormalities in obese rats by modulating the antioxidative status, regulating protein metabolism, and improved insulin resistance in skeletal muscle of HFD-induced insulin resistance in obese rats

Chemical characterization of Passiflora edulis extracts and their in vitro antioxidant, anti-inflammatory, anti-lipid activities, and ex-vivo vasodilation effect

Passion fruit is a dietary plant with the protective proterties against many diseases such as cardiovascular diseases. The aim of this study was to explore the biological properties (anti-oxidant, anti-inflammatory, anti-lipid, and vascular relaxation) of the P. edulis extracts obtained from seed (PSEE) and fruit (PFWE). Thin-layer chromatography (TLC) and HPLC were used to analyze the phytochemical constituents in the extracts. Antioxidant and enzyme inhibition properties were examined. Anti-inflammatory activities of PFWE and PSEE were evaluated in lipopolysaccharide (LPS)-induced macrophages and ex-vivo vascular relaxation were also determined. A high contents of piceatannol and polyphenolic stilbene were found in PSEE extracts. On the other hand, beta-carotene and gamma-tocopherol were predominant in PFWE. PFWE exhibited stronger anti-oxidant activity than PSEE. Both PSEE and PFWE showed significant inhibition of lipase and cholesterol esterase activities. However, only PFWE showed minimal inhibitory effect against HMG-CoA reductase. PSEE and PFWE caused a significant reduction of nitric oxide level in LPS-induced inflammation in RAW264.7 cells. Both extracts also showed ex-vivo vasorelaxation of rat aortic rings. It has been demonstrated that PFWE and PSEE possesses anti-oxidant activity, anti-inflammatory activity, pancreatic lipase and cholesterol esterase, and ex-vivo vasorelaxation of rat aortic rings, however, the activity of HMG-CoA reductase was inhibited by only PFWE. These findings suggest the beneficial effect of PSEE and PFWE against hyperlipidemia thus preventing the development of hypertension. However, further investigations in animal are needed to elucidate

Cardiac endothelial ischemia/reperfusion injury-derived protein damage-associated molecular patterns disrupt the integrity of the endothelial barrier

Human cardiac microvascular endothelial cells (HCMECs) are sensitive to ischemia and vulnerable to damage during reperfusion. The release of damage-associated molecular patterns (DAMPs) during reperfusion induces additional tissue damage. The current study aimed to identify early protein DAMPs in human cardiac microvascular endothelial cells subjected to ischemia-reperfusion injury (IRI) using a proteomic approach and their effect on endothelial cell injury. HCMECs were subjected to 60 min of simulated ischemia and 6 h of reperfusion, which can cause lethal damage. DAMPs in the culture media were subjected to liquid chromatography-tandem mass spectrometry proteomic analysis. The cells were treated with endothelial IRI-derived DAMP medium for 24 h. Endothelial injury was assessed by measuring lactate dehydrogenase activity, morphological features, and the expression of endothelial cadherin, nitric oxide synthase (eNOS), and caveolin-1. The top two upregulated proteins, DNAJ homolog subfamily B member 11 and pyrroline-5-carboxylate reductase 2, are promising and sensitive predictors of cardiac microvascular endothelial damage. HCMECs expose to endothelial IRI-derived DAMP, the lactate dehydrogenase activity was significantly increased compared with the control group (10.15 ± 1.03 vs 17.67 ± 1.19, respectively). Following treatment with endothelial IRI-derived DAMPs, actin-filament dysregulation, and downregulation of vascular endothelial cadherin, caveolin-1, and eNOS expressions were observed, along with cell death. In conclusion, the early protein DAMPs released during cardiac microvascular endothelial IRI could serve as novel candidate biomarkers for acute myocardial IRI. Distinct features of impaired plasma membrane integrity can help identify therapeutic targets to mitigate the detrimental consequences mediated of endothelial IRI-derived DAMPs