Satyrium nepalense, a high altitude medicinal orchid of Indian Himalayan region : chemical profile and biological activities of tuber extracts

The present study investigated antioxidant and antibacterial activities of 5 different extracts and derived fractions from the S. nepalense tubers. Identification of the most active fractions, their phytochemical characterization, total phenolic and flavonoid contents, and biological activities were also evaluated. Petroleum ether, chloroform, ethyl acetate, methanol, water extracts and methanol fractions were screened for their antibacterial activity at 10, 50 and 100 mg/mL doses against ten Gram-negative and Gram-positive bacterial strains by disc diffusion method. Their total antioxidant activity was measured by DPPH and ABTS assays. Identification of the main compounds was performed by LC-MS/MS. Methanol extract exhibited the highest antioxidant (IC50= 30.79 \u3bcg/mL and 24.53 \u3bcg/mL for DPPH and ABTS, respectively) and antibacterial (MIC 71.5 to > 100 \u3bcg/mL) activities in comparison with the other extracts. Levels of phenolics and flavonoids were also the highest in the same extract, i.e. 19.2 mg GAE/g and 11.20 mg QE/g, respectively. Phytochemical investigation of the active fractions of the methanol extract led to the isolation of gallic acid (19.04 mg/g) and quercetin (23.4 mg/g). Therefore, methanol extract showed an interesting potential for both antioxidant and antibacterial activities, thus deserving attention for future applications in the fields of medicinal plants and food supplements

Hypoglycaemic effect of <i>Ficus arnottiana </i>Miq. bark extracts on streptozotocin induced diabetes in rats

478-482Different species of the genus Ficus Linn. such as F. bengalensis Linn., F. glomerata Roxb. and F. cunia Buch.-Ham. have been studied for their antidiabetic potential and used in folklore system of medicine for diabetes. In the present study, the effect of different extracts of F. arnottiana Miq. bark was evaluated on fasting and posts prandial blood sugar in normal and non-insulin dependent diabetes mellitus (NIDDM) rats. Diabetes was induced by streptozotocin in neonates. Oral administration of petroleum ether, chloroform, acetone and methanol extracts of the bark (100 mg/kg, p.o.) for 21 days caused a decrease in fasting blood sugar (FBS) in diabetic rats. Among all the extracts, acetone extract was found to lower the FBS significantly (PPF. arnottiana possess antidiabetic potential

Effect of an isolated active compound (Cg-1) of Cassia glauca leaf on blood glucose, lipid profile, and atherogenic index in diabetic rats

Objectives: The objective of present study was to evaluate the effect of active principle (Cg-1) from Cassia glauca leaf on serum glucose and lipid profile in normal and diabetic rats. Materials and Methods: Diabetes was induced by streptozotocin in neonates. Oral administration of petroleum ether, chloroform, acetone, and methanol of C. glauca leaf (100 mg/kg, p.o.) for 21 days caused a decrease in fasting blood glucose (FBG) in diabetic rats. Among all the extracts, acetone extract was found to lower the FBG level significantly in diabetic rats. Glibenclamide was used as standard antidiabetic drug (5 mg/kg, p.o). Acetone extract was subjected to column chromatography that led to isolation of an active principle, which was given trivial name Cg-1. Cg-1 (50 mg/kg, p.o.) was studied for its hypoglycemic and hypolipidemic potential. The unpaired t-test and analysis of variance (ANOVA) followed by post hoc test was used for statistical analysis. Results: Cg-1 caused a significant reduction in FBG level. It also caused reduction in cholesterol, triglycerides, and LDL levels and improvement in the atherogenic index and HDL level in diabetic rats. Conclusion: Improvement in the FBG and the atherogenic index by Cg-1 indicates that Cg-1 has cardioprotective potential along with antidiabetic activity and provides a scientific rationale for the use as an antidiabetic agent

Temporal lipid profiling in the progression from acute to chronic heart failure in mice and ischemic human hearts

Background and aims: Myocardial infarction (MI) is a leading cause of heart failure (HF). After MI, lipids undergo several phasic changes implicated in cardiac repair if inflammation resolves on time. However, if inflammation continues, that leads to end stage HF progression and development. Numerous studies have analyzed the traditional risk factors; however, temporal lipidomics data for human and animal models are limited. Thus, we aimed to obtain sequential lipid profiling from acute to chronic HF. Methods: Here, we report the comprehensive lipidome of the hearts from diseased and healthy subjects. To induce heart failure in mice, we used a non-reperfused model of coronary ligation, and MI was confirmed by echo-cardiography and histology, then temporal kinetics of lipids in different tissues (heart, spleen, kidney), and plasma was quantitated from heart failure mice and compared with naive controls. For lipid analysis in mouse and human samples, untargeted liquid chromatography-linear trap quadrupole orbitrap mass spectrometry (LC-LTQ-Orbitrap MS) was performed. Results: In humans, multivariate analysis revealed distinct cardiac lipid profiles between healthy and ischemic subjects, with 16 lipid species significantly downregulated by 5-fold, mainly phosphatidylethanolamines (PE), in the ischemic heart. In contrast, PE levels were markedly increased in mouse tissues and plasma in chronic MI, indicating possible cardiac remodeling. Further, fold change analysis revealed site-specific lipid biomarkers for acute and chronic HF. A significant decrease in sulfatides (SHexCer (34:1; 2O)) and sphingomyelins (SM (d18:1/ 16:0)) was observed in mouse tissues and plasma in chronic HF. Conclusions: Overall, a significant decreased lipidome in human ischemic LV and differential lipid metabolites in the transition of acute to chronic HF with inter-organ communication could provide novel insights into targeting integrative pathways for the early diagnosis or development of novel therapeutics to delay/prevent HF

Sphingosine-1-phosphate interactions in the spleen and heart reflect extent of cardiac repair in mice and failing human hearts

Sphingosine-1-phosphate (S1P) is a bioactive mediator in inflammation. Dysregulated S1P is demonstrated as a cause of heart failure (HF). However, the time-dependent and integrative role of S1P interaction with receptors in HF is unclear after myocardial infarction (MI). In this study, the sphingolipid mediators were quantified in ischemic human hearts. We also measured the time kinetics of these mediators post-MI in murine spleen and heart as an integrative approach to understand the interaction of S1P and respective S1P receptors in the transition of acute (AHF) to chronic HF (CHF). Risk-free 8-12 wk male C57BL/6 mice were subjected to MI surgery, and MI was confirmed by echocardiography and histology. Mass spectrometry was used to quantify sphingolipids in plasma, infarcted heart, spleen of mice, and ischemic and healthy human heart. The physiological cardiac repair was observed in mice with a notable increase of S1P quantity (pmol/g) in the heart and spleen significantly reduced in patients with ischemic HF. The circulating murine S1P levels were increased during AHF and CHF despite lowered substrate in CHF. The S1PR1 receptor expression was observed to coincide with the respective S1P quantity in mice and human hearts. Furthermore, selective S1P1 agonist limited inflammatory markers CCL2 and TNF-alpha and accelerated reparative markers ARG-1 and YM-1 in macrophages in the presence of Kdo2-Lipid A (KLA; potent inflammatory stimulant). This report demonstrated the importance of S1P/S1PR1 signaling in physiological inflammation during cardiac repair in mice. Alteration in these axes may serve as the signs of pathological remodeling in patients with ischemia. NEW & NOTEWORTHY Previous studies indicate that sphingosine-1-phosphate (S1P) has some role in cardiovascular disease. This study adds quantitative and integrative systems-based approaches that are necessary for discovery and bedside translation. Here, we quantitated sphinganine, sphingosine, sphingosine-1-phosphate (S1P) in mice and human cardiac pathobiology. Interorgan S1P quantity and respective systems-based receptor activation suggest cardiac repair after myocardial infarction. Thus, S1P serves as a therapeutic target for cardiac protection in clinical translation

Temporal lipid profiling in the progression from acute to chronic heart failure in mice and ischemic human hearts

Background and aims: Myocardial infarction (MI) is a leading cause of heart failure (HF). After MI, lipids undergo several phasic changes implicated in cardiac repair if inflammation resolves on time. However, if inflammation continues, that leads to end stage HF progression and development. Numerous studies have analyzed the traditional risk factors; however, temporal lipidomics data for human and animal models are limited. Thus, we aimed to obtain sequential lipid profiling from acute to chronic HF. Methods: Here, we report the comprehensive lipidome of the hearts from diseased and healthy subjects. To induce heart failure in mice, we used a non-reperfused model of coronary ligation, and MI was confirmed by echo-cardiography and histology, then temporal kinetics of lipids in different tissues (heart, spleen, kidney), and plasma was quantitated from heart failure mice and compared with naive controls. For lipid analysis in mouse and human samples, untargeted liquid chromatography-linear trap quadrupole orbitrap mass spectrometry (LC-LTQ-Orbitrap MS) was performed. Results: In humans, multivariate analysis revealed distinct cardiac lipid profiles between healthy and ischemic subjects, with 16 lipid species significantly downregulated by 5-fold, mainly phosphatidylethanolamines (PE), in the ischemic heart. In contrast, PE levels were markedly increased in mouse tissues and plasma in chronic MI, indicating possible cardiac remodeling. Further, fold change analysis revealed site-specific lipid biomarkers for acute and chronic HF. A significant decrease in sulfatides (SHexCer (34:1; 2O)) and sphingomyelins (SM (d18:1/ 16:0)) was observed in mouse tissues and plasma in chronic HF. Conclusions: Overall, a significant decreased lipidome in human ischemic LV and differential lipid metabolites in the transition of acute to chronic HF with inter-organ communication could provide novel insights into targeting integrative pathways for the early diagnosis or development of novel therapeutics to delay/prevent HF