Background and Aim: Brown adipose tissue's (BAT) ability to increase energy expenditure has become a new focus in obesity research. The amount and activity of BAT are inversely correlated with body-mass index and body fat percentage. Bone morphogenetic protein 7 (BMP7) plays a role in the differentiation and development of BAT, which can be increased by bioactive compounds from several medicinal plants. Moringa oleifera (MO) leaves are rich with vitamin, minerals, and bioactive compounds and have been used for treating obesity-related diseases in the past. The aim of this study was to explore the potency of MO leaf extract (MOLE) to modulate BAT differentiation in mice fed a high-fat diet (HFD). Materials and Methods: Twenty-four, 5-week-old male Deutsche Denken Yoken mice (Mus musculus) were randomly divided into four groups: The normal chow diet group was fed a normal diet, the HFD group was fed a HFD, the HFD+MOLE1, and the HFD+MOLE2 groups were fed HFD and MOLE in a dose of 280 and 560 mg/kg body weight (BW)/day, respectively. The experiment was performed for 7 weeks. At the end of the experiment, histological analysis was performed on the interscapular BAT, and blood was drawn for BMP7 protein levels. Results: After 7 weeks, BAT weight in the HFD group was nearly twice in the weight of the HFD+MOLE1 group (125±13.78 mg vs. 75±13.78 mg; p<0.001). There was also a significant increase in BAT cell density in the HFD+MOLE1 group. BMP7 serum protein levels were significantly higher in the HFD+MOLE1 group compared to the HFD group. Conclusion: The administration of MOLE in a dose of 280 mg/kg BW/day in HFD-mice induces BAT differentiation and proliferation by upregulating BMP7 protein levels.
Cogon grass is traditional medicine empirically used in nephritis, fever, hypertension, dyspnea, epitaxy, as a hepatoprotector agent, and has function to lower cholesterol and blood glucose. The compound of cogon grass is potentially served as an herbs medicine. But, the effect on haematology profile is still well unknown. We demonstrated the effect of cogon grass ethanol extract in mice model diabetic induced with STZ. Eight weeks old of male balb/c mice were injected intraperitoneally with STZ dose 130 mg/Kg BW. Seven days later, after DM confirmed, mice were given ethanol extract of cogon grass with dose 90 mg/KGBW (treatment group 1) and dose 115 mg/Kg BW (treatment group 2). After 14 days of extract gavage, haematology profile were estimated using the direct current detection method. We found there is no anemia occur in diabetic mice. But, the platelet and WBCs, were tend to increase in diabetic control group and treatment group 1, in contrast in treatment group 2 was tend to decrease. In conclusion, we suggested that the extract ethanol of cogon grass suppress the leukocyte and platelet count. It has potentially effect as anti-inflammatory and antiplatelet on diabetic mice.
Background. Patients with thalassemia major may suffer from complications due to iron overload. It has been suggested that several adipokines may play a potential role in the development of complications in thalassemia. Fatty acid-binding protein 4 (FABP4) is one of the adipokines, bridging several aspects of metabolic and inflammatory pathways. Little is known about the relationship between this adipokine and cardiac and liver function, especially in patients with thalassemia major. Aims. This study is aimed at determining serum FABP4 levels in patients with thalassemia major and whether its concentration correlated with serum ferritin levels, as well as cardiac and liver function. Methods. Thalassemia major outpatients ( n = 48 ) completed laboratory examination, echocardiography, and electrocardiography. Results. The mean age was 21.9 ± 8.0 years. A negative and weak correlation between serum ferritin and FABP4 was observed ( r = − 0.291 , p < 0.05 ). In addition, there was moderate and positive correlation between left atrial volume index (LAVI) and FABP4 ( r = 0.316 , p < 0.05 ). Conclusions. Serum FABP4 correlated with serum ferritin and cardiac function in patients with thalassemia major. FABP4 may be a potential clinical biomarker for cardiac dysfunction via metabolic and inflammatory pathways due to iron accumulation and toxicity in patients with thalassemia major.
Iron overload (IO) because of multiple blood transfusion as a definite therapy for hematological disease with chronic and severe anemia has become a major concern. Deleterious complication contributed by chemically reactive deregulated iron may affect cellular homeostasis systemically lead to tissue and organ damage. When this toxicity occurred in blood cells, alteration of peripheral hematological profile concerning erythrocyte, leucocyte, and platelet most likely to be modified and imperatively need to be evidenced. The experimental IO mice model was established by injecting a low and high dose of iron dextran intraperitoneally. Peripheral erythrocyte, leucocyte and platelet indices measured by hematology analyzer were analyzed. A dynamic tendency of leucocyte absolute cell number and differential cell count of low and high dose iron treatment and a significant decrease of differential monocyte count were found. In addition, high dose iron treatment showed a significantly lower mean platelet volume. In conclusion, this study verified that IO impaired the cellular hematological indices by selectively suppress monocyte number addressing that this mononuclear phagocyte was the most affected immune cell. Furthermore, low mean platelet volume following acquired platelet function defect was evidenced. This research provided an animal experimental model that could be used for further study in finding alternative therapeutic targets on the pathophysiology of iron overload diseases, such as thalassemia.
Background: Lupus Nephritis (LN) is still the most frequent complication in Systemic Lupus Erythematous (SLE) patients which causing the major and significance morbidity and mortality. Proteinuria and Glomerular Filtration Rate (GFR) serves as objective and routine examinations to assessrenal function. 24-hour proteinuria still regarded as gold standard to quantify amount protein in urine. Estimated GFR (eGFR) is preferably used due its convenient. On the hand, estimated GFR (eGFR) is preferably used due its convenient. However, both of them should be measured in order to determine renal progression and prognosis. Only few studies have been conducted to find out the correlation between 24-hour proteinuria and eGFR in lupus nephritis patients as both of them serve as potential marker in progression of renal involvement. Thisstudy addressed to find out correlation between 24-hour proteinuria and eGFR in lupus nephritis patients.Method: Analytic-correlation study with cross-sectional approach at Dr. Hasan Sadikin Hospital, Bandung was done. Secondary data was used and paralleled with previous study entitled “Correlation of Random Urine Protein Creatinine (P-C) Ratio with 24-Hour Protein Urinein Lupus Nephritis Patients” carried out from October to December 2014.Correlation coefficient was analyzed by Spearmans’ correlation test.Results: Forty five samples were obtained based on inclusion criteria. Spearmans’ correlation test revealed non significant and very weak correlation between 24-hour proteinuria and eGFR (r=-0.095) with p>0.05.Conclusion: The 24-hour proteinuria and eGFR are weakly correlated. Despite the weak correlation, these examinationsshould be considered as important markers to monitor prognosis of renal involvement in lupus nephritis patients Keywords: Estimated glomerular filtration rate (eGFR),Lupus Nephritis (LN), Proteinuria, Systemic Lupus Erythematosus (SLE).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.