ABSTRACT
Aim Carvacrol ( CAR ) , possesses a wide variety of pharmacological properties including antioxi-dant and anti-inflammatory potential. The present stud-y is designed to investigate the effect of CAR on glu-cose and lipid metabolism in type 1 diabetic mice. Methods Diabetes was induced by intraperitoneal( i. p) injection of streptozotocin into male mice at the dose of 45 mg·kg-1 body weight( BW) . Mice were divided into three different groups containing eight to twelve in each. Age matched male C57 mice were used as nor-mal controls. Group I diabetes, Group Ⅱ and Ⅱ in-jected with CAR at 10 and 20 mg · kg-1 BW respec-tively once daily. After CAR injection 2, 4 or 6 weeks, the rats were weighted and the plasma concen-trations of glucose, total cholesterol( TC) , triglycerides (TG), Glutamic oxalacetic transaminase(AST), Ala-nine transaminase( ALT) levels were enzymatically de-termined using commercial kits. Results STZ-induced C57 BL/6 J diabetic mice showed an elevation in serum glucose, TG, ALT, AST and LDH levels. Compared to diabetic mice, administration of CAR resulted in sig-nificant decreases(P <0. 05) in plasma glucose, TG and LDH levels in a dose dependent manner, but no effect on elevated TC, ALT and AST levels. Conclu-sion These major findings provide evidence that CAR has anti diabetic property and it has the potential for development into a drug to prevent hyperglycemia, re-duce blood lipids and protect the dammaged organs.
ABSTRACT
Aim To study the effect of activating Sonic hedgehog( Shh) pathway on the function of endothelial progenitor cells ( EPCs ) in type 1 diabetic mice. Methods EPCs were isolated and cultured by density gradient method from diabetic mice. The effects of Shh N-terminal peptide and agonist SAG on EPCs prolifera-tion were evaluated by using the MTT colorimetric as-say. EPCs migration was measured by Transwell meth-od. EPCs tube formation ability was estimated by Matrigel . EPCs senescence activity was determined by β-galactosidase staining. Results Compared with control mice, the function of EPCs in type 1 diabetic mice was impaired. The proliferation, migration and tube formation of diabetic EPCs could be promoted by Shh peptide and agonist SAG. The senescence of dia-betic EPCs could be decreased by Shh peptide and ag-onist SAG. Conclusion Activating Shh signaling pathway can improve the impared function of diabetic EPCs in type 1 diabetic mice.
ABSTRACT
AIM:ToinvestigatetheprotectiveeffectofquercetinonangiotensinⅡ(AngⅡ)-inducedcardio-myocyte hypertrophy and its possible mechanism .METHODS: Cardiomyocyte hypertrophy was induced by AngⅡ ( 100 nmol/L) in primary neonatal cardiomyocytes and H 9c2 cells.The cells were treated with different concentration of querce-tin (10 μmol/L, 20 μmol/L and 40 μmol/L) for 48 h and then the cardiomyocyte surface areas were measured by immu-nofluorescence .Proteasome activity was detected by fluorescent peptide substrate .The phosphorylated levels of GSK-3α/βand Akt in H9c2 cells were determined by Western blot .RESULTS:Compared with control group , the cardiomyocyte sur-face areas were both increased in primary cultured neonatal cardiomyocytes and H 9c2 cells, while the surface areas were significantly decreased by quercetin , especially at concentration of 20 μmol/L compared with Ang Ⅱgroup (P<0.05). Compared with control group , the chymotrypsin-like, trypsin-like and caspase-like activities of proteasome were all in-creased in H9c2 cells (P<0.05).The trypsin-like and caspase-like activities of proteasome were inhibited by 20 μmol/L and 40 μmol/L quercetin , while chymotrypsin-like activity was inhibited only at 20 μmol/L of quercetin compared with AngⅡgroup (P<0.05).In addition, phosphorylated levels of GSK-3α-Ser21, GSK-3β-Ser9 and Akt-Ser473 in AngⅡgroup were all increased compared with control group , which were obviously inhibited by in 20 μmol/L and 40 μmol/L quercetin ( P<0.05 ) .CONCLUSION: Quercetin decreases cardiomyocyte hypertrophy through proteasome inhibition , which may be related to the inhibition of Akt and therefore increasing activation of GSK -3α/βin H9c2 cells.
ABSTRACT
Aim To investigate the role of physiological concentration of glucocorticoids on the inflammation mediator IL-6 expression in response to LPS in rat alveolar epithelial cells(CCL149).Methods The CCL149 were treated with LPS,H2O2 and glucocorticoid respectively.Flammtory mediator IL-6 protein expression was measured with ELISA,and the activity of histone deacetylase(HDAC) was measured using colorimetric HDAC activity assay kit.Results IL-6 protein levels were increased in cells exposed to 10 mg?L-1 LPS.Hydrocortisone decreased IL-6 protein expression induced by LPS.Such effect of hydrocortisone was blunt by HDAC inhibitor trichostatinA treatment(10 ?g?L-1).LPS decreased HDAC activity.Hydrocortisone increased HDAC activity.The expression of IL-6 protein induced by LPS was further enhanced by H2O2 treatment.Pretreatment with H2O2 resulted in the inhibition of antiflammtion effect of glucocorticoids.Conclusion Physiological concentration of glucocorticoids could suppress inflammatory response,and this effects requires recruitment of HDAC.Oxidants such as H2O2 may cause the failure of glucocorticoids to function effectively,and the reason may be related to the reduction of HDAC activity.This mechanism may contribute to the pathogenesis of pulmonary disorder.
ABSTRACT
AIM To explore the inhibitory effects of simv astatin on ROS generation and cardiac myocytes hypertrophy induced by ET-1. METHODS The study was performed with primary cultured neonatal rat cardiac myocytes. Intrace llular fluorescence signal was assayed by fluorescence convert microscope. The l evel of intracellular ROS was measured by the ROS-specific probe 2′, 7′-dich lorofluorescin diacetate (DCF-DA). The RNA content was determined by RNA-sensitive fluoresce nce probe propidium iodide (PI) and the total protein of cell was measured by th e methods of coomassie brilliant blue. The cell surface area was measured by ima ge analysis program. RESULTS ①Fluorescence intensity of intracel lular DCF-DA and myocyte hypertrophy increased by ET-1 in dose-dependent mann er. Antioxidant catalase(0 2 U?L -1 ) attenuated the ET-1-induced incre ase of fluorescence intensity of intracellular DCF-DA and myocyte hypertrophy.②Simvastatin inhibited the increase of fluorescence intensity of intracellular DCF-DA and cardiac myocyte hypertrophy induced by ET-1(10 -8 mol?L -1 )in a dose-dependent manner. CONCLUSION ET-1 increases int racellular ROS in the cultured neonatal rat cardiac myocytes. Simvastatin inhibi ted the generation of ET-1-induced ROS and cardiomyocytes hypertrophy.
ABSTRACT
Objective To study the value of three dimensional dynamic contrast and digital subtraction MRI in diagnosing breast cancer.Methods 52 patients with breast diseases were enrolled in this study,including 27 malignant lesions and 36 benign lesions verified by histopathology.the morphologic features and enhancement kinetics of breast lesion on MRI were observed.The morphologic manifestation,early-phase enhancement rate,peak enhancement rate,peak time and time-signal intensity curve were evaluated.Results The benign lesions were mainly characterized by regular mass,well-defined border,internal septation,homogeneous enhancement,and the malignant lesions by irregular shape,speculated margin,rim enhancement,inhomogeneous enhancement.The early-phase enhancement rate,peak time and curve type were significantly different between breast benign and malignant lesions(P
ABSTRACT
AIM To examine whether pretreatment with simvastatin protects the heart against free radical injury. METHODS 1 1 diphenyl 2 picryl hydrazyl (DPPH) was used for triggering free radical injury in cardiac tissue. Simvastatin against free radical injury was investigated in a Langendorff fused rat heart. Left ventricular developed pressure (LVDP), maximal velocity of increase of LVP (+d p /d t max ), heart rate (HR) coronary flow (CF) and malondialdehyde (MDA) formation in cardiac tissue were measured. RESULT In the DPPH free radical group, DPPH signficantly decreased LVDP, +d p /d t max , HR was slowed and CF was reduced. The formation of MDA was significantly enhanced. ( P