ObjectiveTo observe the effect of exercise on expression of protein kinase B (PKB) in adipose tissue of insulin resistant rats fed by high fat diet.Methods30 male Wistar rats were randomly divided into the control group (n=10),given basic diet; the model group (n=20), given fat diet. After 4 weeks, the model group was randomly divided into 2 subgroups, the insulin resistant group was continually given high fat diet, the exercise treated group accepted high fat food and swimming training. After 6 week intervention, the expression of PKB stimulated by insulin in adipose tissue was determined with Western blotting at the end of experiment.ResultsAfter long term high fat diet, expression of PKB in adipose tissue of the insulin resistant group decreased by 23.5% comparing with the control group (P<0.01). After 6 weeks swimming training, the expression of PKB of the exercise treated group was increased by 19.2% comparing with the insulin resistant group (P<0.01).ConclusionExercise treatment can significantly elevate the expression of PKB and ameliorate the state of insulin resistance.

Objective To investigate the effects of exercise training(ET)on the expression of glucogen synthase kinase 3 bate(GSK 3?)in the adipose tissues of insulin resistant(IR)rats on a high fat diet(HFD). Methods Thirty male Wistar rats were randomly divided into a control group(n=10)and a model group(M group,n=20).Insulin resistance was established by feeding a HFD to the M group for 4 w,while rats in the control group were fed a normal diet.The IR rats were then randomly divided into two subgroups:an IR group and an ET group.All rats in the IR and ET groups were fed a HFD,but ET was administrated to the ET group for 6w.The expres- sion of GSK 3?protein in the rats'epididymis adipose tissue was detected using Western blotting,and body weight (BW),the concentrations of serum triglyceride and cholesterol(TG and TC),fasting plasma glucose(FPG)and serum insulin(FINS),as well as insulin sensitivity index(ISI)were regularly detected.Results Compared with the con- trol group,BW and the concentrations of serum TG and TC,FPG and FINS in the model group were significantly in- creased(P＜0.05),while ISI was decreased(P＜0.01).Compared with the control group,there was no difference in GSK 3 protein expression in the ET group,but the expression of GSK 3?protein in the ET group was obviously de- creased in comparison with that in the IR group(P＜0.05).Conclusion ET can ameliorate IR by decreasing GSK 3?protein expression in adipose tissues and enhancing the ingestion of glucose and the synthesis of glycogen.

OBJECTIVETo observe the preventive effect of Radix Paeoniae Rubra (RPR) to restenosis after carotid balloon injury in rabbits.

METHODSThe rabbit model of carotid balloon injury was established adopting Clowes method, and treated with extract of RPR. Component of new genesic intima and expression of proliferating cell nuclear antigen (PCNA) and macrophage was determined by immunochemical stain. The collagen of type I was detected by special staining for blood vessels and the area of new genesic intima was measured by image assay system.

RESULTSRPR could remarkably decreased the PCNA positive expression and inhibit the proliferation of collagen type I and reduce the generating of new intima.

CONCLUSIONRPR has significant preventive effect on the restenosis after carotid ballon injury in high fat-diet induced atherosclerotic rabbits.

Angioplasty, Balloon ; adverse effects ; Animals ; Arteriosclerosis ; etiology ; pathology ; therapy ; Carotid Artery Injuries ; etiology ; Carotid Artery, Common ; pathology ; Carotid Stenosis ; etiology ; pathology ; therapy ; Drugs, Chinese Herbal ; pharmacology ; Hypercholesterolemia ; complications ; Muscle, Smooth, Vascular ; pathology ; Paeonia ; Proliferating Cell Nuclear Antigen ; metabolism ; Rabbits ; Secondary Prevention

OBJECTIVETo explore the dynamic changes of transforming growth factor-α (TGF-α) and transforming growth factor-β1 (TGF-β1) of liver cirrhosis induced by multiple pathogenic factors in rats.

METHODSAnimals in the cirrhosis group were fed a mixture of maize flour, lard, cholesterol and alcohol plus subcutaneously injection with carbon tetrachloride (CCl₄), the CCl₄(0.5 ml/100 g · w) was injected at the first day of experiment and the 40% CCl₄oil solution (0.3 ml /100 g · w) was injected at an interval of three days. The thirty-six male SD rats were randomly divided into liver cirrhosis group of the 4th, 6th and 8 th week, and normal control group of the 4th, 6th and 8th week. The contents of alanine transferase (ALT), endotoxin, tumor necrosis factor-α (TNF-α) and homocysteine (Hcy) in plasma were evaluated. Histopathological changes of the liver were observed under microscope with the staining of HE. The expressions of TGF-α and TGF-β1 were analyzed by the method of immunohistochemistry.

RESULTSCompared with the corresponding normal control group, the levels of ALT, endotoxin, TNF-α and Hcy in plasma were gradually significantly increased in liver cirrhosis group of the 4th, 6th and 8th week (P < 0.05); the expression of TGF-α in the liver tissues was significantly increased at the 4th week (P < 0.05); the expression of TGF-β1 in the liver tissues was gradually significantly increased in every model group (P < 0.05).

CONCLUSIONIn the formation process of cirrhosis, the expression of TGF-α was increased in liver of cirrhosis group at the 4th week, and later it was suppressed; the expression of TGF-β1 was continuously increased. The characteristic dynamic changes of TGF-α and TGF-β1 might be related to sustained endotoxemia, the high level of TNF-α and hyperhomocysteinemia.

Alanine Transaminase ; blood ; Animals ; Carbon Tetrachloride ; Endotoxins ; blood ; Homocysteine ; blood ; Liver Cirrhosis ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor alpha ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Tumor Necrosis Factor-alpha ; blood ; metabolism

Acetaminophen (APAP, also known as paracetamol)-induced liver injury is the leading cause of drug-induced liver injury in the world. Wuzhi Tablet (WZ, an ethanol extract of Schisandra sphenanthera) is widely used in clinical practice to protect liver function. Our previous studies have shown that pretreatment with WZ for 3 days can significantly protect against APAP-induced liver injury; however, the effect of different intervals between APAP and WZ treatment on APAP-induced liver injury remains unclear. In this study, the change in liver injury indexes, APAP metabolites, and the activity of cytochrome P450 (CYP450) enzymes after treatment with WZ and APAP at different intervals were determined. The animal experiment was reviewed and approved by the Animal Ethics Committee of Sun Yat-sen University. The results show that 0 h, 0.5 h, and 2 h pretreatment with WZ significantly protected against APAP-induced liver injury in mice, as evidenced by a significant decrease in biochemical parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malonaldehyde (MDA). WZ inhibited the metabolic activation of APAP mediated by CYP450 enzymes and reduced the formation of APAP metabolites. This study further demonstrates that pretreatment with WZ at different intervals (0 h, 0.5 h, and 2 h before APAP dosing) exerts a significant hepatoprotective effect against APAP-induced liver injury, and a single-dose of WZ inhibits the activity of CYP450 enzymes related to APAP metabolic activation, thereby protecting against APAP-induced hepatotoxicity.

Pregnane X receptor (PXR), a member of nuclear receptor superfamily, plays an important role in xenobiotic and endogenous metabolism, endocrine balance, and cell proliferation, etc. Previous study has shown that pregnenolone 16α-carbonitrile (PCN), a mouse PXR agonist, could induce liver enlargement. And we found that the change in hepatocytes exhibits regional distribution characteristics: hepatocyte enlargement occurs around the central vein (CV) area, while hepatocyte proliferation occurs around the portal vein (PV) area. In this study, the dynamic changes of hepatocytes during PXR-induced liver enlargement were determined. Serum and liver samples from male C57BL/6 mice were collected for biochemical and pathological analysis after PCN treatment for 1, 2, 3, 5 days, respectively. The animal experiment was approved by the Animal Ethics Committee of Sun Yat-Sen University. The results showed that with the increase in the PCN treatment days, the feature of this regional change of hepatocyte around the CV and PV areas became more and more obvious. At the same time, the factors related to hepatocyte enlargement, such as the expression of PXR downstream genes and the hepatic content of triglyceride (TG), has gradually increased. The upregulation of proliferation-related proteins and downregulation of cyclin-dependent kinases inhibitor proteins were observed in the early stage of PCN treatment, suggesting that hepatocyte proliferation occurs earlier than hepatocyte enlargement during PXR-induced liver enlargement. This study reveals the dynamic change of hepatocytes during PXR-induced liver enlargement and provides a new insight in liver enlargement promoted via PXR activation.

OBJECTIVETo examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats, and explore the role of p53 and bax in this process.

METHODSWe examined the effect of IPC on delayed neuron death, neuron apoptosis, expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining, flow cytometry, RT-PCR, and immunohistochemistry technique.

RESULTSIPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216 +/- 9 cells/0.72 mm2 vs. 30 +/- 5 cells/0.72 mm2, P < 0.01) , decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06% +/- 0.21% vs. 4.27% +/- 0.08%, P < 0.01 ), and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC.

CONCLUSIONIPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ischemia/reperfusion, and this process may be related to the reduced expressions of p53 and bax.

Animals ; Gene Expression Regulation ; Genes, p53 ; Hippocampus ; injuries ; Ischemic Preconditioning ; methods ; Neurons ; physiology ; Rats ; Reperfusion Injury ; prevention & control ; Tumor Suppressor Protein p53 ; antagonists & inhibitors ; genetics ; bcl-2-Associated X Protein ; antagonists & inhibitors ; genetics

OBJECTIVETo explore the effect of puerarin injection on the amount of GLUT4 protein at the plasma membrane in insulin-resistant rat skeletal muscle.

METHODThe rat model of insulin resistance (IR) was made by being fed with high-fat diet. The animals were divided into three groups (ten in each group): group I: controls; group II: Insulin-resistant rats; group III: Insulin-resistant rats + Puerarin treatment. Insulin-resistant rats were injected with 100 mg puerarin injection per kg body weight through abdominal cavity once a day for 4 weeks. Fasting blood glucose and fasting serum insulin levels were measured before and after Puerarin treatment, respectively. Insulin treatment was achieved by intraperitoneal injection of insulin (1 unit insulin per kg body weight.) 15 minute before killing the animals. The right hindlimb skeletal muscle was rapidly dissected. Then the expression of GLUT4 protein at the plasma membrane in all the animals was assessed with Western blot method.

RESULTThe GLUT4 content at the plasma membrane in insulin-resistant rats skeletal muscle was significantly lower (about 31%) than that of controls (P < 0.01). Puerarin Injection partly corrected fasting blood glucose (from 6.17 +/- 0.67 mmol x L(-1) to 5.54 +/- 0.35 mmol x L(-1)) and fasting serum insulin levels (from 17.09 +/- 2.02 mU x L(-1) to 11.86 +/- 1.35 mU x L(-1)) and increased the GLUT4 content at the plasma membrane by 1.18-fold in insulin-resistant rats skeletal muscle.

CONCLUSIONPuerarin Injection can ameliorate IR, and the mechanism may be involved in increasing cell-surface level of GLUT4 through decreasing fasting blood glucose and fasting serum insulin levels, improving GLUT4 trafficking and intracellular insulin signaling.

Animals ; Cell Membrane ; metabolism ; Glucose Transporter Type 4 ; Injections ; Insulin Resistance ; Isoflavones ; administration & dosage ; isolation & purification ; pharmacology ; Male ; Monosaccharide Transport Proteins ; metabolism ; Muscle Proteins ; metabolism ; Muscle, Skeletal ; metabolism ; pathology ; Plants, Medicinal ; chemistry ; Pueraria ; chemistry ; Rats ; Rats, Sprague-Dawley

OBJECTIVEGas chromatography (GC) was used to investigate the cellular fatty acid (CFA) composition of 141 Acinetobacter baumannii and 32 A. calcoaceticus isolates from different locations in China and to find chemical markers to differentiate these two closely related bacteria.

METHODSWhole cell fatty acid methyl esters (FAMEs) were obtained by saponification, methylation, and extraction for GC analysis, followed by a standardized Microbial Identification System (MIS) analysis.

RESULTSAll A. baumannii and A. calcoaceticus strains contained some major fatty acids, namely, 18:1 ω9c, 16:0, Sum In Feature 3, 12:0, 17:1ω8c, 3-OH-12:0, 17:0, Sum In Feature 2, 2-OH-12:0, and 18:0 compounds. Although most of the total CFAs are similar between A. baumannii and A. calcoaceticus strains, the ratios of two pairs of CFAs, i.e., Sum In Feature 3/18:1 ω9c versus 16:0/18:1 ω9c and Sum In Feature 3/18:1 ω9c versus unknown 12.484/18:1 ω9c fatty acids, could differentiate these two closely related bacteria. A. baumannii could be easily classified into two subgroups by plotting some ratios such as Sum In Feature 3/16:0 versus 17:0 and Sum In Feature 3/2-OH-12:0 versus 17:0 fatty acids.

CONCLUSIONThe ratios of some CFAs could be used as chemical markers to distinguish A. baumannii from A. calcoaceticus.

Acinetobacter baumannii ; classification ; cytology ; metabolism ; Acinetobacter calcoaceticus ; classification ; cytology ; metabolism ; Biomarkers ; metabolism ; Fatty Acids ; metabolism ; Species Specificity

In this study, hydrophilic matrix sustained release tablets of total lactones from Andrographis paniculata were prepared and the in vitro release behavior were also evaluated. The optimal prescription was achieved by studying the main factor of the type and amount of hydroxypropyl methylcellulose (HPMC) using single factor test and evaluating through cumulative release of three lactones. No burst drug release from the obtained matrix tablets was observed. Drug release sustained to 14 h. The release mechanism of three lactones from A. paniculata was accessed by zero-order, first-order, Higuchi and Peppas equation. The release behavior of total lactones from A. paniculata was better agreed with Higuchi model and the drug release from the tablets was controlled by degradation of the matrix. The preparation of hydrophilic matrix sustained release tablets of total lactones from A. paniculata with good performance of drug release was simple.
Andrographis ; chemistry ; Delayed-Action Preparations ; chemistry ; Drug Compounding ; methods ; Drugs, Chinese Herbal ; chemistry ; Hydrophobic and Hydrophilic Interactions ; Kinetics ; Lactones ; chemistry ; Tablets ; chemistry