ObjectiveToestablisharatmodelofatherosclerosiscombinedwithsyndromeofintermingledphlegm and blood stasis , to observe the inflammatory reactions and the treatment effect of prescription ( Danlou tablet ) on the rat model.Methods Thirty-two healthy male SD rats were randomly and equally divided into four groups , namely, normal control group, model control group, atorvastatin group (ATV group), and Danlou group (DLP group).The normal control group was given basic forage , while other three groups were given high fat forage plus intraperitoneal injection of vitamin D 3 and balloon injury of the left common carotid artery to build rat atherosclerosis model combined with syndrome of intermingled phlegm and blood stasis , and then received intragastric administration of saline , atorvastatin suspension and Danlou tablets suspension for 4 weeks, respectively.After intervention, both serum lipid and hs-CRP, IL-6, TNF-α, and LP-PLA2 levels were determined by ELISA , pathological alterations in the thoracic aorta was analyzed using HE staining , the expressions of IL-6, TNF-αand LP-PLA2 mRNA in the thoracic aorta tissue were assessed by real-time fluorescent quantitativePCRtechnology.Results ①Comparedwiththenormalcontrolgroup,thereweresignificantincreasesin serum TC, LDL-C, hs-CRP, IL-6, TNF-α, and LP-PLA2 levels (P<0.05 for all) and decrease of serum HDL-C levels in the model group (P<0.05).The expressions of IL-6, TNF-α, and LP-PLA2 mRNA in the rat aorta were significantly increased ( P<0.05 for all ) .In the model control group , HE staining showed altered arrangement of aortic endothelial cells, irregular intimal thickening , broadened subendothelial space , and accumulation of foam cells and lipid deposition , forming typical atherosclerotic plaques .② Compared with the model control group , the ATV and DLP groups showed significantly decreased serum TC , LDL-C, hs-CRP, IL-6, TNF-α, and LP-PLA2 levels ( P<0.05 for all) as well as the expressions of IL-6, TNF-α, and LP-PLA2 mRNA in the thoracic aorta (P<0.05 for all).There were no significant differences between the ATV and DLP groups (P>0.05).There were also reduced aortic intimal hyperplasia , macrophage infiltration and plaque area compared with those of the model group .Conclusions Rat model of atherosclerosis combined with syndrome of intermingled phlegm and blood stasis can be established by high fat diet feeding combined with the intraperitoneal injection of vitamin D 3 and balloon injury of carotid artery .The prescription ( Danlou tablet ) can inhibit the inflammatory reaction and ameliorate atherosclerotic changes in the rat models .

0.05),while there were significant differences in VEGF mRNA expression among the rest of groups(P

Objective To explore the therapeutic effect and application value of retroperitoneal laparoscopic combined with resectoscopic radical nephroureterectomy for upper tract urothelial carcinoma Methods From Jan.2006 to Jul.2009,fifteen upper tract urothelial carcinoma patients underwent excision of bladder cuff with resectoscope at first,and then retroperitoneal laparoscopic radical nephroureterectomy.All tumors were confirmed to be localized,stage T1-T3.Clinical outcomes of the patients were retrospectively analyzed.Results Mean operative time was 150 (range:120-180) minutes and blood loss volume was 200 (range:100-400)ml.The function of intestinal canal recovered after 24-48 hours,the drainage tube could be removed after 3-4 days.Catheter was kept for 7-10 days.During the follow up for 1-40 months,all the 15 patients survived with one retroperitoneal lymphatic metastasis.There were no severe complications in perioperative and postoperative period.Conclusions Retroperitoneal laparoscopic combined with resectoscopic radical nephroureterectomy may be a practical surgical procedure for upper tract urothelial carcinoma patients with less intraoperative blood loss and early recovery.

Aim To investigate the effects of maternal chronic aluminum exposure on memorial behaviour and hippocampal intracellular Ca2+ concentration ([Ca2+]i)on their offspring after the induction of LTP(long-term potentiation). Methods Adult Wistar rats (150~200 g) were exposed to aluminum by drinking distilled water, the concentration of AlCl3 is 0.015 mol?L-1(2 g?L-1) and 0.03 mol?L-1(4 g?L-1) aluminum chloride (AlCl3) solution, respectively, for 30 days prior to mating and during the whole gestation and suckling period. Their offspring were distributed into three experimental groups: control group; two exposed groups (represented by 0.2%-Al and 0.4%-Al ) administrated aluminum exposure ended at postnatal day 21. The brain tissue and blood aluminum levels were measured by Atomic absorption spectrometry (AAS). Memorial ability of the offspring was tested by Step down test.[Ca2+]i was measured by the technique of Fura-2/AM calcium ions fluorescence indicator. Results The mean aluminum content in blood and brain tissue was significantly higher than the control group(P0.05), but was significantly decreased in 0.4%-Al exposed group(P

OBJECTIVETo evaluate the protective effects of punicosides on alcohol induced acute liver injury in mice and its possible mechanisms as well.

METHODThe 60 mice were randomly divided into normal control, model group, three dose groups of punicosides with low, medium and high, then there is silibinin group. Three dose groups of punicosides and silibinin were given in advance by gavage for 4 weeks, then the mouse model of alcoholic acute liver injury was established. The serum levels of ALT, AST and TG were determined, and the mice were killed to calculate somatic index of liver, thymus as well as spleen. MDA, SOD, GSH-Px and GSH-ST were detected in the liver homogenate. Histopathological changes of the liver were observed by HE staining. The expression of MCP-1 and NF-kappaB in the liver tissues were detected by immunohistochemistry.

RESULTMid and high dose of punicosides reduced the liver index in mice significantly, improved liver steatosis, decreased the level of ALT, AST and TG in serum and the content of MDA in liver homogenate, furthermore the two dose groups increased the activity of SOD, GSH-Px and GSH-ST, inhibited the expression of MCP-1 and NF-kappaB in liver tissue.

CONCLUSIONPunicosides can protect the acute liver damage induced by alcohol.

Alcohols ; adverse effects ; Animals ; Chemical and Drug Induced Liver Injury ; blood ; drug therapy ; metabolism ; pathology ; Chemokine CCL2 ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Gene Expression Regulation ; drug effects ; Liver ; drug effects ; enzymology ; pathology ; Male ; Malondialdehyde ; metabolism ; Mice ; NF-kappa B ; metabolism

Biopsy ; Humans ; Kidney ; pathology ; Staining and Labeling ; methods

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.

ObjectiveTo investigate the protein wasting and energy reserve in chronic renal failure (CRF) patients undergoing maintaining hemodialysis (HD) at different ages.MethodsA total of 129 CRF patients (62 men and 67 women) aged (56.33 ± 14.14) years on HD were enrolled in this study.They were divided into four age groups:below 40,40-69,60-69,and over 70 years.Nutritional status was assessed by body mass index (BMI),normalized protein catabolic rate (nPCR),and biochemical parameters including pre-albumin,cholesterol,and creatinine.Body composition was tested with multi-frequency bioelectric impedance analysis.Meanwhile,83 healthy subjects,matched for age and sex,were enrolled as controls.ResultsBMI showed no significant difference between healthy controls and HD patients.Among HD patients,38％ had an BMI higher than the normal high limit and 6.2％ had a BMI less than 18.5kg/m2 ; patients with a low body weight accounted for 0,6.2％,4.8％,and 11.1％ in the ＜40 years group,40-59 years group,60-69 years group,and above 70 years groups,respectively.nPCR in the above 70 years group was ( 1.46 ±0.28) g/( kg·d),which was significantly lower than that in the 40-59 years group [ (1.54 ±0.28) g/( kg·d) ; P =0.004) ; the serum creatinine in the the above 70 years group was (834.08 ± 184.96) μmol/L,which was significantly lower than that in 40-59 years group [ (976.24 ± 186.86) μmol/l ] ( P=0.037) ; the prealbumin in the the above 70 years group was (272.65 ±79.78) mg/L,which was significantly lower than that in 40-59 year group [ (332.07 ± 73.03 ) mg/L] ( P =0.026).Body cell mass in HD patients was (22.81 ±8.12) kg,which was significantly lower than that in the control group [ (29.95 ±6.73) kg] (P＜0.001) ; furthermore,the lean tissue mass (LTM) [ (40.16±11.90) kg vs.(47.22 ±9.84) kg] and fat [ (17.45± 8.83)vs.(13.66±7.28) kg] were also significantly lower (both P=0.001 ).The lean tissue indicators in the below 40 years group were also significantly lower than those in the healthy controls ( P =0.012).For the fat tissue ingredients,the below 40 years group ( P =0.013 ) and over 70 years group (P =0.039) showed significant differences with the controls,while the 60-69 years group (P =0.191 ) showed no such difference.ConclusionsNutritional status is different among HD patients at different ages.HD patients below 40 years and abover 70 years are more susceptible to malnutrition.Although BMI shows no difference with the normal subjects,protein wasting and increased fat tissue storage do exist in HD patients.The nutrition changes are slightest in 40-59 years old and much severer in over 70 years old patients.

ificantly lower than in both middle and low group(P＜0.05).Conclusion TP may improve the antioxidant ability of experimental aging mice.