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ObjectiveTo evaluate the application of multi-slice CT (MSCT) perfusion scan technique in predicting renal function recovery after unilateral hydronephrosis treatment.MethodsThirtyeight patients with unilateral obstructive hydronephrosis not shown on intravenous urography (IVU) and a normal contralateral kidney were recruited for this study.Patients were divided into detected (D) and undetected (UD) groups depending on whether the IVU detected urinary tract obstruction.All patients underwent plain abdominal X-ray,gray-scale ultrasonography,excretory urography and MSCT perfusion scan before and after the treatment.Patients were followed-up at six months or more after the treatment for a mean duration of 12.5 months (range from 6 to 22 ).ResultsOf the 38 cases,22 cases were in group D,16 cases were in group UD.On MSCT,renal cortex blood flow (BF) and blood volume ( BV ) value after treatment in group D were 561.1 ± 165.4 ml/( 100 g · min) and 35.9 ± 11.3 ml/100 g compared with before treatment rates of 361.6 ±109.7 ml/(100g· min) and24.1 ±10.2 ml/100g,t=-3.38,-2.34,P＜0.01,0.05.In the UD group,the differences of these parameters were after treatment 38.7 ± 15.4 ml/(100 g · min),10.306 ± 4.925 ml/100 g and before treatment 39.1 ± 22.5 ml/( 100 g · min) and 8.7 ± 4.4 ml/100 g,P ＞ 0.05.In the aspects of BF and BV,there were statistically significant differences between group D and group U D both before and after the treatment,t=9.09,4.15,P ＜ 0.01.ConclusionsM SCT perfusion can provide a valuable prediction technique of the renal function recovery in patients with unilateral obstructive hydronephrosis.Improvement of renal function can be expected after relief of obstructive hydronephrosis if the patients have a BF 361.6 ml/( 100 g · min) and BV 24.1 ml/100 g or greater measured by MSCT perfusion.
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Objective To investigate the effect of polygona-polysaccharose on experimental Alzheimer Disease(AD)mice and its possible mechanism. Methods Twenty-six amyloid precursor protein(APP)transgenic mice were randomly divided into high dosage group(HDG),low dosage group(LDG)and model group(MG)which consisted of 9,9 and 8 mice respectively.1 ml of 16%,4% polygona-polysaccharose solution and 1 ml of drinkable tap water were infused into the mouse stomach in HDG,LDG and MG respectively once a day for 45 days.Morris water maze was used to test the mice's proactive learning and memorizing ability.The morphology of cerebral hippocampus was observed by microscope.The content of amyloid-β-protein(Aβ)and the activity of choline acetyltransferase(ChAT)in the cerebral hippocampus were examined by immunochemical staining method. Results Comparisons among treatment groups(including HDG and LDG)and MG showed:(1)Escape delitescence was shortened[at seventh day:(26.0±9.4)s,(31.2±8.7)s and (39.3±10.9)s,P＜0.05];(2)The frequency of finding the hidden platform within 120 seconds was inereased(5.28±0.76)times,(3.00±0.77)times and(1.00±0.63)times,(P＜0.01);(3)The duration of swimming in objective quadrant(the forth quadrant)within 120 seconds was prolonged [(75.50±8.39)s,(51.39±11.9)s and(36.87±1.25)s,(P＜0.05)].HDG provided better results than those in LDG(all P＜0.05);(4)The activity of ChAT was enhanced and Aβ concentration was decreased for which results mice in HDG showed better than in LDG(all P＜0.05);(5)Morphological study in MG showed the sign of neuron apoptosis such as the reduced number of neuron.the shrinking neuron nuclei,the nucleic membrane being irregular and slightly thickened.However.the neuron in treatment groups were more in number,less transformed and more regularly distrIbuted. Conclusions Polygona-polysaccharose can reduce the accumulation of Aβ in the cerebral hippocampus of AD mice and enhance the activity of ChAT.It can significantly improve the learning and memorizing ability of AD mice and thus proves to be an effective experimental drug for treating AD.
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BACKGROUND: Siberian solomonseal rhizome is a sort of Chinese traditional medicine for anti-senilism. The effective component, poly gonati polysaccharide, has the effects of reducing blood glucose and glycosylhemoglobin.OBJECTIVE: To assay regulative effect of polygonati polysaccharide on expression of the key substance of non-enzymic glycosylation of proteinsglycosylated end-product receptor mRNA by reverse transcriptase polymerase chain reaction, so as to develop effective inhibitor for non-enzymic glycosylation of proteins and provide experimental evidences for preventing diabetes and its complications.DESIGN: Randomized control animal trial SETTING: Department of Geriatrics, the Second Xiangya Hospital, Central South University; Department of Cardiology, Haikou Hospital Affiliated to Xiangya Medical College, Central South University.MATERIALS: The experiment was completed in Animal Room of Second Xiangya Hospital of Central South University form March to June 2004. A total of 30 BALB/C mice of clean grade were selected and randomly divided into normal control group, model control group and polygonati polysaccharide group, with 10 in each group.METHODS: Diabetic models were established by intraperitoneal injection with streptozotocin to mice in model control group and polygonati polysaccharide group. Model establishment would be regard as successful if blood glucose of mouse was 8.0 mmoL/L or above. Mice in polygonati polysaccharide group were treated with polygonati polysaccharide (2 mL/kg per day), while mice in normal control group and model control group were treated with injection of 0.5 mL water once a day for 12 consecutive weeks.After medicine had been given to the mice, they were put to death by decapitation. Reverse transcriptase polymerase chain reaction was used to assay expression of glycosylated end-product receptor mRNA in cardiac and renal tissues of experimental animals.MAIN OUTCOME MEASURES: ① Observation of general situation of mice in each group 12 weeks later after model establishment. ② Change of blood glucose of mice in each group before and after model establishment.③ Gel electrophoretic maps of glycosylated end-product receptor mRNA in cardiac and renal tissue of mice in each group. ④ Semi-quantitative assay of glycosylated end-product receptor in cardiac and renal tissue of mice in each groupRESULTS: All the 30 mice entered the results analysis. ① Observation of general situation of mice in each group 12 weeks later after model establishment: mice in normal control group gained weight and moved freely; mice in model control group manifested the symptoms of losing weight, polyuria, listlessness, lags in response etc.; mice in polygonati polysaccharide group manifested milder symptom of polyuria and more sensitive in responses as compared with model control group.② Changes of blood glucose of mice in each group before and after model establishment: blood glucose levels were similar between normal control group and model control group before and after model establishment (P ＞ 0.05), while blood glucose in polygonati polysaccharide group significantly decreased 12 weeks later after model establishment [(10.05±1.16), (7.18±0.84) mmoL/L, P ＜ 0.05]. ③ Gel electrophoretic maps of glycosylated end-product receptor mRNA in cardiac and renal tissue of mice in each group: Compared with normal control group, the expression of glycosylated end-product receptor mRNA increased in cardiac and renal tissue of mice in model control group, while the expression in polygonati polysaccharide group significantly decreased as compared with model control group. ④ Semi-quantitative assay of glycosylated end-product receptor in cardiac and renal tissue of mice in each group: the relative value of glycosylated end-product receptor to β-actin in cardiac and renal tissue of mice in model control group was significantly higher than normal control group (P ＜ 0.01); however, the relative value of polygunati polysaccharide group significantly decreased as compared with model control group (0.760±0.121,0.998±0.202;0.609±0.146;0.765±0.113; P ＜ 0.05).CONCLUSION: Besides reducing blood glucose, polygonati polysaccharide can significantly down regulate high expression of glycosylated endproduct receptor mRNA in cardiac and renal tissue of mice with diabetes, so as to inhibit the combining sites for glycosylated end-products and a series of cytobiological reactions after combined with their receptors, and protect the target organs and tissues from injuring by hyperglycemia.
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OBJECTIVE:To study the regulative function of polygona-polysaccharose on the expression of RAGE mRNA in diabetic rats’brain.METHODS:Diabetic rat model was made by intraperitoneal injection of streptozotocin.RT-PCR method was used to examine the expression of RAGE mRNA in rats’brain.RESULTS:The expression of RAGE mRNA in brain tissue of diabetic rats was increased.The value of RAGE/?-actin in diabetic rats was significantly higher than that in the control group(P
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AIM: To assess the impact of weaver gene on neuronal development,protein expression and vitality. METHODS: DNA encoding the wild-type and mutant ion channel was introduced into immortalized tyrosine hydroxylase-positive CNS-derived neurons named CAD(Cath.a-differentiated,a variant of Cath.a. Cath.a was established by targeted oncogenesis in transgenic mice) cells. DNA clone, immunostaining and Western blotting were used. Three different concentrations (0 25 mg/L, 0 5 mg/L, or 1 0 mg/L) of Girk2 and wv Girk2 expression plasmids were transfected into the CAD cells. The number of transfected cycling cells, protein synthesis and neurites growth were observed between two groups. RESULTS: The number of transfected cycling CAD cells with high concentration of wv Girk2 reduced to about 60%, compared to Girk2-transfected cells. Low concentration of wv Girk2 did not cause cell death but reduced the protein production of transfected genes. Neurite growth was also affected by wv Girk2. MK-801 and Kir2.3 altered the effect of wv Girk2. CONCLUSION: The results indicate that wv Girk2 functions as a blocker in weaver animals, which blockes the wv Girk2 channel to rescue the cells from death. Our data also suggest that the presence of channels and the level of wv Girk2 may have a significant impact on the fate of cells containing wv Girk2.