OBJECTIVE:To observe the clinical efficacy of the formula granula of Siwu decoction for pubertal dysfunctional uterine bleeding.METHODS:A total of 204 pubertal dysfunctional uterine bleeding cases were randomly assigned to receive formula granula of Siwu decoction(n=109,trial group) or western medicine(n=95,control group).RESULTS:The trial group showed higher total effective rate than in the control group,showing significant differences between the two groups(P

Objective:To study the mechanism of immune tolerance induce by protal venous injection of donor spleen cells on the dog model of renal transplantation.Methods:The donor spleen cells were injected through the protal vein during operation,one week later,renal transplantation was performed.IL-2 and IL-6 were studied by method of ELISA.Results:Level of IL-2 and IL-6 in protal venous group and cyclosporin group was higher than that of control group.There were no difference between protal venous group and cyclosporin group.Conclusion:Immune tolerance could be produced by protal venous injection of donor spleen cells.

Objective To investigate the curative effects of curcumin(CUR)or dexamethasone (DXM)on ischemia-reperfusion injury(IRI)of rat lung grafts.Methods Male SD rats were randomly divided 4 groups:CUR group(CUR was administered intraperitoneally to both donors and recipients at 3 h prior to operation);DXM group(DXM was administered intraperitoneally at 30 min prior to operation);vehicle group(Animals were injected with the DMSO to both donors and recipients at 3 h prior to operation);sham group(Time-matched control animals underwent the same surgery,except that no graft was implanted).Six animals were sacrificed at different reperfusion periods of 2 h and 24 h,respectively.Oxygenation indexes(PO_2/FiO_2),lung injury scores,wet/dry ratio(W/D)and myeloperoxidase(MPO)activity in the transplanted lung were measured.Malondialdehyde(MDA), total anti-oxidative capacity(TAOC),tumor necrosis factor(TNF)-?and interleukin(IL)-6 in the transplanted lung and serum were determined.Results The levels of LPV PO_2/FiO_2 were significant- ly higher in the CUR and DXM groups than in the vehicle groups both 2 and 24 h after reperfusion,re- spectively(P

Objective To investigate the pathway of lymphatic drainage of proteins from cerebral parenchyma in subarachnoid hemorrhage rat models. Methods Healthy adult male Wistar rats were divided into Saline group, Evans blue-labeled albumin (EBA) group, and SAH + EBA group. SAH models were produced by double injection of autologous arterial blood into cisterna magna. Using a modified microinjection method, EBA was injected into left candate-putamen of the EBA group and EBA + SAH group rats. In Saline control group, saline was injected. After injection, at 12 hours, 1 day, 2 days, 3 days and 5 days, the animals were sacrificed and the fluorescence signals of EBA were imagined and analyzed along the possible lymphatic drainage pathway, e.g. the brain tissue, the wall of common carotid artery, and cervical lymphatic nodes. Results One day after injection, in EBA group, the fluorescence of EBA initially appeared on the left of the brain, the wall of common carotid artery, left lateral cerebral ventricle, and the perivascular spaces of cerebral vessels. The fluorescence signals gradually expanded to the opposite side.Large amount of fluorescence granules accumulated in the outer layer of common carotid artery. Fluorescence was also found in cervical lymphatic nodes. Two days after injection in this group, the density of fluorescencein the brain became weaker while the density of fluorescence in rhinencephalon became stronger. The fluorescence of EBA was found in lymphatic nodes adjacent to abdominal aorta. In SAH + EBA group,reduced amount and velocity of the drainage of EBA from left caudate-putamen to rhinencephalon, cervical lymphatic nodes, and lymphatic nodes adjacent to abdominal aorta were observed. From 12 hours to 5 days after injection, fluorescence intensity of EBA in deep cervical lymphatic nodes in SAH + EBA group(8.9 ±2. 0, 11.9 ± 2. 5, 17.4 ± 3.7, 26.7 ± 4. 5 and 59.0 ± 8. 1 ) were lower than those in EBA group ( 14. 5 ±3.2, 27.5 ±7.4, 60.3 ±12.3, 138.0±12.0 and 108. 1 ±13.4, F=13. 17, 24.04, 66.81, 302.77 and 59.36, P ＜ 0. 01 ). From 2 to 5 days, fluorescence intensity of EBA in lymphatic nodes adjacent to abdominal aorta was also lower in SAH + EBA group( 11.0 ± 1.5, 12. 5 ±2. 8, 23.6 ±3. 2) than those in EBA group(26. 3 ±5.9, 47.5 ±9.6, 41.0 ±9.3; F =38. 17, 72.52, 19.01, P ＜0.01). Conclusion SAH can result in reduced drainage of macromolecular substances, e.g. protein, from the brain via lymphatic pathway.

Aim To establish a method to evaluate lymphatic drainage of macromolecular tracer in cerebrospinal fluid in rats.Methods Rat cervical lymphatic blockade(CLB)models were established by occlusion of cervical lymphatic tubes and removal of cervical lymphatic nodes.The rats were divided into non CLB(normal controls) and CLB groups.~(125)I-labeled human serum albumin(~(125)I-HSA)was injected into the left lateral cerebral ventricle,and blood samples were collected and ~(125)I-HSA concentrations were detected continually within 24 hours.Concentration-time curve was drawn according to the single compartment model in pharmacokinetics.Parameters of pharmacokinetics such as area under curve(AUC),maximum concentration(C_(max)),transfer rate constant K_a and peak time(T_(max))were derived.The AUC,C_(max),K_a,and T_(max) regarding the lymphatic drainage of ~(125)I-HSA were calculated based on the differences between the two groups.Results AUC,C_(max),K_a of ~(125)I-HSA by lymphatic drainage were 51.97 mg·L~(-1)·h~(-1),2.91 mg·L~(-1),and 0.64 h~(-1),respectively.The proportion of AUC,C_(max),K_a of ~(125)I-HSA by lymphatic drainage to those of drained by both arachnoid granulations and lymphatics was 71.53%,44.02%,58.18%,respectively.T_(max) in CLB group(8.36±0.82 h)was much longer than that in non CLB group(3.57±0.54 h).Conclusions A method to evaluate lymphatic drainage of macromolecular tracer in cerebrospinal fluid in rats is successfully established.The lymphatic drainage pathway plays an important role in eliminating macromolecular substances in cerebrospinal fluid.

Objective To investigate the effects of 12-lipoxygenase (12-LO) and angiotensin Ⅱ (Ang Ⅱ) on the CIP/KIP family of cyclin-dependent kinase inhibitors (CKIs) p21,p27 and p57 related to cell hypertrophy.Methods Mesangial cells were treated with high glucose for 24 hours and 48 hours respectively.12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] and Ang Ⅱ were infused to rats by osmotic mini-pump for 1 week and 2 weeks respectively.Rats fed high fat diet were received low dose streptozotocin (STZ) to make type 2 diabetes (DN).The rats were divided into normal control group,DN group,DN+Ang Ⅱ type 1 receptor blocker (ARB) group or 12-LO inhibitor (CDC) group.DN+ARB rats were treated by losartan for 6 weeks,and DN+CDC rats were treated for 8 weeks.Urine albumin and protein expressions of p21,p27 and p57 were detected by ELISA and Western blotting respectively.Glomeruli injury and expressions of p21 and p27 were detected by PAS staining and immunohistochemistry respectively.Results High glucose increased p21 and p27 protein expression in mesangial cells significantly compared with the relative control (all P ＜ 0.05),but had no effect on p57.Ang Ⅱ increased p27 protein expression in gloneruli significantly (P ＜ 0.05),but had no effect on p21 and p57 protein expression.12(S)-HETE increased both p21 and p27 protein expression in glomeruli significantly (all P ＜ 0.05),but had no effect on p57 protein expression.Blood glucose,kidney/body weight,urinary protein,and glomerular p21 and p27 protein expressions were increased in DN group (all P ＜ 0.05) compared with those in control group,with little change of p57 protein expression (P ＜ 0.05).Moreover,glomerular hypertrophy and extra cellular matrix accumulation were observed in DN group.However,urine protein,kidney/body weight,renal injury,but not blood glucose,were decreased in DN+ARB group and DN+CDC group compared with DN group respectively (P＜ 0.05).Further DN+CDC rats had decreased both p21 and p27 protein expressions in glomeruli,but DN+ ARB rats only had decreased p27 protein expression (all P ＜ 0.05).Conclusions 12-LO may induce both p21 and p27 protein expression in DN glomeruli,but Ang Ⅱ may induce only p27 expression.

Objective To study the changes of endothelin,nitric oxide and vascular endothelial growth factor level in patients with type 2 diabetic retinopathy (DR). Methods Eighty diabetes patients (53 with diabetic retinopathy and 27 without). Another 30 healthy volunteers were recruited as control. Plasma ET and VEGF levels were measured by enzyme-linked immunosorbent assay. NO levels were measured by nitrate reductase method. Results Plasma levels of ET were higher in patients with type 2 diabetes with DR (DR)(80. 68 ± 13.57) mg/L than (65. 33 ± 11.24) mg/L, (45.25 ±9. 06) mg/L, in control and in type 2 diabetes patients without DR (NDR) (Ps ＜ 0, 01 ). Plasna levels of NO in DR group (69. 82 ± 14. 89) μmol/L were higher than (37. 85 ±-9. 11 ) μmol'L, in control group,but lower than (77.52 ±± 18.56) μmol/L in NDR group (Ps ＜ 0. 05 ). Plasma levels of VEGF ( 110. 52 ± 25.65 ) μg/L in DR were significantly increased compared with control (82.42 ± 18. 47 ) μg/L, and NDR(97.55 ±25.61)μg/L, (Ps ＜0.05).Conclusion ET, NO and VEGF may be involved in the pathogenesis of type 2 diabetic retinopathy.

OBJECTIVE: To observe the effects of intermedin preconditioning on hypoxic injury in rat's cardiac myocytes and to provide the hypothetical mechanism of sudden cardiac death in the field of forensic pathology. METHODS: The H9c2 cultured rat cardiac myocytes were randomly divided into control group, hypoxia group and IMD group. The myocardial cell viability, cellular ultrastructure, intracellular calcium concentration and apoptosis rate were determined by MTT assay, transmission electron microscopy, laser scanning confocal microscope and flow cytometry, respectively. RESULTS: Compared with the control group, cell viability obviously decreased with inner ultrastructure injury in the hypoxia group (P<0.05), while cell viability significantly increased in the IMD group by reducing the hypoxia injury of cardiac myocytes (P<0.05). Compared with the control group, [Ca2+]i (fluorescence intensity) and apoptosis rate significantly increased in the hypoxia group, but decreased in the IMD group (P<0.05). CONCLUSION IMD increases the cell survival rate and decreases the cell apoptosis inhibited by intracellular calcium overload from hypoxia. This finding may reveal the mechanism of protective effects of myocardial hypoxia, and provide a scientific basis for the identification sudden cardiac death.
Animals ; Apoptosis ; Calcium ; Cell Hypoxia ; Cell Survival ; Hypoxia ; Myocardial Ischemia ; Myocardium/cytology* ; Myocytes, Cardiac/physiology* ; Rats ; Rats, Sprague-Dawley

Objective To investigate the inhibitory effects of rosiglitazone on the synthesis of reactive oxygen species (ROS) and the expression of monocyte chemoattractant protein 1 (MCP-1) induced by high glucose in rat mesangial cells. Methods The mesangial cells were divided into six groups: control group ( C, 5.6 mmol/L glucose), mannitol group (M, 24.2 mmol/L mannitol+group C), high glucose group( H, 30 mmol/L glucose), R1 group(R1, group H+10 μmol/ L rosiglitazone), R2 group (R2, group H+20 μmol/L rosiglitazone), N-acetylcysteine (NAC) group (N, group H+5 mmol/L NAC, NAC was added 1 h before the stimulation of high glucose). The level of ROS was measured by confocal laser scanning microscopy. The mRNA and the protein expression of MCP-1 were semi-quantitatively determined with reverse transcription-polymerase chain reaction and ELISA respectively. Results No significant differences of ROS and MCP-1 were found between control group and mannitol group. The intracellular ROS induced by high DOI:10.3760/cma.j.issn. 1001-7097.2009.01.011glucose increased by 4.1-fold compared to control group (P<0.01), which was prevented by rosiglitazone (20 μmol/L) and NAC respectively. The MCP-1 mRNA expression in group R2 and group N was significantly lower than that in group H (P<0.01). The MCP-1 protein level in group H [(940.9±20.3) ng/L] was higher than that in group C [(403.0±8.1) ng/L] (P<0.01), and the expression of MCP-1 protein in group R2 [(562.5±15.3) ng/L] and group N [(539.8±8.3) ng/L] was lower than that in group H (P<0.01). Conclusion Rosiglitazone may suppress high glucose-induced MCP-1 expression by reducing the level of ROS, which may be one of the mechanisms that rosiglitazone plays a direct role in the protection of kidney.

AIM:To determine the injured effect of cerebrospinal fluid(CSF) from subarachnoid hemorrhage(SAH) after cerebral lymphatic blockage(CLB) on PC12 cells. METHODS:SAH and CLB models of adult New Zealand rabbits were used. CSF was obtained from experimental animals after 5 d of modeling and was added into cultured PC12 cells. The cells were randomly divided into blank control(F12 Ham's),normal CSF,SAH CSF,and SAH+CLB CSF groups. At different time points,the survival rate of PC12 cells was measured by MTT assay. LDH leakage was detected. Expression of Bax and heat-shock protein 70(HSP70) was determined by immunohistochemical staining. RESULTS:MTT assay and detection of LDH leakage revealed that the survival rate of PC12 cells was obviously inhibited and the leakage of LDH increased in SAH CSF group and SAH+CLB CSF group. CSF from normal rabbit did not damage the PC12,as compared to blank controls. Above effects were more obvious in SAH+CLB CSF group than those in SAH CSF group. Bax and HSP70 protein expression was found in both SAH CSF group and SAH+CLB CSF group. Expression of Bax protein in SAH+CLB CSF group was stronger than that in SAH CSF group in a time dependent manner. At 0.5 h and 1 h,the expression of HSP70 protein in SAH+CLB CSF group was stronger than that in SAH CSF group,whereas the expression became weaker at 2 h and 4 h in that group. CONCLUSION:Blockage of cerebral lymphatic drainage pathway deteriorates the damage of CSF from SAH on PC12 cells,indicating this pathway may acts as an endogenous protective mechanism in SAH.