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OBJECTIVE:To compare the an ti-hepatocarcinoma effects of curcumin (CUR)and its derivative hydrazincurcumin (HZC),and to explore the mechanism. METHODS :MTT assay was used to detect the effects of CUR or HZC (2.5,5,10,20, 40,80 μmol/L)on the proliferation of HepG 2 cells. Flow cytometry was used to detect the effects of CUR or HZC (10,20,40 μmol/L)on cell cycle distribution and apoptosis of HepG 2 cells. Western blotting assay was used to detect the effects of CUR or HZC(10,20,40 μmol/L)on the expression of apoptosis-related protein in HepG 2 cells. The male SD rats were randomly divided into normal control group (n=10),CUR control group (n=10),HZC control group (n=10),model group (n=30),CUR protection group (n=30)and HZC protection group (n=30). CUR control group and HZC control group were given CUR 85917439。E-mail:zhaoji-an-88@163.com or HZC (80 mg/kg) intraperitoneally. Model group ,CUR protection group and HZC protection group were given diethylnitrosamine (50 mg/kg)intraperitoneally to establish hepatocarcinoma model ;at the same time ,2 protection groups were given CUR or HZC (80 mg/kg)intraperitoneally,twice a day,for consecutive 12 weeks. During medication ,the change of body weight and death of rats were recorded. Twenty four weeks later,liver index of rats was calculated and appearance was observed ;the number of cancer nodules was counted ;HE staining was used to observe the pathological changes of liver tissue and calculate the nuclear division index of hepatocarcinoma ;the proliferating cell nuclear antigen (PCNA)index was detected by immunohistochemistry. RESULTS :CUR and HZC could increase the inhibitory rate of HepG 2 cells(P<0.05),and increased the percentage at G 0/G1 phase and apoptotic rate of HepG 2 cells(P< 0.05). CUR and HZC could significantly decrease the protein expression of p-JAK 2,p-STAT3,Bcl-2 and Bcl-xl ,while increased the protein expression of Bax ,Cyt-c,Caspase-9,Caspase-3 and PAPR (P<0.05). Above effects of HZC were significantly better than those of CUR (P<0.05). The results of animal experiment showed that there was no death ,no liver canceration and no pathological changes in liver appearance and tissue section of the three control groups ;there was no statistical significance in body weight and its increased weight ,liver index ,nuclear division index of carcinoma or PCNA index (P>0.05). Compared with model group, survival rate of rats were increased significantly in CUR protection group and HZC protection group , while hepatocarcinoma incidence and the number of cancer nodules were decreased significantly (P<0.05);body weight and its increased weight were increased significantly ,while liver index ,nuclear division index of carcinoma and PCNA index were decreased significantly (P<0.05). There were some pathological changes in liver appearance and tissue section ;cancerous lesions with focal necrosis or cancerous lesions with patchy necrosis were observed. There was no statistical significance in the improvement of above indexes in 2 protection groups (P>0.05). CONCLUSIONS :HZC could inhibit the proliferation and induce apoptosis of HepG 2 cells by inhibiting JAK 2/STAT3 signaling pathway and regulating the activation of mitochondrial endogenous pathway,which shows stronger anti-hepatocarcinoma effect in vitro than CUR. On the other hand ,there was no significant difference in the improvement of liver caner indexes in hepatic cancer model rats between HZC and CUR.
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Objective To evaluate whether Vitamin B supplementation could prevent ischemic stroke recurrence.Methods Randomized controlled trials (RCTs) observing Vitamin B supplementation in patients with stroke was performed in databases including ScienceDirect, PubMed/Medline, China National Knowledge Infrastructure, Chinese Biomedical Data-Base, Wanfang Database, and VIP Chinese Science and Technology Journal Database to find related studies in English or Chinese published before August 2016. The patients in control group received a placebo or basic therapy without Vitamin B, and those in experimental group was treated with Vitamin B alone or Vitamin B on the basis of conventional treatment. The data were collected by two researchers independently and the quality of studies was assessed by the modified Jadad Scale. The Meta-analysis was performed using Stata 12.0, funnel plot was drawn, and Egger and Begg regressions were used to evaluate the publication bias, and sensitivity was also analyzed. Results Seven RCTs studies were enrolled to analyze with a total number of 9846 stroke patients, 4755 patients in control group, and 5091 in experimental group, respectively. ① Vitamin B supplementation for prevention of recurrent stroke: heterogeneity test results showed a heterogeneity in literatures enrolled (I2 = 62.9%,P = 0.009), and a random effect model was used for Meta-analysis. It was shown that the incidence of recurrent stroke in the experimental group was significantly lower than that in the control group [pooled relative risk(RR) = 0.64, 95% confidence interval (95%CI) = 0.47-0.87], which indicated that the supplementation of Vitamin B could prevent the recurrence of stroke. Cumulative Meta-analysis showed that Vitamin B supplementation exhibited positive effects in the prevention stroke recurrence from 2012. The 95%CI tended to be stable while demonstrating good change trend as sample growing. The publication bias evaluation results showed that the funnel plot was not symmetrical by visual inspection, further quantitative analysis showed thatP value from Egger regression was 0.008, while that from Begg regression was 0.035, bothP 0.05, which indicating that there was no evidence of publication bias in the study included.Conclusions Vitamin B supplementation was associated with a lower risk of recurrent stroke in stroke patients and could significantly improve the quality of secondary prevention of stroke. Furthermore, supplementation of Vitamin B could reduce plasma Hcy levels in stroke patients which might contribute to its effect in preventing stroke recurrence.
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Objective To explore whether glutamine can ameliorate oxidative stress injury in mice with sepsis in order to provide an experimental basis for clinical application.Methods Thirty 5-week old Qunming male mice were randomly divided into three groups: control, model and glutamine groups, 10 mice in each group. Lipopolysaccharide (LPS) 5 mL/kg was injected into intraperitoneal cavity to establish septic model in model and glutamine groups, and an equal amount of normal saline was injected into the cavity in control group. After the septic model was successfully established, propylene ammonia acyl-glutamine 0.75 g/kg was immediately injected through tail vein in the glutamine group, and an equal amount of sterile normal saline was injected into the vein in the model and control groups. After 6 hours, the experiment was terminated, the blood was collected from the orbital cavity and the animal was sacrificed; serum, liver and renal tissue homogenates were taken to detect the indexes of oxidative stress, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lipid metabolite malonaldehyde (MDA).Results Compared with the control group, the levels of SOD activities and GSH-Px of serum and liver, kidney tissue in the model group were significantly lower, and the MDA content was significantly higher. Compared with the model group, the levels of SOD activities and GSH-Px of serum and liver, kidney tissue in the glutamine group were significantly higher, and the MDA content was significantly lower [SOD in the serum (U/mL): 134.78±3.74 vs. 124.60±3.49, SOD in the liver (U/mg): 56.71±1.35 vs. 49.84±0.86, SOD in the kidney (U/mg): 46.22±1.22 vs. 43.22±1.52; GSH-Px in serum (U/mL): 325.15±21.86 vs. 267.04±13.5, GSH-Px in liver (U/mg): 91.35±1.59 vs. 83.40±1.33, GSH-Px in kidney (U/mg): 136.08±0.58 vs. 132.97±0.74; MDA in serum (μmol/L): 9.20±0.32 vs. 13.67±1.24, MDA in liver (nmol/mg): 1.85±0.10 vs. 4.88±0.17, MDA in kidney (nmol/mg): 2.47±0.12 vs. 3.52±0.27, allP < 0.01].Conclusion Sepsis can cause oxidative stress and oxidative damage, glutamine not only can improve the levels of antioxidant enzymes of GSH-Px and SOD, enhance antioxidant capacity, reduce the MDA content of lipid metabolites, but also can reduce the toxic metabolites, so as glutamine has the effect of ameliorating oxidative stress injury.
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Objective To investigate the effect of nutrition support team (NST) on the clinical outcomes in surgically treated children with congenital heart disease (CHD).Methods Totally 60 surgically treated CHD children from January 2010 to June 2010.In March 2010,they were divided into two groups based on the interventions:before the intervention (BET group) and after the intervention (AET group).Nutritional risk screening rate,enteral nutrition (EN) application rate,all-in-one parenteral nutrition (PN) application rate,postoperative mechanical ventilation time,length of ICU stay,average hospitalization days,expenses directly related to nutrition,and hospitalization expenses were compared between these two groups.Results The nutritional risk screening rate,EN application rate,and all-in-one PN application rates before and after intervention of NST were 13.3% (4/30) vs 100% (30/30),43.3% (4/30) vs 63.3% (19/30),and 35.3% (6/17) vs 100% (11/11),respectively,in AET group and BET group (x2 =132.11,19.65,and 24.73,respectively,all P < 0.05).Mechanical ventilation time [(7.03 ± 1.76) h vs (8.09 ±2.56) h],length of ICU stay [(24.81 ±2.52) h vs (37.01 ±3.47) h],average hospitalization days [(17.96 ±4.03) d vs (19.60 ±4.53) d],nutritionrelated expenses [(4 132.27 ±416.27) yuan vs (2 754.03 ±323.47) yuan],and hospitalization expenses [(25 725.11 ±515.68) yuan vs (31 975.53 ±600.56) yuan] were also significantly favorable in AET group (t =5.76,3.04,2.05,32.07,and 43.30,respectively; all P < 0.05).Conclusion NSP is an effective approach to promoting the standard efficacious nutrition support therapy in clinical settings and can improve the therapeutic effectiveness and clinical outcomes in surgically treated CHD children.
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OBJECTIVE: With the prolongation of life span, more and more people care their health. In this paper we summarized the studies about correlative factors of mandible osteoporosis so as to investigate the cause of osteoporosis and how to inhibit or postpone the occurrence of mandible osteoporosis and improve people's quality of life.DATA SOURCES: We searched Qsinghua Tongfang Database for papers about mandible osteoporosis published between January 1991 and May 2005 with the key words of "osteoporosis, mandible bone, alveolar bone"in Chinese. Meanwhile, related English literatures were also searched in Medline between January 1975 and May 2005 with the same key words.STUDY SELECTION: The literatures included all the related papers of correlative factors of mandible osteoporosis. Inclusive criteria were: the study types were randomized controlled trials, drug stress test and clinical drug effect test; the samples were both human and animals. Exclusive criteria: Reviews and literatures without controls were excluded.DATA EXTRACTION: Totally 182 literatures related to the correlative factors of mandible osteoporosis were collected, and 36 were accorded with the inclusive criteria. The excluded were 146 papers of repeated drug effect study.DATA SYNTHESIS: A total of 36 papers including 5 321 human and 152 animals analyzed the data of correlative factors of mandible osteoporosis in age, sex, hormones, biting force, physical training and living habit,etc., respectively, which included 6 interfere-test papers of ovariactomized rats.CONCLUSION: It is concluded that mandible osteoporosis can result in a part of bone mine loss, which is related to age, sex, hormones, biting force,physical exercise and living habits, and so on.