To discuss the effect of dexamethasone in preventing fat embol ism syndrome (FES) in cemented hi p arthroplasty patients. Methods Forty patients scheduled for unilateral cemented hi p arthroplasty between January 2008 and December 2009 were randomly divided into trial group (n=20) and control group (n=20). In trial group, there were 6 males and 14 females with an average age of 73.2 years (range, 54-95 years), including 4 cases of osteoarthritis, 3 cases ofavascular necrosis of femoral head, and 13 cases of femoral neck fracture; the disease duration was 4 days to 6 years (median, 0.8 year). In control group, there were 10 males and 10 females with an average age of 71.9 years (range, 59-91 years), including 2 cases of osteoarthritis, 3 cases of avascular necrosis of femoral head, and 15 cases of femoral neck fracture; the disease duration was 3 days to 5 years (median, 0.6 year). There was no significant difference in gender, age, or disease duration (P gt; 0.05) between 2 groups. Cemented total or bipolar hip arthroplasty (with the same brand of cement and prosthesis) in 2 groups were performed by a group of surgeons. The patients were given intravenously injected with dexamethasone (20 mg) in trial group before 1 hour of cement injection and intravenously injected with normal sal ine (2 mL) in control group. Amount of 5 mL vein blood were withdrawn before surgery, after 4, 8, and 24 hours of cement injection to test the number and average diameter of fat droplets. According to Gurd diagnosis standard, related FES symptoms and signs were inspected. Results Primary heal ing of incision was achieved in all cases of 2 groups. According to Gurd standard of diagnosis, no FES occurred in each group at 2 weeks postoperatively; deep venous thrombosis occurred in 2 cases (10%) of trial group and in 5 cases (25%) of control group, showing significant difference (P lt; 0.05). The number and diameter of fat droplets in trial group were significantly lower than those in control group at 4, 8, and 24 hours of cement injection (P lt; 0.01). All cases were followed up 7.4 months on average (range, 3-13 months). The postoperative Harris score was 89.5 ± 6.1 in trial group and 87.9 ± 8.3 in control group, showing no significant difference (P gt; 0.05). No loosening occurred during follow-up period. Conclusion Intravenous injection withdexamethasone can effectively reduce the number and diameter of venous fat droplets in cemented hip arthroplasty, which can decrease the risk of postoperative FES.
Objective
To explore the paracrine effect of bone marrow mesenchymal stem cells (BMSCs) on dexamethasone-induced inhibition of osteoblast function in vitro.
Methods
The serum free conditioned medium of mouse BMSCs cultured for 24 hours was prepared for spare use. The 3rd passage of MC3T3-E1 cells were divided into 4 groups: the control group (group A), dexamethasone group (group B), dexamethasone+BMSCs conditioned medium (1:1) group (group C), and BMSCs conditioned medium group (group D). After 24 hours of culture, the alkaline phosphatase (ALP) content was determined; the protein expressions of RUNX2 and Osteocalcin were detected by Western blot; and the gene expressions of collagen type I-α 1 (COL1A1), RUNX2, ALP, and Osteocalcin were detected by real-time fluorescence quantitative PCR (RT-qPCR); alizarin red staining was used to observe calcium nodules formation at 21 days.
Results
After cultured for 24 hours, ALP content was significantly lower in groups B, C, and D than group A, and in group B than groups C and D (P < 0.05), but no significant difference was found between groups C and D (P > 0.05). The relative protein expression of RUNX2 of group B was significantly lower than that of groups A, C, and D (P < 0.05), but difference was not significant between groups A, C, and D (P > 0.05). The relative protein expression of Osteocalcin was significantly lower in group B than groups A, C, and D, in groups A and C than group D (P < 0.05), but difference had no significance between groups A and C (P > 0.05). The relative gene expressions of RUNX2, Osteocalcin, COL1A1, and ALP of groups B, C, and D were significantly lower than those of group A (P < 0.05); the relative gene expressions of RUNX2, Osteocalcin, and ALP were significantly higher in group D than groups B and C, in group C than group B (P < 0.05). The gene expression of COL1A1 was significantly higher in group D than group B (P < 0.05), but difference was not significant between groups B and C, and between groups C and D (P > 0.05). The cells of group A all died at 6 days after culture; at 21 days, the calcium no dule staining was positive by alizarin red in groups B, C and D, and the degree of the staining gradually increased from groups B to D.
Conclusion
BMSCs conditioned medium can alleviate the inhibitory effect of dexamethasone on osteoblasts function.
The aim of this study is to investigate the apoptotic inhibition and its molecular mechanism of dexamethasone (DEX) acting on cisplatin (CDDP)-induced apoptosis of human lung adenocarcinoma cell SPC-A1. SPC-A1 cells were pre-cultured in vitro for 24 hours with DEX in different concentrations and then CDDP was added in different concentrations for culturing for further 48 hours. The survival rates of the cells were determined by MTT. The expression of serum/glucocorticoid-induced kinase (SGK-1) and mitogen-activated protein kinase phosphatase-1 (MKP-1) in SPC-A1 cells after being cultured by 1 μmol/L DEX at different time was detected by semi-quantitative RT-PCR technology. The expression of glucocorticoid receptor (GR) in SPC-A1 cells was measured by immunohistochemistry (IHC) with biotin-labeled anti-GR. The results of MTT showed that SPC-A1 cells had resistance to CDDP-induced apoptosis with pre-cultured DEX and the resistance intensity presented DEX concentration-dependent. The expressing quantity of SGK-1 in SPC-A1 cells stimulated by DEX could be elevated and increased with intention of time, but the express of MKP-1 was not detected. Up-regulated expression of GR in SPC-A1 cells stimulated by DEX was detected by IHC. The number of cells expressing GR in SPC-A1 cells was significantly higher than that in the control group. The results showed that DEX inhibited apoptosis of SPC-A1 cells induced by CDDP. The possible molecular mechanism is that elevated expression of GR induced by DEX up-regulates the expression of SGK-1 which locates at the downstream of anti-apoptosis pathway. The apoptosis resistance of SPC-A1 cells may account for all above the factors.
ObjectiveTo study the effects of continuous regional arterial infusion (CRAI) of dexamethasone on plasma inflammatory factors of severe acute pancreatitis (SAP) rabbits. MethodsTwentyfour rabbits were randomly divided into sham operation group, SAP group, intravenous infusion of dexamethasone group and CRAI of dexamethasone group (each group 6 rabbits) by random number table. The serum tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, and amylase (AMY) levels in rabbits were tested at hour 0.5, 3, 6, 9, and 12 after modeling succeed. The pathological changes of pancreas and the survival were observed on day 3 after modeling succeed. ResultsCompared with the sham operation group, the serum levels of IL-6 significantly increased at 3 h and reached the peak at 6 h, decreased at 9 h (all Plt;0.05); levels of IL-10 significantly increased at 6 h, continuously elevated at 9 h and 12 h (all Plt;0.001); levels of TNF-α significantly increased at 0.5 h (Plt;0.001), reached the peak at 6 h (Plt;0.001) and decreased at 9 h (Plt;0.05); levels of AMY significantly increased at 9 h, continuously elevated at 12 h (all Plt;0.05) in the SAP group. Compared with the SAP group, the serum levels of IL-6 and IL-10 in the CRAI of dexamethasone group all significantly decreased at 6 h, 9 h, and 12 h (Plt;0.001); levels of IL6 significantly decreased only at 6 h in the intravenous infusion of dexamethasone group; levels of TNF-α in the CRAI of dexamethasone group significantly decreased at 3 h, 6 h, 9 h, and 12 h (all Plt;0.001), which in the intravenous infusion of dexamethasone group significantly decreased only at 6 h (Plt;0.05); levels of AMY in the CRAI of dexamethasone group and intravenous infusion of dexamethasone group all significantly decreased at 12 h (Plt;0.05). Compared with the intravenous infusion of dexamethasone group, the serum levels of IL-6 and IL-10 in the CRAI of dexamethasone group all significantly decreased at 6 h (Plt;0.05) and 12 h (Plt;0.001); levels of TNF-α all significantly decreased at 3 h, 6 h, 9 h, and 12 h (all Plt;0.001); levels of AMY were not significantly different (Pgt;0.05). The pathological changes of pancreas in the CRAI of dexamethasone group were obvious, the death of rabbits reduced on day 3 after modeling succeed. ConclusionCRAI dexamethasone can effectively reduce the systemic inflammatory response and pancreatic inflammation, and reduce mortality.
Objective To explore the value and clinical safety of low-dose dexamethasone used after operation of anastomotic colorectal resection with fast-track surgery in patients with colorectal cancer. Methods Between January 2008 and December 2009, 470 patients undergoing anastomotic colorectal resection were analyzed retrospectively, who were divided into dexamethasone group and control group according to the use of low-dose dexamethasone treatment or not after operation. Postoperative adverse effect, complications, and early rehabilitations were studied. Results There was no statistical significance in postoperative incidence of adverse effect or complications between two groups (Pgt;0.05). In early rehabilitation, first ambulation of patients in the dexamethasone group was significantly earlier than that in the control group (Plt;0.05), while there was no statistical significance in first time of passing flatus, stool, and oral intake, the retain time of nasogastric tubes, urinary catheter, and drains, and postoperative hospital stay (Pgt;0.05). Conclusion Using low-dose dexamethasone after operation anastomotic colorectal resection in patients with colorectal cancer is safe and may have potential to enhance recovery after operation.
Objcetive To assess the efficacy and safety of lenalidomide plus dexamethasone (LD) compared with placebo plus dexamethasone (PD) for relapsed or refractory multiple myeloma. Methods Data were searched in The Cochrane Library (Issue 3, 2010), MEDLINE (with PubMed, 1966 to Nov. 2010), EMbase (1984 to Nov. 2010), CBMdisc (1978 to Nov. 2010), and CNKI (1979 to Nov. 2010), and also searched in clinical trials register for ongoing studies and completed studies with unpublished data. The references of the included studies and relevant supplement or conference abstracts were handsearched. Randomized controlled trials were included. The data were extracted, and then the quality of the included studies was assessed by two reviewers independently. RevMan 5.0 software was used for meta-analyses for studies with low heterogeneity. Results Two studies involving 704 participants were included. One was high quality study, while the other was unclear about randomization and allocation concealment. The adverse outcomes of LD, such as mortality (RR=0.78, 95%CI 0.62 to 0.97, P=0.03) and incidence of disease progression (RR=0.16, 95%CI 0.08 to 0.34, Plt;0.000 01), were better than those of PD, which had significant differences. The overall response rate was higher in the LD group than in the PD group (RR=2.75, 95%CI 2.22 to 3.41, Plt;0.000 01). The incidence of thrombotic event (RR=3.20, 95%CI 1.78 to 5.73, Plt;0.000 1), the Grade Three and Grade Four neutropenia (RR=10.20, 95%CI 5.76 to 18.08, Plt;0.000 01), the Grade Three and Grade Four thrombocytopenia (RR=2.08, 95%CI 1.28 to 3.38, P=0.003), and the incidence of drug withdrawal or dosage reduction due to adverse reactions (RR=1.34, 95%CI 1.21 to 1.49, Plt;0.000 01) were all higher in the LD group than in the PD group. Conclusion The efficacy of LD is superior to that of PD for relapsed or refractory multiple myeloma, but the incidence of drug adverse events, such as thrombosis, Grade Three or Grader Four neutropenia or thrombocytopenia, is also higher than that of PD, which has to be prevented positively.
Objective To investigate the mechanism of dexamethasone in the treatment of acute necrotizing pancreatitis (ANP). Methods The ANP of 48 SD rats were induced by retrograde infusion of sodium taurocholate through biliopancreatic duct.After 30 minutes,the therapy group was administrated with dexamethasone at a dose of 0.2 mg/100 g alone. The control group was administrated with the same amount of 0.9% saline solution.At fourth hour and twelfth hour,8 rats of each group were sacrificed to examine the levels of serum tumor necrosis factor-alpha(TNFα) and serum amylase,to score the degree of pancreatic necrosis and to evaluate acinar cell apoptosis by in situ hybridization by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL). The survial period of 8 rats in each group were observed. Results In therapy group, the level of TNFα was (17.8±2.7) pg/ml and (8.5±1.6) pg/ml,the apoptosis index was （36.94±4.12）% and （ 32.79±3.31）%,the survival period was (33.4±21.5) h.While the control group with the indexes mentioned above were as follows: (53.6±18.7) pg/ml and (37.2±11.1) pg/ml ( P＜0.01),（4.37±1.24）% and （5.12±2.11）% （P＜0.01）,(14.6±5.7) h (P＜0.01) ,the histologic scoring for ANP between therapy group and control group was a significantly distinct (P＜0.01). Conclusion Dexamethasone can induce pancreatic acinar cell apoptosis in this model. Proper leves of TNFα may play an important role in regulating the apoptosis.Apoptosis can protect pancreas from necrosis in ANP.
Objective To investigate the effect of dexamethasone, recombinant human fibroblast growth factor (rhFGF) and recombinant human bone morphogenetic protein 2 (rhBMP-2) on the proliferation and differentiation of marrow stromal stem cells (MSCs) for their further application in tissue engineering. Methods MSCs were isolated and cultured in vitro, and then exposed to different dose of dexamethasone (10-8 mol/L,10-7 mol/L,10 -6 mol/L), rhFGF (50 ng/ml,200 ng/ml,500 ng/ml) and rhBMP-2 (50 ng/ml,500 ng/ml,1 000 ng/ml) respectively. The total protein and alkaline phosphatase (ALP) activity of each group was measured on 4th and 7th day. Results Exposure of MSCs with 10-6mol/L dexamethasone inhibited protein synthesis without obvious effects on ALP expression. The application of rhFGF significantly promoted cell proliferation but inhibited ALP activity. In comparison, ALP expression was significantly enhanced by treatment of rhBMP-2 at concentration of 500 ng/ml，1 000 ng/ml. Conclusion The exposure of dexamethasone as well as rhBMP-2 to MSCs with an appropriate concentration promotes osteogenic expression without reverse effects on cell proliferation, which indicates the great potential value in cell-based strategy of bone tissue engineering.
ObjectiveTo observe the effects of bulbar subconjunctival and periocular injection of dexamethasonone on blood glucose levels of type 1 diabetic mellitus (T1DM)rats.
Methods80 healthy adult male Sprague-Dawley rats were randomly divided into GroupⅠ(n=40) and GroupⅡ(n=40). GroupⅠrats received intraperitoneal (IP) injection of streptozotocin to induce T1DM model, while GroupⅡrats received IP injection of citrate buffer solution and was the control group.GroupⅠrats and GroupⅡrats were further divided into four subgroups:A (n=10), a (n=10), B (n=10), and b (n=10). Subgroup-A rats received bulbar subconjunctival injection of dexamethasone, subgroup-a rats received bulbar subconjunctival injection of saline, subgroup-B rats received periocular injection of dexamethasone, subgroup-b rats received periocular injection of saline. After the injection, rats were fasted but could drink water. Tail vein blood samples were collected and the blood glucose level was measured by glucose monitor.
ResultsAfter modeling, the blood glucose level of GroupⅠand GroupⅡrats was(9.31±1.79) mmol/L and (5.72±0.80) mmol/L respectively, the difference was statistically significant (P < 0.05). The blood glucose level of GroupⅠrats reached the peak in 3h after injection. In 6-24 h after injection, the blood glucose level of GroupⅠA rats was obviously increased than that of the blood glucose level of Group Ia rats and the difference was statistically significant (P < 0.05). In 3-24 hours after injection, the blood glucose level of GroupⅠB rats was obviously increased than that of the blood glucose level of GroupⅠb rats and the difference was statistically significant (P < 0.05). Comparing the blood glucose level during different injection time between GroupⅠA rats and GroupⅠB rats, between GroupⅠa rats and GroupⅠb rats, the difference was not statistically significant (P > 0.05). In 3-24 hours after injection, the blood glucose level of GroupⅡA rats was obviously increased than that of the blood glucose level of GroupⅡa rats and the difference was statistically significant (P < 0.05); the blood glucose level of GroupⅡB rats was obviously increased than that of the blood glucose level of GroupⅡb rats and the difference was statistically significant (P < 0.05). Comparing the blood glucose level during different injection time between GroupⅡA rats and GroupⅡB rats, between GroupⅡa rats and GroupⅡb rats, the difference was not statistically significant (P > 0.05).
ConclusionBulbar subconjunctival injection and periocular injection of dexamethasone could both increase the blood glucose of TIDM rats, but these two injection methods had no differences on the blood glucose level.
