OBJECTIVE: To investigate the effects of dexamethasone on the proliferation and differentiation of bone marrow stromal cells(MSC). METHODS: MSC were isolated and cultured in vitro. After treatment with different concentrations of dexamethasone (0, 10-10, 10-9, 10-8, 10-7 and 10-6 mol/L), the proliferation and alkaline phosphatase (ALP) activity of MSC were measured to evaluate the effect of dexamethasone on the biological characteristics of MSC. RESULTS: Dexamethasone inhibited cell proliferation. With the increase of concentration of dexamethasone, the effect was enhanced, which was more significant when the concentration of dexamethasone was over 10-8 mol/L. At the same time, dexamethasone promoted the activity of ALP. This effect was enhanced with the increase of concentration of dexamethasone, but the alteration was small when the concentration of dexamethasone was over 10-8 mol/L. The effects increased with the time. The activity of ALP was enhanced 2 to 4 times with the dexamethasone for 6 days. CONCLUSION: Dexamethasone inhabit the proliferation of MSC, while induce them to differentiate into osteoblasts. The appropriate concentration of dexamethasone was 10-8 mol/L.
Purpose
To evaluate the prostag landins(PG) levels and to identify the effect of dexamethasone(DXM) on PG in response to photochemical insult in rat retina.
Methods
The experiments were performed on 36 SD rats which were separated into two groups,control and treated groups,and the latter received daily intraperitoneal injections of DXM (1 mg/kg) for 5 consecutive days,starting 3 days before light exposure.The animals were continually exposed to green fluorescent light(510-560 nm)with an illuminance level of (1900plusmn;106.9)lx for 24 hrs.The retinal concentration of PGE 2 and 6-keto-PGF1alpha; were tested at 6hrs,1,3,7 and 14 days after light exposure.
Results
The PGE2 and 6-keto-PGF1alpha; levels of the control groups (37.50plusmn;2.75,48.06plusmn;4.0 4,81.90plusmn;4.89) pg/mg and (4.68plusmn;0.69,7.50plusmn;0.57,10.40plusmn;0.71) pg/mg had significantly higher values than those of the treated rats(20.60plusmn;4.28,37.36plusmn; 3.34,54.85plusmn;4.57) pg/mg and (2.50plusmn;0.59,4．68plusmn;0.81,6.87plusmn;1.10)pg/mg (Plt;0.01) after 6 hrs,1 and 3 days light exposure respectively.
Conclusion
By inhibition of PG synthesis,the DXM may play an ameliorative effect on retinal photochemical injury of rats.
(Chin J Ocul Fundus Dis,1999,15:94-96)
Objective To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils.Methods The rats were randomly divided into 3 groups.The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils,tumor necrosis factor α （TNF-α）, and interleukin 10 （IL-10） concentrations were measured. Results The flap survival areas in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A andC on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-α concentration reached the maximum level at 1 h,while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-α concentration was lower than that in Group B and decreased dramatically at 6 h. The IL-10 concentration was the lowest at 1 h, and increased rapidly at 3 h. Thus, ischemia reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils. Conclusion Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.
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 systematically review the effect of pre-treating the catheters with dexamethasone for preventing PICC-associated phlebitis.
MethodsWe electronically searched PubMed, EMbase, The Cochrane Library (Issue 4, 2012), CNKI, CBM, WanFang Data and CQVIP for studies about pre-treating the catheters with dexamethasone to prevent PICC-associated phlebitis from inception to March 2013. Relevant studies including grey literature were also manually searched. Two reviewers independently screened studies according to the inclusion and exclusion criteria, extracted data and evaluated the methodological quality of the included studies. Then meta-analysis was performed using the software RevMan 5.0.
ResultsA total of 13 studies involving 1 965 cases (1 025 cases in the dexamethasone group, and 940 cases in the control group) were included. The results of meta-analysis showed that pre-treating the catheters with dexamethasone could significantly decrease the incidence of PICC-associated phlebitis (RR=0.29, 95%CI=0.22 to 0.39, P < 0.000 1). However, no significant difference was found for the PICC-associated other complications, such as pipe blockage, bleeding, swelling of puncture site, allergy and atopic catheter.
ConclusionPre-treating the catheters with dexamethasone soltion before inserting could reduce the incidence of PICC-associated phlebitis. The aforementioned conclusion needs to be further validated by more high-quality and large-scale randomized controlled trials.
OBJECTIVE: To study the hemorheology of island flap after ischemia-reperfusion injury and modulation of dexamethasone. METHODS: Sixty Wister rats were made ischemia-reperfusion injury model, and divided into two groups randomly(Group I: intraperitoneal injection of normal saline 2 ml/kg as control group; Group II: intraperitoneal injection of dexamethasone 5 mg/kg as experimental group). Flap survived areas were measured and neutrophil necrosis numbers in flaps were counted. Erythrocytes and neutrophil hemorheology were observed. RESULTS: Area survived flap in group II was larger than that in group I. Neutrophil necrosis numbers were less in group II than in group I (P lt; 0.05). Whole blood hyposhear viscosity, erythrocyte aggregation, Casson yield stress and nerutrophil adhesion ability were higher in group I than in group II (P lt; 0.05); and the neutrophil deformability was lower in group I than in group II. CONCLUSION: Flap inchemia-reperfusion can increase erythrocyte aggregation index and neutrophil adhesion ability. Dexamethasone can improve these and decrease neutrophil necrosis numbers, so as to prevent flap from ischemia-reperfusion injury.
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.
ObjectiveTo observe the changes of microstructure of rats'sciatic nerves with non-freezing cold injury after treated with dexamethasone.
MethodsTwelve male Wistar rats were randomly divided into cooling group and treating group.Unilateral sciatic nerves of the rats in the cooling group received cooling treatment with 3-5℃ for 2 hours;while unilateral sciatic nerves of the rats in the treating group received cooling treatment with 3-5℃ for 2 hours and underwent the celiac injection with dexamethasone in addition.The other sciatic nerves were exposed,as the control.The bilateral sciatic nerves of rats in each group were harvested after 24 hours.The microstructure of nerves was examined under the light microscope and electron microscope.
ResultsLight microscopic examination revealed extensive myelinated fibre degeneration in form of giant empty axons or shrunken dark axons on the first day after cooled.And the endoneurial capillary lumen was narrowed because of swollen endothelial cells.After the treatment,myelinated fibre degeneration was still similar to that before the treatment,but the endoneurial capillary lumen and endothelial cells were normal.By electron microscopy,sciatic nerves showed extensive myelinated fiber degeneration,and swollen endothelial cells.But unmyelinated fibers and tight junction were preserved on the first days after cooled.Aggregated red cells and platelet thrombus were not found.After the treatment,myelinated fibre degeneration was still similar to that before the treatment.Unmyelinated fibers and tight junction were preserved.The endoneurial capillary lumen and endothelial cells were normal.
ConclusionAfter the treatment,the damage of endoneurial capillary had improved,but myelinated fiber degeneration was similar to that before the treatment.It suggested that dexamethasone may only improve the vascular system in non-freezing cold injury of sciatic nerve.
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 role of IFN-γ in suppressing bleomycin-induced pulmonary fibrosis in rats.Methods Seventy-five SD rats were randomly divided into five groups (15 rats in each group)，ie.a normal group，a bleomycin-induced pulmonary fibrosis model group，a dexamethasone-treated group，a high-dose IFN-γ-treated group (150 000 U/kg) and a low-dose IFN-γ-treated group (50 000 U/kg).Five rats in each group were randomly killed in 7th day，14th day and 28th day after relative treatment respectively，and lung tissue samples were harvested for histopathology study.HE and Masson staining were used to determine the extent of alveolus inflammation and pulmonary fibrosis respectively.Histoimmunochemical method were adapted to determine protein levels of TGF-β1，CTGF，type Ⅰcollagen and type Ⅲ collagen in pulmonary tissues.Results Histopathological study showed that treatment with either dexamethasone or IFN-γ (both high dose and low dose) remarkably meliorated the extent of alveolus inflammation and suppressed pulmonary fibrosis (compared with model group，all Plt;0.05).Histoimmunochemical study suggested that both dexamethasone and IFN-γ could inhibit the expression of TGF-β1，CTGF，type Ⅰand type Ⅲ collagen (compared with model group，all Plt;0.05)，and the suppression of TGF-β1，type Ⅰand type Ⅲ collagen expression was more obvious in high-dose IFN-γ-treated group than those in low-dose group (Plt;0.05).Conclusions INF-γ possesses apparent anti-fibrosis effect that is similar to dexamethasone but with less side effect.Such effect may resulted from reduced production of type Ⅰand type Ⅲ collagen through expression inhibition of cytokines such as TGF-β1 and CTGF.
