Objective To investigate the expression of aquaporin-1( AQP1 ) in visceral and parietal pleura in SD rats and to examine the effect of AQP1 on pleural fluid turnover. Methods Five groups( n = 24 ) of SD rats were randomly assigned to received intrapleural injection of dexamethasone,lipopolysaccharide, erythromycin, hypertonic saline and normal saline, respectively. The AQP1 protein in pleural was detected with immunohistochemistry. The mRNA expression of AQP1 under stimulations at different time points was measured by real time RT-PCR. Results AQP1 was immunolocalized predominantly to the microvessels and mesothelial cells of visceral and parietal pleura. The extent of AQP1expression in parietal pleura was less than that in visceral pleura[ ( 4. 14 ±1. 12) ×104 copy /μg vs ( 7. 43 ±2. 02) ×104 copy / μg, P lt;0. 05] . AQP1 expression increased at all phases in the dexamethasone group andthe hypertonic saline group, whereas decreased in the erythromycin group and the lipopolysaccharide group.Conclusion The stimulations of dexamethasone, lipopolysaccharide, erythromycin and hypertonic saline can significantly change the AQP1 expression in pleura, which indicate that AQP1 may contribute to the accumulation and clearance of pleuritic fluids.
ObjectiveTo study the effect of transforming growth factor β3 (TGF-β3), bone morphogenetic protein 2 (BMP-2), and dexamethasone (DEX) on the chondrogenic differentiation of rabbit synovial mesenchymal stem cells (SMSCs). MethodsSMSCs were isolated from the knee joints of 5 rabbits (weighing, 1.8-2.5 kg), and were identified by morphogenetic observation, flow cytometry detection for cell surface antigen, and adipogenic and osteogenic differentiations. The SMSCs were cultured in the PELLET system for chondrogenic differentiation. The cell pellets were divided into 8 groups: TGF-β3 was added in group A, BMP-2 in group B, DEX in group C, TGF-β3+BMP-2 in group C, TGF-β3+DEX in group E, BMP-2+DEX in group F, and TGF-β3+BMP-2+DEX in group G; group H served as control group. The diameter, weight, collagen type II (immuohistochemistry staining), proteoglycan (toluidine blue staining), and expression of cartilage related genes [real time quantitative PCR (RT-qPCR) technique] were compared to evaluate the effect of cytokines on the chondrogenic differentiation of SMSCs. Meanwhile, the DNA content of cell pellets was tested to assess the relationship between the increase weight of cell pellets and the cell proliferation. ResultsSMSCs were isolated from the knee joints of rabbits successfully and the findings indicated that the rabbit synovium-derived cells had characteristics of mesenchymal stem cells. The diameter, weight, collagen type II, proteoglycan, and expression of cartilage related genes of pellets in groups A-F were significantly lower than those of group G (P<0.05). RT-qPCR detection results showed that the relative expressions of cartilage related genes (SOX-9, Aggrecan, collagen type II, collagen type X, and BMP receptor II) in group G were significantly higher than those in the other groups (P<0.01). Meanwhile, with the increase of the volume of pellet, the DNA content reduced about 70% at 7 days, about 80% at 14 days, and about 88% at 21 days. ConclusionThe combination of TGF-β3, BMP-2, and DEX can make the capacity of chondrogenesis of SMSCs maximized. The increase of the pellet volume is caused by the extracellular matrix rather than by cell proliferation.
Objective Dexamethasone (DXM) can regulate the balance of neutrophil and cytokine and enhance the ischemia-reperfusion tolerance of the skin flap; amlodipine besylate (AB) can selectively expand the peripheral blood vesselsand rel ieve the vascular smooth muscle spasm. To investigate the percutaneous penetration abil ity of DXM/AB compound gel and evaluate its effect on survival of ischemic skin flap. Methods Sodium carboxymethylcellulose was used to make blank gel, which was mixed in DXM, AB, azone (AZ), and progylene glycol (PG) respectively to make the compound gel containing 0.3%DXM/0.5%AB only (group D), the compound gel containing 3%AZ/2%PG, 3%AZ, and 2%PG (groups A, B, and C), the 0.3%DXM gel containing 3%AZ/2%PG (group E), the 0.5%AB gel containing 3%AZ/2%PG (group F). The accumulative penetration of DXM and AB in compound gel, 0.3%DXM gel, 0.5%AB gel through excised rat skin and its penetration within flap tissue were investigated by ultraviolet spectrophotometry. Fifty SD rats were selected to make 100 mm × 10 mm random flap at the back, and were randomly divided into 5 groups according to different gels which were used to treat flaps (n=10): compound gel group (group A1), 0.3%DXM gel group (group B1), 0.5%AB gel group (group C1), blank gel group (group D1), and peritoneal injection of DXM (5 mg/kg) and AB (2 mg/kg) (group E1). The survival area of ischemic random skin flap was measured on the 7th day by planimetry. Twenty-four SD rats were selected to make 100 mm × 10 mm random flap at the back, and were randomly divided into 2 groups (n=12). The accumulative penetration of DXM and AB within skin flap were also detected at 2 and 6 hours after appl ication of 2 g of compound gel containing 3%AZ/2%PG (group A2) and peritoneal injection AB (2 mg/kg) / DXM (5 mg/kg) (group B2). Results The accumulative penetration of DXM and AB in compound gel were increased in time-dependent manner (P lt; 0.05), and it was the highest in group A, and was significantly higher than that in group B and group C (P lt; 0.01), but there was no significant difference when compared with group E or group F (P gt; 0.05). The accumulative penetration of DXM and AB in groups A, B, and C were significant higher than that in group D (P lt; 0.05). After 7 days, the survival area of flaps in groups A1, B1, C1, D1, and E1 were (695.0 ± 4.6), (439.3 ± 7.1), (477.5 ± 14.5), (215.2 ± 3.8), and (569.4 ± 9.7) mm2, respectively; group A1 was significantly higher than other groups (P lt; 0.05). After 2 and 6 hours, the quantities of DXM and AB in skin flap of group A2 were significantly higher than that of group B2 (P lt; 0.05). Conclusion In 0.3%DXM/0.5%AB compound gel, DXM and AB might penetrate into skin tissue, which could significantly increase the survivalarea of ischemic skin flap.
Diabetic macular edema (DME) is the most threatening complication of diabetic retinopathy that affects visual function, which is characterized by intractability and recurrent attacks. Currently, the clinical routine treatments for DME mainly include intravitreal injection, grid laser photocoagulation in the macular area, subthreshold micropulse laser, periocular corticosteroid injection, and vitrectomy. Although conventional treatments are effective for some patients, persistent, refractory, and recurrent DME remains a clinical challenge that needs to be urgently addressed. In recent years, clinical studies have found that certain combination therapies are superior to monotherapy, which can not only restore the anatomical structure of the macular area and effectively reduce macular edema but also improve visual function to some extent while reducing the number of treatments and the overall cost. This makes up for the shortcomings of single treatment modalities and is highly anticipated in the clinical setting. However, the application of combination therapy in clinical practice is relatively short, and its safety and long-term effectiveness need further exploration. Currently, new drugs, new formulations, and new therapeutic targets are still under research and development to address different mechanisms of DME occurrence and development, such as anti-vascular endothelial growth factor agents designed to anchor repetitive sequence proteins with stronger inhibition of vascular leakage, multiple growth factor inhibitors, anti-inflammatory agents, and stem cell therapy. With the continuous improvement of the combination application of existing drugs and treatments and the development of new drugs and treatment technologies, personalized treatment for DME will become possible.
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.
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 observe the effect of dexamethasone to intracellular free Ca2+ of frozen RPE cells. METHODS:The cultured human RPE cells were frozen for 30s at --70deg;C. The RPE cells were loaded with Fura-2/AM and analyzed using a digital imaging microscopy system,the effect of dexamethasone to intracellular free Ca2+ was measured at a serial concentration of 40, 60,100,150,200mu;g/ml. RESULTS:The concentration of intracellular free Ca in frozen human RPE cells was increased to 18.6%~29.8% by dexamethasone at concenlration of 40mu;g/ml~60mu;g/ml,while was decreased to 28.4%~35.2% at 150mu;g/ml~200mu;g/ml. CONCLUSIONS:Effect of dexamethasone showed two aspects of effect to frozen cultured human RPE ceils,that it was inhibitor at high concentration and stimulator at low concentration （Chin J Ocul Fundus Dis,1997,13: 86-88）
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.
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 compare the effect of intravenous 20% mannitol or dexamethasone (DM) on low back and leg pain after minimally invasive transforaminal lumbar interbody fusion (MI-TLIF). MethodsBetween October 2012 and September 2013, 100 patients with degenerative lumbar diseases underwent MI-TLIF and percutaneous pedicle screw fixation. All patients were randomly divided into 3 groups:34 patients received intravenous 20% mannitol after operation (mannitol group); 32 patients received intravenous DM after operation (DM group); and 34 patients received neither dehydrating agent nor steroid after operation (control group). There was no significant difference in gender, age, disease duration, clinical symptoms, lesion types, and lesion segments between groups (P>0.05). The serum levels of inflammatory factors[tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6] were measured by ELISA at pre-operation and 3, 24, 48, 72, and 96 hours after operation. Low back and leg pain was determined by using visual analogue scale (VAS) score after operation. ResultsAll procedures were smoothly performed without major complications of nerve root injury, hematoma, or infection. There was no significant difference in operation time and intraoperative blood loss between groups (P>0.05). The VAS score of low back pain showed no significant difference between groups at all time points after operation (P>0.05); the VAS score of leg pain in the DM group was significantly lower than that in the control group at all time points (P<0.05), and than those in the mannitol group at 3, 24, 48, and 96 hours after operation (P<0.05). The serum level of TNF-α in the DM group was significantly lower than that in the control group at all time points (P<0.05), and than that in the mannitol group at 3, 48, 72, and 96 hours after operation (P<0.05). The serum level of IL-1β in the DM group was significantly lower than that in the control group at 3, 24, 48, and 72 hours after operation (P<0.05), and than that in the mannitol group at all time points after operation (P<0.05). The serum level of IL-6 in the DM group was significantly lower than that in the control group at 3 and 24 hours after operation (P<0.05), and than that in the mannitol group at 3, 24, and 48 hours after operation (P<0.05). ConclusionIntravenous 20% mannitol may has no effect on postoperative low back and leg pain, while DM can markedly relieve leg pain after MI-TLIF.