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Objective:To investigate the effect of oxycodone hydrochloride injection pretreatment on focal cerebral ischemia-reperfusion injury in rats.Methods:Seventy-two male SD rats weighing 200-250 g were randomly divided into 3 groups( n=24 each group): sham operation group (sham group), focal cerebral I/R group (I/R group), and oxycodone hydrochloride injection group (Oxy group). Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 h followed by reperfusion. In the Oxy group, oxycodone hydrochloride 0.5 mg/kg was injected iv at 5 min before ischemia. While the same volume of saline (1 mL) was injected in the sham group and I/R group. The neurological deficit score (NDS) was assessed at 24 h of reperfusion, the rats were then sacrificed, and their brains were immediately removed for determination of brain water content and the infarct volume, and the histopathological changes were observed after HE staining. The levels of cytokines (TNF-α, IL-1β and IL-10) in the ischemia cortex were quantified by ELISA. MPO activity in the ischemia cortex was assessed. Western blot was used to detect the expression of NF-κB in the ischemia cortex. The data were analyzed using SPSS 20.0 software, multiple-group comparisons were performed using one-way ANOVA, and LSD- t test was used for pairwise comparison between groups. A P<0.05 was considered statistically significant different. Results:Compared with the sham group, NDS, brain water content, relative infarction volume and rate of nerve cell necrosis were significantly increased in the I/R and Oxy groups (all P<0.05). Levels of TNF-α, IL-1β, IL-10, NF-κB and the activities of MPO were increased in the ischemia cortex (all P<0.05). Compared the Oxy group with the I/R group, NDS, brain water content, relative infarction volume and rate of nerve cell necrosis were significantly decreased [(1.7±0.9) vs (2.6±1.1);(79.2±2.4)% vs (84.7±4.2)%; (23.0±5.4)% vs (34.8±6.0)%; (25.2±12.4)% vs (54.8±14.8)%, all P<0.05]. The levels of TNF-α, IL-1β, relative expression of NF-κB, and the activities of MPO were significantly decreased in the ischemia cortex [(4.4±1.2) pg/mg vs (6.5±1.2) pg/mg; (5.4±0.7) pg/mg vs (7.8±0.8) pg/mg; (0.83±0.11) vs (1.23±0.33); (0.27±0.09) U/g vs (0.36±0.14) U/g, all P<0.05] , while the concentration of IL-10 was significantly increased [(20.9±4.5) pg/mg vs (9.2±1.6) pg/mg, t=6.036, P=0.000 1]. Conclusions:Oxycodone hydrochloride can attenuate focal cerebral I/R injury through inhibiting NF-κB activity.
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Objective@#To evaluate the effect of irisin preconditioning on global cerebral ischemia-reperfusion (I/R) injury in rats.@*Methods@#Thirty-six healthy male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, were divided into 3 groups (n=12 each) using a random number table method: sham operation group (group S), global cerebral I/R group (group I/R) and irisin preconditioning group (group I). Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg) in anesthetized rats.At 30 min before ischemia, irisin 10 μg/kg (diluted to 10 μg/ml in normal saline) was intravenously injected in group I, and the equal volume of normal saline was intravenously injected in S and I/R groups.Morris water maze test was performed at day 3 of reperfusion to assess the cognitive function.Rats were sacrificed after the end of morris water maze test, and brains were removed for determination of histopathologic changes in hippocampal CA1 region (using HE staining), neuronal apoptosis in hippocampal CA1 region (Tunel staining), glial fibrillary acidic protein (GFAP) expression (by Western blot), myeloperoxidase (MPO) activity in the hippocampal tissues (by colorimetric assay), and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in hippocampal tissues (by enzyme-linked immunosorbent assay). The cell necrosis rate and apoptotic rate were calculated.@*Results@#Compared with group S, the escape latency was significantly prolonged on 1-5 days in group I/R and on 1-3 days in group I, the time of staying at 1st quadrant was significantly shortened, the cell necrosis rate and apoptotic rate were increased, the expression of GFAP was up-regulated, and the activity of MPO and contents of TNF-α and IL-1β were increased in I/R and I groups (P<0.05 or 0.01). Compared with group I/R, the escape latency was significantly shortened on 1-5 days, the time of staying at 1st quadrant was prolonged, the cell necrosis rate and apoptotic rate were decreased, the expression of GFAP was down-regulated, and the MPO activity and contents of TNF-α and IL-1β were decreased in group I (P<0.05 or 0.01).@*Conclusion@#Irisin preconditioning can reduce the global cerebral I/R injury in rats, and the mechanism may be related to inhibiting activation of astrocytes in hippocampus and reducing inflammatory responses.
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Objective To evaluate the effect of irisin preconditioning on global cerebral ischemiareperfusion (I/R) injury in rats.Methods Thirty-six healthy male Sprague-Dawley rats,aged 8-10 weeks,weighing 250-300 g,were divided into 3 groups (n=12 each) using a random number table method:sham operation group (group S),global cerebral I/R group (group I/R) and irisin preconditioning group (group I).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg) in anesthetized rats.At 30 min before ischemia,irisin 10 μg/kg (diluted to 10 μg/ml in normal saline) was intravenously injected in group I,and the equal volume of normal saline was intravenously injected in S and I/R groups.Morris water maze test was performed at day 3 of reperfusion to assess the cognitive function.Rats were sacrificed after the end of morris water maze test,and brains were removed for determination of histopathologic changes in hippocampal CA1 region (using HE staining),neuronal apoptosis in hippocampal CA1 region (Tunel staining),glial fibrillary acidic protein (GFAP) expression (by Western blot),myeloperoxidase (MPO) activity in the hippocampal tissues (by colorimetric assay),and contents of tumor necrosis factor-alpha (TNF-cα) and interleukin-1 beta (IL-1β) in hippocampal tissues (by enzyme-linked immunosorbent assay).The cell necrosis rate and apoptotic rate were calculated.Results Compared with group S,the escape latency was significantly prolonged on 1-5 days in group I/R and on 1-3 days in group I,the time of staying at 1st quadrant was significantly shortened,the cell necrosis rate and apoptotic rate were increased,the expression of GFAP was up-regulated,and the activity of MPO and contents of TNF-α and IL-1β were increased in I/R and I groups (P＜0.05 or 0.01).Compared with group I/R,the escape latency was significantly shortened on 1-5 days,the time of staying at 1st quadrant was prolonged,the cell necrosis rate and apoptotic rate were decreased,the expression of GFAP was down-regulated,and the MPO activity and contents of TNF-α and IL-1β were decreased in group I (P＜0.05 or 0.01).Conclusion Irisin preconditioning can reduce the global cerebral I/R injury in rats,and the mechanism may be related to inhibiting activation of astrocytes in hippocampus and reducing inflammatory responses.
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Objective To evaluate the effect of quercetin pretreatment on the permeability of blood-brain barrier in a rat model of global cerebral ischemia-reperfusion ( I∕R). Methods Sixty-three clean-grade healthy male Sprague-Dawley rats, weighing 300-350 g, aged 4-5 months, were divided into 3 groups (n＝21 each) using a random number table method: sham operation group ( group S), group I∕R and quercetin pretreatment group ( group Q). Global cerebral I∕R was induced by occlusion of bilateral common carotid arteries combined with hypotension ( mean arterial pressure was maintained at 35-45 mmHg) in chloral hydrate-anesthetized rats. Quercetin 25 μmol∕kg was injected intraperitoneally twice a day for 3 consecutive days starting from 3 days before establishment of the model in group Q, while the e-qual volume of normal saline was given instead at the corresponding time points in group S and group I∕R, respectively. The animals were sacrificed at 24 h of reperfusion and brains were removed to determine the brain water content, Evans blue ( EB) content and expression of occludin protein in cerebral cortex ( by Western blot) and to observe the ultrastructure of blood-brain barrier. Results Compared with group S, the brain water content and EB content were significantly increased, the expression of occludin protein was down-regulated (P＜0. 05), and the injury to ultrastructure of blood-brain barrier was accentuated in I∕R and Q groups. Compared with group I∕R, the brain water content and EB content were significantly de-creased, the expression of occludin protein was up-regulated (P＜0. 05), and the injury to ultrastructure of blood-brain barrier was significantly attenuated in group Q. Conclusion Quercetin pretreatment can de-crease the permeability of blood-brain barrier and attenuate brain edema, and the mechanism may be related to up-regulated expression of occludin protein in a rat model of global cerebral I∕R.
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Objective To evaluate the effect of oxycodone on acute lung injury (ALI) induced by lipopolysaecharide (LPS) in rats. Methods Thirty-six pathogen-free healthy male Sprague-Dawley rats, weighing 250-300 g, were divided into 3 groups (n= 12 each) using a random number table: sham opera-tion group (group S), LPS-induced ALI group (group A) and oxycodone group (group O). ALI was in-duced by injecting LPS 8 mg∕kg intravenously in A and O groups, while the equal volume of normal saline was given instead in group S. Oxycodone 2 mg∕kg was injected intravenously at 10 min before LPS injection in group O, while the equal volume of normal saline was given instead in S and A groups. Rats were sacri-ficed at 6 h after LPS injection, and the broncho-alveolar lavage fluid (BALF) was collected for detection of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) concentrations by enzyme-linked im-munosorbent assay. Pulmonary specimens were obtained for microscopic examination of the pathological changes and for determination of wet∕dry weight ratio (W∕D ratio) and expression of Toll-like receptor 4 (TLR4) in lung tissues (using real-time polymerase chain reaction and Western blot). Results Compared with group S, the TNF-α and IL-1β concentrations in BALF, W∕D ratio, pathological scores and expres-sion of TLR4 were significantly increased at 6 h after LPS injection in A and O groups (P<0. 05). Com-pared with group A, the TNF-α and IL-1β concentrations in BALF, W∕D ratio, pathological scores and expression of TLR4 were significantly decreased at 6 h after LPS injection in group O (P<0. 05). Conclu-sion Oxycodone can attenuate LPS-induced ALI in lung tissues, and the mechanism is related to down-regulating the expression of TLR4 and inhibiting inflammatory responses of rats.
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Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.
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Objective To investigate the etiology and novel treatment of plasma cell mastitis (PCM).Methods 145 cases of PCM undergoing massage dredge,ductal lavage and local amalgesic injection from Jan.2011 to Dec.2012 were retrospectively analyzed.Results 145 cases of PCM underwent conservative treatment for 2 to 8 weeks,among whom 128 cases were cured and the other 17 cases underwent surgical treatment for poor outcome.Among the 128 cases undergoing conservative treatment,9 cases had relapse during the follow-up of 12 to 36 months.Conclusions The combined treatment of massage dredge,ductal lavage and partial closed treatment is effective for patients with PCM,and it can keep patients from having mastectomy and reduce the recurrent rate.
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PURPOSE: Synuclein-gamma (SNCG), which was initially identified as breast cancer specific gene 1, is highly expressed in advanced breast cancers, but not in normal or benign breast tissue. This study aimed to evaluate the effects of SNCG siRNA-treatment on breast cancer cells and elucidate the associated mechanisms. METHODS: Vectors containing SNCG and negative control (NC) siRNAs were transfected into MDA-MB-231 cells; mRNA levels were determined by real-time polymerase chain reaction. Cell proliferation was evaluated using the MTT assay, cell migration was assessed by the Transwell assay, apoptosis and cell cycle analyses were conducted with the flow cytometer, and Western blot analysis was performed to determine the relative levels of AKT, ERK, p-AKT, and p-ERK expression. RESULTS: SNCG mRNA levels were significantly reduced in MDA-MB-231 cells transfected with SNCG siRNA. Our results indicate that in SNCG siRNA-treated cells, cell migration and proliferation decreased significantly, apoptosis was induced, and the cell cycle was arrested. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the SNCG siRNA-treated groups, than in the control and NC groups. CONCLUSION: SNCG siRNA could decrease the migration and proliferation of breast cancer cells by downregulating the phosphorylation of AKT and ERK.
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Apoptosis , Blotting, Western , Breast , Breast Neoplasms , Cell Cycle , Cell Migration Assays , Cell Movement , Cell Proliferation , Extracellular Signal-Regulated MAP Kinases , Phosphorylation , Proto-Oncogene Proteins c-akt , Real-Time Polymerase Chain Reaction , RNA, Messenger , RNA, Small Interfering , SynucleinsABSTRACT
Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.
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Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.
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Objective To investigate the effect of lipoxin A4 ( LXA4 ) on the permeability of blood-brain barrier (BBB) after focal cerebral ischemia-repeffnsion (I/R) in rats. Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups ( n = 18 each): group Ⅰ sham operation (group S); group Ⅱ focal cerebral I/R ( group I/R) and group Ⅲ LXA4 ( group L). Focal cerebral I/R was produced by middle cerebral artery occlusion (MCAO) with a 4-0 nylon thread with rounded tip inserted into right internal jugular vein and threaded cranially in group Ⅱ and Ⅲ . In group Ⅲ LXA4 100 ng was injected into right lateral ventricle of the brain after MCA was successfully occluded. MCAO was maintained for 2 h. The neurological deficit was evaluated and scored (0 = no deficit, 5 = death) at 24 h of reperfusion. 2% Evans blue 4 ml/kg was injected via femoral vein at 1 h before the animals were sacrificed. The animals were killed and their brains were immediately removed for determination of brain water content, Evans blue content and expression of matrix metalloproteinase-9 (MMP-9)in the ischemic cortex. Results The neurologic deficit scores, the brain water and Evans blue content and MMP-9 protein expression in the cortex were significantly higher in I/R group than in S group. The cerebral I/R-induced changes were significantly attenuated in LXA4 group. Conclusion LXA4 can protect blood-brain barrier against cerebral I/R injury by inhibiting MMP-9 protein expression in the brain tissue.
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Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P ＜ 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P ＜0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P ＜ 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats.
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Objective To investigate the effects of simvastatin pretreatment on ischemia-reperfusion (I/R)injury to the spinal cord in rats. Methods Ninety-six healthy male SD rats weighing 220-280 g were randomly divided into 3 groups (n=32 each): Ⅰ group sham operation (group S); Ⅱ group I/R and Ⅲ group simvastatin pretreatment (group Si). The animals were anesthetized with 10% chloral hydrate 0.4 ml/100g. I/R to the spinal cord was induced by cross-clamping the aorta below renal artery for 45 min followed by reperfusion according to Zivin in group Ⅱ and Ⅲ. In group Ⅲ simvastatin 20 mg/kg was administered via gastric tube in the morning for 3 days before operation. Neurological function was assessed and scored (0 = no spontaneous movement of the hindlimbs, 7 = normal gait) at 2, 6, 12 and 24 h (n = 8 at each time point). The animals were then sacrificed and the lumbar segment (L2-5) of the spinal cord was removed for microscopic examination and determination of expression of TLR4 mRNA, NF-κB protein activity and TNF-α and ICAM-1 contents in the spinal cord. Results I/R to the spinal cord significantly increased TLR4 mRNA expression, NF-κB protein activity and TNF-α and ICAM-1 content in the spinal cord and decreased neurological scores in group Ⅱ compared with group C. Simvastatin pretreatment significantly attenuated the I/R-induced increase in the above-mentioned variables and ameliorated I/R-induced neurological dificit and histopathological damage. Conclusion Simvastatin pretreatment has neuroprotective effects on the spinal cord against I/R injury by attenuating inflammatory response.
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Objective To investigate the effect of lipoxin A4(LXA4) on inflammatory response in a rat model of permanent focal cerebral ischemia (PFCI). Methods Seventy-two adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n = 24 each):group Ⅰ sham operation (group S); group Ⅱ PFCI and group Ⅲ LXA4. PFCI was induced by thread occlusion of right middle cerebral artery according to the method described by Longa in group Ⅱ and Ⅲ. In group Ⅲ LXA4 100 ng/5 μl was injected into right ventricle of the brain after PFCI was successfully induced, while in group Ⅰ and Ⅱ equal volume of normal saline was injected instead of LXA4. Six animals were killed at 6, 12 and 24 h of ischemia. Their brains were immediately removed for microscopic examination and determination of myeloperoxidase (MPO) activity, TNF-α, IL-10 and transforming growth factor-β1 (TGF-β1) contents in the ischemic cortex. The expression of glial fibrillary acidic protein (GFAP)was measured by immuno-histochemistry. Apoptosis in neurons was assessed using TUNEL. Results PFCI significantly increased MPO activity, TNF-α, IL-10 and TGF-β1 contents and GFAP expression in the ischemic cortex and neuronal apoptosis in group Ⅱ as compared with group S. LXA4 significanfly decreased MPO activity,TNF-α content, GFAP expression and neuronal apoptosis and increased IL-10, TGF-β1 contents at 12,24 h of ischemia. LXA4 significantly ameliorated PFCI-induced cerebral histopathologic damage. Conclusion LXA4 can protect the brain against PFCI injury by inhibiting inflammatory response.
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Objective To investigate the effects of flurbiprofen pretreatment on the permeability of bloodbrain barrier in a rat model of global cerbral ischemia-reperfusion (I/R) injury. Methods Forty-five male SD rats weighing 300-350 g were randomly divided into 3 groups (n = 15 each): sham operation group (group S); global cerebral I/R group (group I/R); flurbiprofen 10 mg/kg + global cerebral I/R group (group F). Global cerebral ischemia was induced by 20 min occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg). In group F, flurbiprofen 10 mg/kg was injected iv at 15 min before ischemia. Evans blue 3 ml/kg was injectcd iv at 24 h of reperfusion, then the rats were sacrificed and their brains were immediately removed for determination of the apoptosis rate, brain water content, Evans blue content, TNF-α, IL-1β and IL-10 content, and microscopic examination. Results The apoptosis rate, brain water content, Evans blue content, and TNF-α, IL-1β and IL-10 content were significantly higher in group I/R and F than in group S (P ＜ 0.05 or 0.01).The apoptosis rate, brain water content, and Evans blue content and TNF-α and IL-1β content were significantly lower, while IL-10 content was higher in group F than in group I/R (P ＜ 0.01). Global cerbral I/R-induced changes were significantly attenuated in group F. Conclusion Pretreatment with flurbiprofen can protect bloodbrain barrier against cerebral I/R injury by inhibition of the inflammatory reaction.
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Objective:To investigate the effect of flurbiprofen axetil on the pain after artifical abortion and its mechanism. Methods: A total of 120 ASAⅠ~Ⅱ induced abortion patients were randomly divided into 4 groups(n=30 each). Group F50 was treated with flurbiprofen axetil(50 mg) combined with propofol,Group F75 with flurbiprofen axetil(75 mg) combined with propofol,Group C with blank emulsion combined with propofol and Group K with ketamine combined with propofol.All patients took Misoprostol tablet by mouth 2 hours before artifical abortion, patients of group F50,group F75 and group C were intravenousely injected flurbiprofen axetil or blank emulsion five minutes before propofol, and patients of group K were administered mixed solution of ketamine and propofol. HR, BP, side effect,and pain of VAS score after artifical abortion were recorded. Reslts: Pain of VAS score after artifical abortion in group C and group K were higer than those of group F50 and group F75 at the same time(P
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PONV (Postoperation nausea and vomiting) is one of the most possible problems after operation, and it has been a barraier to recovery of patients who had been orperationed, This review will focus on risk factors and prophylactic antiemetic therapy for PONV.
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AIM: To investigate the short-term efficacy and safety of sulfasalazine (SASP) 3 g per day in the treatment of patients with mild and moderate ulcerative colitis (UC). METHODS: 122 patients were treated with SASP ( 1 g, t.i.d.) for 6 weeks. The data of clinical manifestations, colonoscopic and histological involvements were compared before and after the treatment of UC. The short-period efficacy and adverse reactions were evaluated in 110 patients. RESULTS: The therapeutic project was carried out in the 110 out of 122 patients. After 110 patients were treated for 6 weeks, the clinical, colonoscopic and histological remission were 71.8%, 21.8% and 16.4%, respectively. Among the 79 patients with clinical remission, 58.2% and 67.1% of them remained grade 1 in colonoscopic and histological findings, respectively. The curative rates and the effective rates were 63.9% and 82.0%, respectively. Among the 122 patients treated with SASP, 21 of them ( 17.2%) had adverse reactions. Except 4 patients suffered urticaria and leukopenia, no patients quitted the treatment because of obvious adverse reaction. CONCLUSION: SASP ( 3 g per day) can be an effective and safe medicine in treatment of patients with mild and moderate UC, but more than half of the patients in clinical remission still have light inflammation in colonoscopy and histology.
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Objective To study the value of BCSG1 on evaluating the curative effect of neoadjuvant chemotherapy(NC) for breast cancer.Methods The expression of BCSG1 in cancer tissue was assayed by immunohistochemistry and RT-PCR in 36 cases of breast cancer patients before and after receiving NC of CEF(cyclophosphamide,epirubicin and fluorouracil) regimen.The therapeutic response of NC was evaluated by morphological and pathological observation.The relationship between expression of BCSG1 and morphological response to NC was analyzed.Results Among the studied cases,the diameter of tumor significantly decreased(P
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Objective To assess the clinical significance of endoscopic ultrasonography (EUS) in the diagnosis and preoperative staging of gastric cancer. Methods EUS was carried out in 22 patients inclu-ding 17 gastric cancer patients and 5 patients in suspicion. Helical CT scanning was performed in all of the patients and fine needle aspiration biopsies ( FNAB) were administrated to 5 suspicious patients. Compared the results of operation and pathology with those of tumor staging by estimating the depth of tumor invasion ( T) , local lymph node metastasis ( N) and metastasis to neighboring or remote organs ( M) in order to esti-mate the accuracy of diagnosis and TNM staging. The sensitivity and specificity of tumor-node-metastasis staging of gastric cancer by EUS were compared with those of the spiral CT according to the final histopatho-logical results. Results In 5 suspicious patients specimens were successfully obtained by FNAB under the guide of EUS with the pathological diagnosis of adenocarcinoma in 4 cases and signet ring cell carcinoma, 1 case. All patients underwent radical gastrectomy except one in T1N0M0, staging was treated by endoscopic mucosal resection (EMR). The sensitivity and specificity of EUS in T, N, and M stage were 84.9% and 74. 2% , 92. 1% and 77. 1% , 63. 4% and 87. 5% respectively; whereas those of CT in T, N, and M stage were 27. 3% and 75% , 31.5% and 100% , 50% and 100% respectively. The sensitivity of EUS in T and N staging were higher than those of CT with significant statistical difference (P