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81.
目的 探讨JNK信号通路在小鼠术后肠麻痹(POI)发病机制中的作用。方法 将野生型C57/BL6小鼠(WT)及同品系的JNK-/-小鼠均随机分成假手术组(Sham组,n=6)和肠麻痹组(POI组,n=6)。采用经典小肠操作方法诱导POI模型,术后24h给小鼠碳末灌胃,20min后麻醉小鼠,开腹取小肠评估肠动力,取回肠评估组织学改变,检测髓过氧化物酶(MPO)、IL-1β、IL-6水平及Claudin-2蛋白表达。结果 与Sham组小鼠相比,无论WT或JNK-/-小鼠其POI组的小肠排推率(分别为21%与33%)均明显降低(P=0.034及P=0.045,均P<0.05),小肠组织MPO活性水平(分别为0.608U/g与0.433U/g)明显升高(均P<0.05);与WT小鼠POI组比较,JNK-/-小鼠POI组的小肠运动功能及其组织病理变化有所改善,炎症介质如MPO、IL-1β及IL-6水平均有明显降低(均P<0.05),小肠Claudin-2蛋白表达也降低(P<0.01)。结论 JNK基因敲除减轻小鼠肠道炎症反应、改善POI,表明JNK信号通路参与POI的发病过程。  相似文献   
82.
Summary We report a study of a 22-year-old woman with a plasma-cell granuloma (PCG), a rare intracranial lesion characterized by a non-neoplastic polyclonal proliferation of plasma cells and other mononuclear cells. She presented after a generalized seizure and CT-scan and magnetic resonance images demonstrated a left temporo-basal tumour mass involving both the meningeal layers and the brain parenchyma. Histopathological examination of a biopsy led to the diagnosis of a typical PCG. After a short course of steroid administration, the clinical and radiological features improved and complete regression of the lesion was shown after one year and persisted at four-year follow-up. This dramatic regression of an intracranial PCG shows that neither surgical removal nor radiation therapy is required to treat a broad skull base PCG.  相似文献   
83.
【摘要】 目的 比较甲基强的松龙(甲强龙)与地塞米松治疗术后早期炎性肠梗阻的疗效。方法 回顾性分析2002年7月至2012年7月收治的66例炎性肠梗阻患者的临床资料,依据使用不同激素分为甲强龙组和地塞米松组,观察比较两组疗效及不良反应。结果 66例患者均采用保守方法治愈,无中转手术病例。甲强龙组腹胀、腹痛缓解时间,肛门排气时间和治愈时间均少于地塞米松组,具有统计学差异(P<0.05)。结论 甲强龙治疗术后早期炎性肠梗阻疗效优于地塞米松。  相似文献   
84.
肺部孤立性炎性病变CT分析   总被引:2,自引:1,他引:2  
目的 旨在提高对肺部孤立性炎性病变的认识 ,提高对该病的正确诊断率。方法 肺部孤立性炎性病变 2 1例 ,其中 4例手术治疗 ,4例经皮CT引导下肺穿刺活检 ,13例抗炎治疗后CT随访复查。 2 1例病灶部位均行 2~ 5mm薄层CT扫描。结果 ①病变形态呈方形、三角形及不规则形 13例。②病灶边缘部分清楚 ,部分模糊 ,在肺窗清楚 ,纵隔窗消失 12例。③病变周边密度较低 ,呈带状低密度 9例。④抗炎治疗 2~ 10周病灶逐渐吸收 11例 ,2例残留条索阴影。结论 病灶形态呈方形或不规则形 ,病灶中央密度较高 ,边缘密度较低且边缘部分清楚 ,部分模糊 ,肺窗清楚 ,纵隔窗消失 ,对肺部孤立性炎性病变的诊断有很大价值 ,必要时再行经皮CT引导下肺穿刺活检 ,能提高肺部孤立性炎性病变的正确诊断率。另外 ,对基层医院而言 ,薄层CT扫描尤其必要  相似文献   
85.
Systemic inflammatory responses in patients receiving cardiac surgery with the use of the cardiopulmonary bypass (CPB) significantly contribute to CPB‐associated morbidity and mortality. We hypothesized that insufflated hydrogen gas (H2) would provide systemic anti‐inflammatory and anti‐apoptotic effects during CPB, therefore reducing proinflammatory cytokine levels. In this study, we examined the protective effect of H2 on a rat CPB model. Rats were divided into three groups: the sham operation (SHAM) group, received sternotomy only; the CPB group, which was initiated and maintained for 60 min; and the CPB + H2 group in which H2 was given via an oxygenator during CPB for 60 min. We collected blood samples before, 20 min, and 60 min after the initiation of CPB. We measured the serum cytokine levels of (tumor necrosis factor‐α, interleukin‐6, and interleukin‐10) and biochemical markers (lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase). We also measured the wet‐to‐dry weight (W/D) ratio of the left lung 60 min after the initiation of CPB. In the CPB group, the cytokine and biochemical marker levels significantly increased 20 min after the CPB initiation and further increased 60 min after the CPB initiation as compared with the SHAM group. In the CPB + H2 group, however, such increases were significantly suppressed at 60 min after the CPB initiation. Although the W/D ratio in the CPB group significantly increased as compared with that in the SHAM group, such an increase was also suppressed significantly in the CPB + H2 group. We suggest that H2 insufflation is a possible new potential therapy for counteracting CPB‐induced systemic inflammation.  相似文献   
86.
We previously reported Rho kinase is involved in vessel hyper-permeability caused by burns. Here we further explore the Rho kinase downstream signaling, it is found that its specific inhibitor Y27632 significantly diminishes the activation of JNK and p38 MAPKs but not ERK that induced by serum from burned rats (burn-serum). JNK activation was found involved in the expression of HUVEC adhesion molecules following thermal injury, although not in the process of stress fiber formation. Inhibition of various MAPKs by specific inhibitors showed that SB203580 (inhibitor of p38), but neither SP600125 (inhibitor of JNK) nor PD98059 (inhibitor of ERK), abolish activation of the p38 downstream kinase MK2. Demonstration of stress fibers by fluorescent-labeled phalloidin showed that inhibition of MK2, either by its specific inhibitor or by dominant negative adeno-viral-carried constructs, significantly reduced burn-serum-induced HUVEC stress-fiber formation, while inhibition of another downstream p38 MAPK kinase, PRAK, had no such effects. Transfection of dominant negative adeno-viral MK2 (Ad-MK2(A)) significantly inhibited thermal injury-induced blood vessel hyper-permeability in rats and, moreover, prolonged the survival of burned rats beyond 72 h following thermal injury. One of the mechanisms behind these phenomena is that Ad-MK2(A) causes a significant depression of burn-serum-induced HSP27-phosphorylation, while the adeno-viral transported dominant negative PRAK (Ad-PRAK(A)) does not block. Although the effect of blockade of MK2 through its adeno-viral approach requires further study and investigation of alternatives to know for sure, we may have found a new pathway behind thermal-injury-induced blood vessel hyper-permeability, namely: Rho kinase > p38 > MK2 > HSP27.  相似文献   
87.

Background

Operations on the infrarenal aorta can cause ischemic-reperfusion (IR) injury in local tissues, which could result in remote organ (e.g., lung) damage. Treatment of such injuries remains an unresolved problem.

Objectives

Our aim was to reduce remote lung damage after lower limb IR by means of postconditioning.

Materials and methods

Male Wistar rats were divided into three groups: Sham-operated, IR, and Postconditioned (PostC). In the latter two groups rats underwent 180 min of exclusion of the infrarenal aorta. The reperfusion time was 4 h. Serum-free radical levels, tumor necrosis factor-α and interleukin-6 concentrations, histologic changes in the lung, wet/dry-ratio, myeloperoxidase activity, heat shock protein 72 level and blood gas changes were investigated.

Results

Postconditioning reduced histological damage in the lung (P < 0.05). Free radical levels and tumor necrosis factor-α concentrations were significantly lower in the PostC group than in the IR group (P < 0.05 and P < 0.01, respectively). Interleukin-6 concentrations did not significantly differ in the PostC group. Compared with the IR group, lung myeloperoxidase activity was lower in the PostC group. Decreased pulmonary heat shock protein 72 level was observed in the PostC group compared with the IR group and the wet/dry-ratio was also significantly lower in the PostC group (P < 0.05). A noticeably higher arterial pO2 level was manifest in the PostC group after 2 and 4 h of reperfusion (P < 0.05).

Conclusions

Postconditioning reduced lung damage under experimental conditions, in the early period of reperfusion after lower limb IR injury.  相似文献   
88.
Cerebralcare Granule(CG) improves cerebral microcirculation and relieves vasospasm,but studies investigating its therapeutic effect on cerebral ischemia/reperfusion injury are lacking.In the present study,we administered CG(0.3,0.1 and 0.03 g/m L intragastrically) to rats for 7 consecutive days.We then performed transient occlusion of the middle cerebral artery,followed by reperfusion,and administered CG daily for a further 3 or 7 days.Compared with no treatment,high-dose CG markedly improved neurological function assessed using the Bederson and Garcia scales.At 3 days,animals in the high-dose CG group had smaller infarct volumes,greater interleukin-10 expression,and fewer interleukin-1β-immunoreactive cells than those in the untreated model group.Furthermore,at 7 days,high-dose CG-treated rats had more vascular endothelial growth factor-immunoreactive cells,elevated angiopoietin-1 and vascular endothelial growth factor expression,and improved blood coagulation and flow indices compared with untreated model animals.These results suggest that CG exerts specific neuroprotective effects against cerebral ischemia/reperfusion injury.  相似文献   
89.
洪丽莉 《武警医学》2022,33(12):1062-1064
 目的 探讨伏诺拉生治疗重症反流性食管炎(RE)的疗效及其对胃泌素和炎症因子的影响。方法 选取2021-02至2022-02在武警安徽总队医院消化科门诊确诊为重症RE患者62例,随机分为伏诺拉生组(31例)和对照组(31例)。伏诺拉生组采用伏诺拉生和依托必利治疗,对照组采用雷贝拉唑和依托必利治疗。比较两组治疗后临床有效率,以及治疗前后内镜评分、胃泌素、TNF-α、IL-6。结果 伏诺拉生组的有效率为87.10%,显著高于对照组(64.52%),差异有统计学意义(χ2=4.309,P<0.05);治疗后,两组内镜评分(0.30±0.13, 0.64±0.26)均明显低于治疗前(3.42±0.51,3.38±0.48),并且伏诺拉生组改善得更显著(t=-6.51,P<0.01)。伏诺拉生组的胃泌素水平[(88.93±11.37) pg/ml]明显高于对照组[(60.78±7.98) pg/ml],而TNF-α[(5.95±0.68) pg/ml]、IL-6[(5.55±0.67) pg/ml]水平明显低于对照组[(7.88±0.99)pg/ml,(8.24±0.92)pg/ml],且差异均有统计学意义(P<0.01)。两组均发生1例不良反应(3.23%)。结论 伏诺拉生治疗重症RE可明显提升有效率,可修复损伤的胃黏膜,同时可显著调整血清胃泌素及炎症因子水平而不增加不良反应。  相似文献   
90.
目的:观察麝香、乳香配伍组合对虎杖提取物治疗慢性非细菌性前列腺炎模型大鼠前列腺组织病理及炎症因子表达的影响。方法:53只健康雄性Wistar大鼠,5只用于大鼠前列腺蛋白提纯液的制备,48只随机分为麝香配伍乳香+虎杖提取物组、虎杖提取物、模型组、正常对照组共4组。除正常对照组外,应用大鼠前列腺蛋白提纯液辅以免疫佐剂制备实验性慢性非细菌性前列腺炎大鼠模型,造模60 d时正常对照组、模型组予生理盐水,虎杖提取物、麝香配伍乳香+虎杖提取物组分别予生药量虎杖1.575 g/(kg.d)、麝香0.021 g/(kg.d)、乳香1.05 g/(kg.d)按组别选用连续灌胃,各组给药14 d时处死,检测指标包括病理学,ELISA法检测前列腺组织匀浆TNF-α、IL-1β、IL-6、IL-8水平,RT-PCR及Western印迹方法检测炎症因子MCP-1(CCL2)、CCR2 mRNA及蛋白表达。结果:麝香配伍乳香+虎杖提取物组前列腺组织结构改善,无明显炎性细胞浸润,虎杖提取物组可见炎性细胞浸润。麝香配伍乳香+虎杖提取物组明显降低前列腺组织炎症因子(TNF-α:11.04±4.07、IL-1β:16.94±4.26、IL-6:110.08±28.42、IL-8:26.28±7.36,pg/ml),优于单纯虎杖提取物组(TNF-α:63.21±21.37、IL-1β:41.32±14.62、IL-6:177.64±42.65、IL-8:96.37±37.61,pg/ml),差异有统计学意义(P<0.05,P<0.01)。麝香配伍乳香+虎杖提取物组大鼠前列腺组织炎症趋化因子MCP-1(CCL2)及其受体CCR2的mRNA(MCP-1:0.32±0.17;CCR2:0.28±0.11)及蛋白(MCP-1:0.28±0.15;CCR2:0.11±0.04)表达水平与模型组(MCP-1 mRNA:1.15±0.39;MCP-1蛋白:0.93±0.34;CCR2 mRNA:0.83±0.26;CCR2蛋白:0.93±0.34)比较显著降低(P<0.01),显著优于虎杖提取物组(MCP-1 mRNA:0.65±0.27;MCP-1蛋白:0.56±0.22;CCR2 mRNA:0.78±0.24;CCR2蛋白:0.25±0.09),差异有统计学意义(P<0.05,P<0.01)。结论:麝香乳香配伍组合的应用具有促进虎杖提取物对慢性前列腺炎的治疗,降低炎症反应程度,从而促进前列腺组织结构修复的作用。  相似文献   
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