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1.
目的：通过康脑液干预观察其对脑缺血再灌注损伤大鼠血管内皮生长因子（vascular endothelial growth factor,VEGF）、脑源性神经生长因子（brain derived neurotrophic factor,BDNF）、基质金属蛋白酶（matrix metalloproteinase-9,MMP-9）表达的影响,探讨康脑液对脑缺血再灌注损伤的保护机制.方法：将雄性SD大鼠随机分为假手术组、脑缺血再灌注模型组及康脑液28.6、14.3、7.15 g·kg-1·d-1剂量组（灌胃给药7 d）,改进Longa等线栓法制备大鼠右侧大脑中动脉阻塞（middle cerebral artery occlusion,MCAO）再灌注模型.于缺血2h后再灌注（分别于再灌注后6h、12h、24 h、72 h、7d处死大鼠）;采用TTC染色法观察大鼠的脑梗死面积;免疫组织化学法观察大鼠脑组织VEGF、BDNF、MMP-9的表达.结果：比较各组缺血再灌注24 h大鼠脑梗死灶面积,发现28.6、14.3 g·kg--1·d-1剂量组较脑缺血再灌注模型组明显减小（P＜0.05）;与脑缺血再灌注模型组相比,28.6、14.3 g·kg--1·d-1剂量组各时间点的VEGF、BDNF表达量明显上调（P＜0.01）,MMP-9表达的阳性细胞明显减少（P＜0.01）,差异有统计学意义.结论：康脑液可促进大鼠局灶性脑缺血后脑组织中VEGF,BDNF的表达,同时抑制脑内MMP-9的表达,缩小脑梗死面积,发挥对神经血管单元（neurovascular unit,NVU）的保护作用,减轻脑缺血再灌注损伤.  相似文献   

2.

Objective

The aim of this study was to evaluate the concentrations of C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and the degree of homeostasis model assessment-insulin resistance (HOMA-IR) in patients with morbid obesity exposed to a three-week low-calorie diet and balneotherapy.

Methods

The study included 33 patients (25 females and 8 males; mean age 46 years) with body mass index (BMI) values of >40 kg/m2. Evaluations of CRP, IL-6, TNF-α, lipid profile, HOMA-IR, and fasting glucose were carried out before (baseline data) and three weeks after the treatment. The control group consisted of 20 healthy volunteers (15 females and 5 males) with a mean age of 39 years and BMI values of ≤24.9 kg/m2.

Results

In the blood of patients with morbid obesity we found significantly elevated levels of CRP, TNF-α, triglycerides, HOMA-IR and fasting glucose, but a decreased level of high density lipoprotein (HDL)-cholesterol, compared with the healthy individuals. The treatment resulted in about a 9.4% reduction in body weight from 122.5 to 111.0 kg and a significant decrease in the concentration of CRP, but no change in TNF-α or IL-6. HOMA-IR was significantly reduced.

Conclusion

The decrease in CRP level without changes in TNF-α or IL-6 concentrations after the low-calorie diet and balneological treatment, suggests that an essential amount of adipose tissue must be removed before proper adipocyte function is restored. The decrease in HOMA-IR indicates an improvement in insulin sensitivity, which is beneficial in obese patients.
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3.
目的：探讨前期研究筛选出的丹参七种水溶性有效成分最优配伍组合样品A2、B4、C11对脑缺血再灌注（ischemia reperfusion）小鼠学习记忆的保护作用。方法：采用改进的Himori法暂时性阻断两侧颈总动脉制备小鼠脑缺血再灌注损伤模型,应用水迷宫实验,观察配伍组合样品对脑缺血再灌注小鼠记忆功能的保护作用,检测小鼠断头耐缺氧存活时间,脑组织中超氧化物歧化酶（superoxi dedismutase,SOD）、过氧化氢酶（catalase,CAT）、乙酰胆碱酯酶（aeetyleholine esterase,ACHE）活力及丙二醛（malondialdehyde,MDA）含量。免疫组织化学方法检测小鼠海马神经元凋亡相关天冬氨酸特异性半胱氨酸蛋白酶-3（cysteine-asparate protease-3,caspase-3）和神经生长因子（nerve growth factor,NGF）的表达。结果：丹参7种水溶性有效成分配伍组合样品B4、C1l可明显改善小鼠脑缺血再灌注所致的记忆障碍,增强耐缺氧能力,提高脑内SOD,CAT活性,降低AChE活性和MDA含量;抑制凋亡蛋白caspase．3表达,上调NGF表达。其中以B4（2．8μm01·L-1）、C11（30．0iμmol·L-1）组作用最为明显（P〈0．01）,A2各个剂量组效果不显著（P〉0．05）。结论：丹参7种水溶性有效成分配伍组合样品B4、C11对脑缺血再灌注损伤小鼠记忆功能有保护作用,其机制可能通过提高清除脑内自由基能力,抑制小鼠神经细胞凋亡,促进神经再生,来减轻脑缺血再灌注引起的脑组织损伤。  相似文献   

4.
INTRODUCTION GM1 ganglioside (GM1) is the main kind ofgangliosides in mammalia, and most abundant inbrain tissue (Duchemin et al., 2002). It was reportedthat GM1 could protect cerebral ischemia in vivo andin vitro, one protective mechanism of which is thatGM1 could reduce neural injury induced by toxicityof excitatory amino acid via N-methyl-D-aspartate receptor (NMDAR) (Kharlamov et al., 1993; Simon et al., 1993; Garofalo and Cue…  相似文献   

5.

Objective

Keloids are exuberant cutaneous scars that form due to abnormal growth of fibrous tissue following an injury. The primary aim of this study was to assess the efficacy and mechanism of hyperbaric oxygen therapy (HBOT) to reduce the keloid recurrence rate after surgical excision and radiotherapy.

Methods

(1) A total of 240 patients were randomly divided into two groups. Patients in the HBOT group (O group) received HBOT after surgical excision and radiotherapy. Patients in the other group were treated with only surgical excision and radiotherapy (K group). (2) Scar tissue from recurrent patients was collected after a second operation. Hematoxylin and eosin (H&E) staining was used to observe keloid morphology. Certain inflammatory factors (interleukin-6 (IL-6), hypoxia-inducible factor-1α (HIF-1α), tumor necrosis factor-α (TNF-α), nuclear factor κB (NF-κB), and vascular endothelial growth factor (VEGF)) were measured using immunohistochemical staining.

Results

(1) The recurrence rate of the O group (5.97%) was significantly lower than that of the K group (14.15%), P<0.05. Moreover, patients in the O group reported greater satisfaction than those in the K group (P<0.05). (2) Compared with the recurrent scar tissue of the K group, the expression levels of the inflammatory factors were lower in the recurrent scar tissue of the O group.

Conclusions

Adjunctive HBOT effectively reduces the keloid recurrence rate after surgical excision and radiotherapy by improving the oxygen level of the tissue and alleviating the inflammatory process.
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6.

Objective

Bovine endometritis is one of the most common reproductive disorders in cattle. The aim of this study was to investigate the anti-inflammation potential of punicalagin in lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and to uncover the underlying mechanisms.

Methods

bEECs were stimulated with different concentrations (1, 10, 30, 50, and 100 μg/ml) of LPS for 3, 6, 9, 12, and 18 h. MTT assay was used to assess cell viability and to identify the conditions for inflammatory injury and effective concentrations of punicalagin. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess gene expression of pro-inflammatory cytokines. Western blotting was used to assess levels of inflammation-related proteins.

Results

Treatment of bEECs with 30 μg/ml LPS for 12 h induced cell injury and reduced cell viability. Punicalagin (5, 10, or 20 μg/ml) pretreatment significantly decreased LPS-induced productions of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) in bEECs. Molecular research showed that punicalagin inhibited the activation of the upstream mediator nuclear factor-κB (NF-κB) by suppressing the production of inhibitor κBα (IκBα) and phosphorylation of p65. Results also indicated that punicalagin can suppress the phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).

Conclusions

Punicalagin may attenuate LPS-induced inflammatory injury and provide a potential option for the treatment of dairy cows with Escherichia coli endometritis.
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7.
目的为进一步探讨细胞因子在类风湿关节炎中的作用．方法５０只ＳＤ大鼠以完全弗氏佐剂（ＦＣＡ）形成ＡＡ动物模型．随机分为Ⅰ组（２周）、Ⅱ组（３周）、Ⅲ组（４周）、Ⅳ组（８周）以及Ⅴ组（正常对照）．分别对各组大鼠血清前炎症细胞因子ＴＮＦ－α、ＩＬ－６以及抑制性细胞因子 ＩＬ－４、 ＩＬ－ １０水平进行测定（ＥＬＩＳＡ法）．同时检查炎症指标血沉（ＥＳＲ）、关节肿胀度、病理切片，所有结果进行对比并做动态分析．结果ＡＡ大鼠Ⅰ－Ⅲ组ＥＳＲ水平及关节肿胀度与对照组均有显著差异（Ｐ＜０．０１）；ＴＮＦ－α组水平各组均高于正常（Ｐ＜０．０５，Ｐ＜０．０１，Ｐ＜０．００１）；ＩＬ－６水平Ⅱ组（Ｐ＜０．０５）、Ⅲ组高于正常；ＩＬ－４水平Ⅰ组、Ⅱ组低于正常组，Ⅲ组、Ⅳ组高于正常组，但均无显著性意义；与正常组比较，ＩＬ－１０水平Ⅰ组（Ｐ＜０．００１）、Ⅱ组（Ｐ＜０．０５）、Ⅲ组均低于正常，Ⅳ组高于正常组并有非常显著性意义（Ｐ＜０．０１）；细胞因子动态观察结果，ＴＮＦ－α、ＩＬ－ ６水平随急性期（第２周）开始而升高，高峰水平随急性期过去（第８周）而下降．而调节性因子ＩＬ－４、ＩＬ－１０高峰时间滞后于炎症因子，并随慢性期延长而升高．结论ＡＡ大?  相似文献   

8.
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9.
吸入麻醉药因其安全、可靠、稳定、易于控制等特性广泛应用于临床全麻手术中。近年来研究表明,吸入麻醉药可以通过减轻细胞损伤,降低梗死面积等方式在分子和细胞水平对脑、心脏、肝脏、肾脏等器官的缺血再灌注损害起到一定的保护作用。吸入麻醉药可通过激活离子通道、抑制细胞凋亡、基因调控、减少自由基产生等多种途径发挥保护作用。该文综述了吸入麻醉药对机体脏器的保护作用及其机制。  相似文献   

10.
观察适应性运动对大鼠大强度离心运动后不同时相骨骼肌结构及血浆IL《变化的影响。方法：80只大鼠分为对照组和实验组,实验组进行两周离心跑台训练。两周后观察各组在运动前及完成一次性跑台离心运动后即刻、24h、48h和72h观察比目鱼肌结构及血浆IL-6的变化。结果：（1）运动后两组大鼠比目鱼肌均出现损伤性改变,尤以对照组更为明显,且以运动后24-48小时较为严重。（2）对照组运动后即刻血浆IL-6显著增高,随后逐渐下降,72h再次显著增高。实验组运动后48h达峰值。实验组运动后血浆IL-6水平低于对照组。结论：适应性运动有助于减轻离心运动导致的骨骼肌超微结构损伤,对血浆IL-6水平的升高有抑制作用。血浆IL-6可能与由剧烈运动导致的肌肉损伤有关。  相似文献   

11.
目的:探讨大鼠脑损伤后脑微循环障碍、脑缺血及神经组织超微结构的变化规律,为临床改善脑损伤后脑微循环障碍、治疗脑缺血、促进神经功能恢复提供理论依据。方法:采用Feeney's自由落体撞击法建立急性局灶性脑挫裂伤模型,共81只大鼠,随机均分为9组,每组6只行内源性过氧化物酶(EGPO)组织化学染色、脑含水量测定,并进行图象分析。每组3只电镜观察微血管内皮细胞和神经组织超微结构改变。结果:①脑损伤后30min伤区可见出血灶,伤区内无血管染色,伤区周围存在"微无血管区"。"微无血管区"的存在持续至伤后72h。②脑损伤后30min微血管面密度明显下降,伤后48h达到高峰,直到伤后168h才有所恢复,但仍未达到正常水平。③脑损伤后30 min微血管平均光密度明显下降,伤后24h、48h回升,72h再次下降,至168h仍未恢复正常。④脑损伤后30 min,微血管内皮细胞有轻度受损迹象,伤后2h毛细血管腔内有微绒毛形成,伤后6h微绒毛增多。伤后12~72h毛细血管腔明显狭窄。⑤脑损伤后30min,神经细胞超微结构改变不明显,随时间的延长,神经细胞超微结构逐渐恶化,至伤后168h细胞结构完全丧失。结论:EGPO组织化学染色方法能准确反应脑损伤后脑微循环的改变;脑损伤后即发生脑缺血改变,神经细胞、毛细血管内皮细胞的损害继发于脑损伤后的缺血性改变,而脑缺血的发生源于脑损伤后脑微血管结构的破坏和微循环灌注的不足。  相似文献   

12.
Objective： To investigate the effect of activated protein C （APC） on inflammatory responses in human umbilical vein endothelial cells （HUVEC） stimulated with lipopolysaccharide （LPS）. Methods： The second passage of collagenase digested HUVEC was divided into the following groups： serum free medium control group （SFM control）, phosphate buffer solution control group （PBS control）, LPS group with final concentration of 1 μg/ml （LPS group）, APC group with final concentration of 7 μg/ml, Pre-APC group （APC pretreatment for 30 min prior to LPS challenge）, and Post-APC group （APC administration 30 min after LPS challenge）. Supernatant was harvested at 0, 4, 8, 12 and 24 h after LPS challenge. Interleukin-6 （IL-6） and Interleukin-8 （IL-8） levels were analyzed with ELISA. Cells were harvested at 24 h after LPS challenge, and total RNA was extracted. Messenger RNA levels for IL-6 and IL-8 were semi-quantitatively determined by RT-PCR. Results： Compared with control group, IL-6 and IL-8 levels steadily increased 4 to 24 h after LPS stimulation. APC treatment could increase LPS-induced IL-6 and IL-8 production. The mRNA levels of IL-6 and IL-8 exhibited a similar change. Conclusion： APC can further increase the level of IL-6 and IL-8 induced by LPS. The effect of these elevated cytokines is still under investigation.  相似文献   

13.
[目的]针刺预处理对全脑缺血大鼠微血管损伤及脑水肿的保护作用.[方法]采用四动脉阻断法制作大鼠全脑缺血模型,针刺预处理组:术前给予针刺,针刺7 d后给予全脑缺血10 min,干湿法测脑组织水含量,应用HE染色、TUNEL染色及透射电镜技术,观察大鼠脑缺血后,组织病理学及超微结构改变.[结果]与脑缺血组相比,针刺预处理组不引起明显的神经元损伤,全脑缺血10 m in后72 h,微血管损伤及脑水肿明显减轻,血管内皮细胞凋亡减少.[结论]针刺预处理能够通过减轻微血管损伤及脑水肿对脑缺血产生保护作用.  相似文献   

14.
Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer’s lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuate...  相似文献   

15.
To investigate the inhibiting effect of β-Aescin on nuclear factor-κB(NF-κB)activation and the expression of tumornecrosis factor-α(TNF-α)protein after traumatic brain injury(TBI)in the rat brain,62 SD rats were subjected to lateral corticalimpact injury caused by a free-falling object and divided randomly into four groups:(1)sham operated(Group A);(2) injured(Group B);(3)β-Aescin treatment(Group C);(4) pyrrolidine dithocarbamate(PDTC) treatment(Group D).β-Aescin was ad-ministered in Group C and PDTC treated in Group D immediately after injury.A series of brain samples were obtained directly 6h,24 h and 3 d respectively after trauma in four groups.NF-κB activation was examined by Electrophoretic Mobility Shift Assay(EMSA);the levels of TNF-α protein were measured by radio-immunoassay(RIA);the water content of rat brain was measuredand pathomorphological observation was carried out.NF-κB activation,the levels of TNF-α protein and the water content of ratbrain were significantly increased(P＜0.0  相似文献   

16.
The signaling pathway for tumor necrosis factor-α (TNF-α) and its receptors is up-regulated during extracorporeal circulation (ECC), and recruits blood neutrophil into the lung tissue, which results in acute lung injury (ALI). In this study, we evaluated the role of tumor necrosis factor receptor 1 (TNFR1) in ECC-induced ALI by blocking TNF-α binding to TNFR1 with CAY10500. Anesthetized Sprague-Dawley (SD) rats were pretreated intravenously with phosphate buffered saline (PBS) or vehicle (0.3 ml ethanol IV) or CAY10500, and then underwent ECC for 2 h. The oxygenation index (OI) and pulmonary inflammation were assessed after ECC. OI was significantly decreased, while TNF-α and neutrophil in bronchoalveolar lavage fluid (BALF) and plasma TNF-α increased after ECC. Pretreatment of CAY10500 decreased plasma TNF-α level, but did not decrease TNF-α levels and neutrophil counts in BALF or improve OI. Lung histopathology showed significant alveolar congestion, infiltration of the leukocytes in the airspace, and increased thickness of the alveolar wall in all ECC-treated groups. CAY10500 pretreatment slightly reduced leukocyte infiltration in lungs, but did not change the wet/dry ratio in the lung tissue. Blocking TNF-α binding to TNFR1 by CAY10500 intravenously slightly mitigates pulmonary inflammation, but cannot improve the pulmonary function, indicating the limited role of TNFR1 pathway in circulating inflammatory cell in ECC-induced ALI.  相似文献   

17.
Fulminant hepatic failure is a severe clinical condition associated with extremely poor outcomes and high mortality. A number of studies have demonstrated the ability of plasma transfusion to successfully treat fulminant hepatic failure, but the underlying mechanisms are not well understood. The aim of the present study is to define the mechanisms of plasma transfusion treatment in lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced mice. LPS/D-GalN treatment in mice causes significant hepatic failure, including increasing serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, histopathological changes in centrilobular necrosis and inflammatory cells, and the up-regulation of inflammation (tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)). When LPS/D-GaIN-induced mice were treated with plasma, these changes were halted. Results showed that plasma transfusion significantly reduced mortality, and decreased the levels of AST, ALT, and inflammation factors such as TNF-α and IL-6. The expression levels of cleaved Caspase-3, BAX, and p53 were down-regulated and Bcl-2 was up-regulated, suggesting that plasma can reduce LPS/D-GalN-induced apoptosis. The protective mechanism of plasma against LPS/D-GalN-induced fulminant hepatic failure is related to the inhibition of the inflammatory response and the reduction in apoptosis through the down-regulation of the p53-induced apoptotic pathway.  相似文献   

18.
目的：探讨大鼠类风湿性关节炎（RA）动物模型的制备、病理组织学观察及血清细胞因子IL-1、TNF-α检测。方法：以实验大鼠为对象,Ⅱ型胶原（CII）和完全弗氏佐剂（Complete Freund＇s Adjuvant,CFA）混合注射,不同时间点实验组大鼠（O、7、14、28、42d）所获得血样用于做IL-1、TNF-α检测,膝关节标本进行组织病理学研究。结果：模型组血清IL-1、TNF-α在急性期增高明显,与对照组差异有统计学意义（P〈0.05）。模型组关节组织标本观察到滑膜组织增生,其局部骨吸收破坏明显,软骨表层胶原纤维溶解、软骨细胞变性坏死,软骨表面凹凸不平。结论：采用异种CII与CFA制备的RA模型,可以用于RA组织病理学、发病机理及治疗方面的研究。  相似文献   

19.
如今延长溶栓时间窗、减轻再灌注损伤是缺血性脑血管病亟待解决的的问题,缺血后适应提供了一种可能的解决方法,故成为研究的热点。缺血后适应通常指的是在组织缺血-再灌注之后进行的一系列短暂血管闭塞/血管再灌注,诱导组织针对缺血-再灌注损伤产生内源性保护作用,减少组织器官缺血-再灌注损伤。该文将综述缺血后适应脑保护的基本机制：减少缺血-再灌注后脑血流的改变,减少氧化应激产物的产生,抗炎,相关信号传导通路改变。  相似文献   

20.
目的通过肺组织NF-κB的表达,研究羟乙基淀粉130/0.4复苏对失血性休克大鼠肺损伤保护作用的可能机制.方法健康雄性SD大鼠54只,体重230~280 g,随机分为3组：对照组（C组）、乳酸林格氏液复苏组（RL组）、6%羟乙基淀粉130/0.4复苏组（HES组）,按照Wiggers改良法复制失血性休克模型.于复苏后1 h、2 h4、h采用免疫组织化学的方法检测肺组织NF-κB的表达;光镜下观察肺组织形态学改变.结果 RL组与HES组肺组织NF-κB免疫组化染色细胞核阳性百分率较C组明显升高,RL组升高的程度较HES组明显（P〈0.01）.免疫组化染色光镜观察显示：HES组比RL组的组织损伤明显减轻.结论 6%羟乙基淀粉130/0.4复苏失血性休克可以抑制肺组织NF-κB活性,减轻休克及复苏过程造成的肺损伤.  相似文献   

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