梅州香樟挥发油抗炎活性试验

目的:探究梅州香樟挥发油的抗炎活性。方法:采用角叉菜胶致大鼠足跖炎症模型评价梅州香樟挥发油及其脂质体凝胶的抗炎活性。结果:梅州香樟挥发油及其脂质体凝胶对大鼠足肿胀抑制率分别为26.92%和33.75%,而其脂质体凝胶肿胀抑制率高于市售红花油(32.03%)。结论:梅州香樟挥发油制成脂质体凝胶具有明显的抗炎活性,该实验为梅州香樟的综合利用及进一步药用开发提供科学的参考依据。     

清炎颗粒清咽、抗炎作用研究

[目的]研究清炎颗粒清咽、抗炎作用研究。[方法]采用2,4-二硝基苯酚溶液致热作用,采用二甲苯致小鼠耳肿胀法复制小鼠炎症模型观察清炎颗粒抗炎作用。[结果]清咽抗炎颗粒剂量组对2,4-二硝基苯酚致大鼠体温升高均有明显的抑制作用,对二甲苯致大鼠耳片急性炎症反应均有明显的抑制作用,清咽抗炎颗粒组对1%角叉菜胶引起的大鼠足跖肿胀性炎症反应均有明显的抑制作用。与空白对照组比较,差异均具有统计学意义(均P0.05)。[结论]清炎颗粒具有清咽、抗炎作用。     

祛痘化妆品用中药提取物的抗炎作用研究

为研究祛痘化妆品川中药组方提取物的抗炎活性,采用二甲苯致小鼠耳廊肿胀、1％角叉荣胶致小鼠后足跖肿胀方法．测定致炎小鼠两耳的质量差和后足炎症因子IL-1α、PGE2及蛋白含量,研究中药组办提取物的抗炎活性。结果发现．中药提取物高（200mg／kg）、中（100mg／kg）和低（50mg／kg）剂量组明显抑制了耳肿胀的发生;高剂量组在造模2h后能减轻角叉菜胶所致的足肿胀．与阴性对照组相比有显著性差异,其他组其他时间点未见明显区别;药物组动物IL-1a、PGE2的释放均旺著下降。试验表明祛痘化妆品用中药组方提取物具有显著的抗炎活性。     

中药竹黄不同提取部位抗炎镇痛活性的研究

目的研究竹黄不同提取部位的抗炎、镇痛的药理活性,为竹黄的进一步深入研究提供科学依据。方法采用两种炎症模型和两种疼痛模型。用二甲苯致小鼠耳廓肿胀、小鼠棉球肉芽肿法、醋酸扭体法和热板法观察竹黄不同提取部位的抗炎、镇痛作用。结果竹黄的水极性提取部位对小鼠抗炎的影响差异显著(P0.05),其他极性提取部位对小鼠炎症模型也有一定的影响,但差异不显著;在小鼠的疼痛模型中,竹黄的各极性提取部位对小鼠的影响在统计学意义上均不显著,但也具有一定的镇痛作用,其中水极性部位的提取物镇痛作用最为明显。结论竹黄具有抗炎镇痛作用,以水提物部位作用最佳。     

虎床方提取物的抗过敏及抗炎作用研究

目的:选用虎杖、蛇床子、苦参、川芎等四味中药按中医配伍理论组成虎床方,并探讨组方提取物的抗过敏及抗炎作用。方法:采用煎煮法提取其有效组分,分为低中高三个剂量组,分别为1,2,3 g/m L;通过高浓度的DNCB致敏和低浓度的DNCB多次激发,构建湿疹小鼠模型,给药后测定小鼠耳肿胀厚度、脾指数和胸腺指数、耳组织中TNF-α的水平;通过对二甲苯致小鼠耳部急性炎症的抗炎模型,测定小鼠的耳廓肿胀度。结果:虎床方低、中、高剂量均能显著抑制湿疹小鼠的耳肿胀度,并且中剂量时可显著抑制湿疹小鼠的耳肿胀度,同时中剂量时显著降低耳组织表皮厚度和肥大细胞数,亦可降低湿疹小鼠的脾指数,并抑制胸腺指数;虎床方中剂量能显著减少湿疹小鼠耳组织TNF-α及血清Ig E和TNF-α含量,减轻炎性皮损;虎床方中、高剂量组显著降低二甲苯致小鼠耳廓肿胀度。结论:虎床方具有一定的抗过敏及抗炎作用。     

叶绿素铜钠盐牙膏的抗炎止血效果试验

目的：研究叶绿素铜钠盐牙膏的抗炎止血效果。方法：以二甲苯致小白鼠耳廓急性炎症肿胀为模型，在急性炎症肿胀耳廓局部涂抹受试物，观察样品对急性炎症肿胀的抗炎效果；用小白兔实质器官肝脏局部创面损伤出血的止血时间为评价指标，观察样品的止血效果。结果：与牙膏空白基质组比较，牙膏试验组的抗炎、止血效果均具有显著性差异。结论：叶绿素铜钠盐牙膏具有较好的抗炎止血效果。     

黑果腺花楸不同极性物质抗氧化及抗炎镇痛研究

为了高效的提取及分离黑果腺花楸活性物质,以黑果腺花楸为原料,不同极性溶剂作为溶媒(石油醚、乙酸乙酯、正丁醇和水),采用超声波辅助提取法,分别提取到不同极性物质(石油醚相、乙酸乙酯相、正丁醇相和水相)。利用不同的抗氧化模型(铁还原力、清除羟基自由基(OH)·能力、清除ABTS自由基能力、抗肝组织自发性脂质过氧化能力和花生油氧化能力)、炎症模型(小鼠耳廓肿胀和小鼠肉芽肿胀)和镇痛模型(小鼠热板痛阈值和冰醋酸致小鼠扭体次数)来评价黑果腺花楸不同极性物质的活性。结果表明,正丁醇相具有较强的抗氧化能力和消炎镇痛能力。正丁醇可以作为提取黑果腺花楸活性物质及分离抗氧化活性及抗炎镇痛成分的溶剂。     

杜鹃花活性提取物镇痛抗炎作用的初步研究

目的:研究中药杜鹃花活性提取物总黄酮的抗炎镇痛作用,为进一步临床应用开发提供依据。方法:采用热板法致小鼠疼痛观察杜鹃花的镇痛作用,通过大鼠足注射弗氏完全佐剂诱导大鼠足肿胀,通过测定不同时间点的足趾容积评价抗炎作用。结果:杜鹃花中、高剂量可明显延长小鼠热板舔足反应潜伏期,与空白对照组比较有显著性差异(p0.01),且有一定的量效关系。杜鹃花低、中、高剂量组对大鼠足肿胀具有明显的抑制作用,与模型组比较有显著性差异(p0.01)。结论:杜鹃花活性提取物总黄酮具有显著的镇痛抗炎作用,且抗炎效果较好,为该药物临床上用于关节炎的治疗提供了依据。     

甘草酸二钾在牙膏中的抑菌作用

测试了甘草酸二钾对牙龈卟啉单胞菌的最小抑菌浓度,并研究了含0.2%甘草酸二钾的牙膏对牙龈卟啉单胞菌的抑菌作用及对二甲苯致小鼠耳廓肿胀的影响。实验结果表明,甘草酸二钾对牙龈卟啉单胞菌具有抑制作用,最小抑菌浓度为1.875 g/L;含0.2%甘草酸二钾的牙膏具有抑制牙龈卟啉单胞菌的作用,抑菌环直径为20.5 mm;在二甲苯致小鼠耳廓肿胀的抗炎模型上,含0.2%甘草酸二钾的牙膏具有超过醋酸氟轻松软膏的效果。     

黄河三角洲产地管花肉苁蓉不同极性提取物抗炎镇痛活性的研究

目的:研究比较黄河三角洲产地管花肉苁蓉不同极性提取物抗炎镇痛的活性,为其临床试验和进一步应用提供参考依据。方法:采用耳肿胀法和棉球肉芽组织增生法致炎,研究管花肉苁蓉不同极性提取物灌胃给药对急性炎症的作用。采用热板法和醋酸扭体法致痛,研究管花肉苁蓉不同极性提取物灌胃给药的镇痛作用。结果:管花肉苁蓉不同极性提取物对小鼠的耳肿胀、棉球肉芽肿、热板痛阈值时间以及扭体次数有抑制作用,但同模型对照组比较差异不显著。结论:管花肉苁蓉有一定的抗炎镇痛作用。     

Anti-Inflammatory Effects of 4-Methylcyclopentadecanone on Edema Models in Mice

The present study evaluated the anti-inflammatory effects of 4-methylcyclopentadecanone (4-MCPC) on edema models in mice and aimed to determine the safety of 4-MCPC after acute exposure. The acute toxicity of 4-MCPC was evaluated by oral administration to rats of single doses of 0, 5, 50, 500 and 5000 mg/kg. Toxic symptoms were observed for 14 days. The anti-inflammatory activity was evaluated in xylene-induced mouse ear edema and carrageenan-induced mouse paw edema. The animals were treated with 4-MCPC once every day for seven consecutive days. Edema index, % inhibition, IL-1β, TNF-α, PGE₂ and MPO levels in paws were detected after the treatment with xylene or carrageenan. Our results indicated that the LD₅₀ value of 4-MCPC in rats is greater than 5000 mg/kg. The ED₅₀ of 4-MCPC in xylene-induced mouse ear edema model was 7.5 mg/kg. 4-MCPC (8 or 16 mg/kg) remarkably inhibited carrageenan-induced mouse paw edema. Further study revealed that 4-MCPC treatment also decreased IL-1β, TNF-α, PGE₂ and MPO levels in mice paws. Intragastric administration of 4-MCPC exhibited more significant anti-inflammatory activity than muscone at a dose of 16 mg/kg. Taken together, our results suggest that 4-MCPC has potent anti-inflammatory activity and the mechanisms might be related to the decreases of the levels of IL-1β, TNF-α, PGE₂ and MPO in inflamed paws.     

42例产妇宫颈水肿的治疗体会

目的观察利多卡因+阿托品对产妇分娩时宫颈水肿的治疗作用。方法回顾性分析2007年以来用利多卡因+阿托品治疗的42例产妇宫颈水肿的病例,并与同期发生宫颈水肿产前未经任何处理的产妇做对比。结果治疗组无一例需进行剖宫产,对照组有12例(40.0%)因滞产而行剖宫产,2组比较有统计学差异(P=0.00732,P<0.01)。治疗组宫口全开时间较对照组短(P=0.02183,P<0.05);治疗组产妇VAS疼痛评分更低(P=0.00465,P<0.01);治疗组分娩出血量更小(P=0.00687,P<0.01);治疗组新生儿无一例窒息,Apgar评分均在4分以上例数多于对照组例数(P=0.00891,P<0.01)。结论应用利多卡因+阿托品多点注射治疗宫颈水肿可取得良好疗效,帮助产程顺利进行,值得临床推广。     

Involvement of Cytokines in the Pathogenesis of Diabetic Macular Edema

Diabetic macular edema (DME) is a critical complication of diabetic retinopathy, a condition that arises from the breakdown of the blood–retinal barrier and the consequent increase in vascular permeability. Over the years, attempts have been made to treat DME by various approaches, including laser photocoagulation, steroid triamcinolone acetonide, and vitrectomy. However, treatment was unsatisfactory until research identified vascular endothelial growth factor (VEGF) as a factor in the pathogenesis of DME. Intraocular anti-VEGF agents show good efficacy in DME. Nevertheless, in some patients the condition recurs or becomes resistant to treatment, suggesting that other factors may be involved. Because inflammation and retinal hypoxia are seen in DME, research has examined the potential role of cytokines and other inflammatory mediators. In this review, we provide an overview of this research and describe feedback mechanisms that may represent a target for novel treatments.     

2-Arachidonyl-lysophosphatidylethanolamine Induces Anti-Inflammatory Effects on Macrophages and in Carrageenan-Induced Paw Edema

2-Arachidonyl-lysophosphatidylethanolamine, shortly 2-ARA-LPE, is a polyunsaturated lysophosphatidylethanolamine. 2-ARA-LPE has a very long chain arachidonic acid, formed by an ester bond at the sn-2 position. It has been reported that 2-ARA-LPE has anti-inflammatory effects in a zymosan-induced peritonitis model. However, it’s action mechanisms are poorly investigated. Recently, resolution of inflammation is considered to be an active process driven by M2 polarized macrophages. Therefore, we have investigated whether 2-ARA-LPE acts on macrophages for anti-inflammation, whether 2-ARA-LPE modulates macrophage phenotypes to reduce inflammation, and whether 2-ARA-LPE is anti-inflammatory in a carrageenan-induced paw edema model. In mouse peritoneal macrophages, 2-ARA-LPE was found to inhibit lipopolysaccharide (LPS)-induced M1 macrophage polarization, but not induce M2 polarization. 2-ARA-LPE inhibited the inductions of inducible nitric oxide synthase and cyclooxygenase-2 in mouse peritoneal macrophages at the mRNA and protein levels. Furthermore, products of the two genes, nitric oxide and prostaglandin E₂, were also inhibited by 2-ARA-LPE. However, 1-oleoyl-LPE did not show any activity on the macrophage polarization and inflammatory responses. The anti-inflammatory activity of 2-ARA-LPE was also verified in vivo in a carrageenan-induced paw edema model. 2-ARA-LPE inhibits LPS-induced M1 polarization, which contributes to anti-inflammation and suppresses the carrageenan-induced paw edema in vivo.     

Effect of polyphenols on oxidative stress and mitochondrial dysfunction in neuronal death and brain edema in cerebral ischemia

Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti-inflammatory, anti-carcinogenic, anti-viral, anti-ulcer, and anti-apoptotic properties. One important consequence of ischemia is neuronal death and oxidative stress plays a key role in neuronal viability. In addition, neuronal death may be initiated by the activation of mitochondria-associated cell death pathways. Another consequence of ischemia that is possibly mediated by oxidative stress and mitochondrial dysfunction is glial swelling, a component of cytotoxic brain edema. The purpose of this article is to review the current literature on the contribution of oxidative stress and mitochondrial dysfunction to neuronal death, cell swelling, and brain edema in ischemia. A review of currently known mechanisms underlying neuronal death and edema/cell swelling will be undertaken and the potential of dietary polyphenols to reduce such neural damage will be critically reviewed.     

A Two-Step Multicomponent Synthetic Approach and Anti-inflammatory Evaluation of N-Substituted 2-Oxopyrazines

Inflammation is widely reported as a main factor for the development of chronic diseases such as cancer, diabetes, and even metabolic syndrome. Thus, the search for novel anti-inflammatory compounds is required. Herein we describe the synthesis of a collection of peptidic pyrazinones by a convenient approach involving a multicomponent isocyanide-based reaction followed by a tandem deprotection/oxidative cyclization step. This series of compounds were tested for their potential anti-inflammatory capacity in an in vivo murine model, and four compounds were identified to inhibit tetradecanoylphorbol acetate (TPA)-induced edema by more than 75 %. The two most active compounds, N-benzyl-2-(4-hydroxy-3,5-dimethoxyphenyl)-2-[2-oxopyrazin-1(2H)-yl]acetamide ( 10 o ) and N-cyclohexyl-2-[2-oxopyrazin-1(2H)-yl]-2-[4-(trifluoromethyl)phenyl]acetamide ( 10 x ), with methyl and trifluoromethyl groups, were also able to decrease myeloperoxidase activity and leukocyte infiltration. Moreover, 10 x decreased the thickness of TPA-treated mouse ears, as observed in histological analysis of the tissues.     

Identifying Genetic Biomarkers Predicting Response to Anti-Vascular Endothelial Growth Factor Injections in Diabetic Macular Edema

Intraocular anti-vascular endothelial growth factor (VEGF) therapies are the front-line treatment for diabetic macular edema (DME); however, treatment response varies widely. This study aimed to identify genetic determinants associated with anti-VEGF treatment response in DME. We performed a genome-wide association study on 220 Australian patients with DME treated with anti-VEGF therapy, genotyped on the Illumina Global Screening Array, and imputed to the Haplotype Reference Consortium panel. The primary outcome measures were changes in central macular thickness (CMT in microns) and best-corrected visual acuity (BCVA in ETDRS letters) after 12 months. Association between single nucleotide polymorphism (SNP) genotypes and DME outcomes were evaluated by linear regression, adjusting for the first three principal components, age, baseline CMT/BCVA, duration of diabetic retinopathy, and HbA1c. Two loci reached genome-wide significance (p < 5 × 10⁻⁸) for association with increased CMT: a single SNP on chromosome 6 near CASC15 (rs78466540, p = 1.16 × 10⁻⁹) and a locus on chromosome 12 near RP11-116D17.1 (top SNP rs11614480, p = 2.69 × 10⁻⁸). Four loci were significantly associated with reduction in BCVA: two loci on chromosome 11, downstream of NTM (top SNP rs148980760, p = 5.30 × 10⁻⁹) and intronic in RP11-744N12.3 (top SNP rs57801753, p = 1.71 × 10⁻⁸); one near PGAM1P1 on chromosome 5 (rs187876551, p = 1.52 × 10⁻⁸); and one near TBC1D32 on chromosome 6 (rs118074968, p = 4.94 × 10⁻⁸). In silico investigations of each locus identified multiple expression quantitative trait loci and potentially relevant candidate genes warranting further analysis. Thus, we identified multiple genetic loci predicting treatment outcomes for anti-VEGF therapies in DME. This work may potentially lead to managing DME using personalized treatment approaches.     

应用BiPAP无创机械通气治疗急性心源性肺水肿的疗效观察

目的评价BiPAP无创机械通气治疗急性心源性肺水肿的疗效。方法对我院收治的急性心源性肺水肿随机分为两组,治疗组25例急性心源性肺水肿患者在传统常规治疗同时加用BiPAP呼吸机经鼻(面)罩双水平气道正压通气治疗,对照组23例在传统常规治疗上加用鼻导管给氧治疗。结果BiPAP组通气治疗后,23例患者临床症状明显改善,血气分析中pH、PaO2、PaCO2、SaO2等参数比较有显著性差异(P<0.05),总有效率为92.0%,避免了气管插管机械通气。对照组总有效率为73.9%。结论BiPAP无创机械通气治疗急性心源性肺水肿能迅速纠正缺氧、改善心功能,可作为抢救急性心源性肺水肿的一种安全有效的方法。     

Vascular Permeability in Diseases

Vascular permeability is a selective mechanism that maintains the exchange between vessels, tissues, and organs. The regulation was mostly studied during the nineteenth century by physiologists who defined physical laws and equations, taking blood, tissue interstitial, and oncotic pressure into account. During the last decades, a better knowledge of vascular cell functions and blood-vessel interactions opens a new area of vascular biology. Endothelial cell receptors vascular cell adhesion molecule (VCAM), intercellular cell adhesion molecule (ICAM), vascular endothelial growth factor receptor (VEGFR-2), receptor for advanced glycation end products (RAGE), and mediators were identified and their role in homeostasis and pathological situations was described. The molecular differences of endothelial cell junctions (tight, gap, and adherens junctions) and their role in vascular permeability were characterized in different organs. The main mediators of vasomotricity and permeability, such as prostaglandins, nitric oxide (NO), prostacyclin, vascular growth factor (VEGF), and cytokines, have been demonstrated to possess major functions in steady state and pathological situations. Leukocytes were shown to adhere to endothelium and migrate during inflammatory situations and infectious diseases. Increased vascular permeability is linked to endothelium integrity. Glycocalyx, when intact, may limit cancer cell metastasis. Biological modifications of blood and tissue constituents occurring in diabetes mellitus were responsible for increased permeability and, consequently, ocular and renal complications. Vascular pressure and fluidity are major determinants of pulmonary and cerebral edema. Beside the treatment of the infectious disease, of the blood circulation dysfunction and inflammatory condition, drugs (cyclooxygenase inhibitors) and specific antibodies anti-cytokine (anti-VEGF) have been demonstrated to reduce the severity and the mortality in diseases that exhibited enhanced vascular permeability.