The effect of rosiglitazone in the prevention of intra-abdominal adhesion formation in a rat uterine horn model

BACKGROUND: Effects of rosiglitazone in the prevention of adhesion formation were evaluated. METHODS: Eighty Wistar albino rats were randomly grouped into eight equally sized groups. A 2-cm segment of the antimesenteric surface of the right uterine horn was traumatized to form a standardized lesion, using bipolar cautery. A dose-response study was performed with 0.1, 0.3, 1 and 3 mg/kg/day rosiglitazone. Fifteen days later, adhesions were evaluated clinically and histopathologically. A time-response study was performed with 1 mg/kg/day rosiglitazone (the minimum dose found to significantly affect adhesion formation). Rosiglitazone was given for 7 days post-operatively and results were compared with those of control and the 15-day group (time-response). In all these studies, rosiglitazone was orally administered 3 days before the operation and continued post-operatively. In two further experimental groups, rosiglitazone was only administered pre-operatively or post-operatively. RESULTS: Approximately 1 mg/kg/day rosiglitazone was found to reduce adhesion scores both clinically and histopathologically. Duration of treatment was also found to affect the extent of adhesion formation. However, giving rosiglitazone either just pre-operatively or post-operatively did not significantly reduce adhesion formation. CONCLUSION: Rosiglitazone with peroxisome proliferator-activated receptor (PPAR)-gamma agonist activity reduced the formation of i.p. adhesion possibly by reducing the initial inflammatory response and the subsequent exudation in this study.     

Prevention of postoperative adhesion formation in rat uterine horn model by nimesulide: a selective COX-2 inhibitor

BACKGROUND: Pelvic surgery is one of the main causes of intraperitoneal (i.p.) adhesions that create various medical problems including pelvic pain, bowel obstructions and female infertility. A rat model was used to investigate the efficacy of nimesulide, a selective cyclooxygenase-2 inhibitor, in the prevention of adhesion formation. METHODS: Fifty Wistar-Albino rats underwent bilateral uterine horn injury with a unipolar cautery. Study groups were as follows: (i) control group, no adjuvant therapy; (ii) i.p. Ringer's lactate group, 2 ml Ringer's lactate solution was instilled i.p.; (iii) i.p. Ringer's lactate plus nimesulide group, 1 ml Ringer's lactate plus 1 ml nimesulide (0.5 mg/ml) were given i.p.; (iv) intramuscular (i.m.) nimesulide group, 1 ml i.m. nimesulide (0.5 mg/ml) was given preoperatively for 5 days; and (v) i.p. nimesulide group, 1 ml nimesulide (0.5 mg/ml) was instilled i.p. At the end of the study all animals were killed, and a standard adhesion scoring system was applied by a blinded examiner. RESULTS: The mean adhesion extent in study groups was as follows: 1.33 +/- 0.76 in control group, 1.40 +/- 0.90 in i.p. Ringer's lactate group, 0.75 +/- 0.70 in i.p. Ringer's lactate plus nimesulide group, 0.25 +/- 0.44 in i.m. nimesulide group and 0.31 +/- 0.70 in i.p. nimesulide group. The mean +/- SD adhesion severities of control, i.p. Ringer's lactate, i.p. Ringer's lactate plus nimesulide, i.m. nimesulide, and i.p. nimesulide groups were 0.58 +/- 0.35, 0.30 +/- 0.41, 0.27 +/- 0.3, 0.12 +/- 0.28 and 0.15 +/- 0.35 respectively. The lowest adhesions were found in the groups treated with nimesulide i.m. and nimesulide i.p. ( P < 0.05). CONCLUSIONS: This study showed that preoperative i.m. or postoperative i.p. administration of nimesulide to the site of injury reduced the formation of postoperative adhesions in a rat uterine horn model.     

Prevention of post-surgical adhesion formation using aspirin in a rodent model: a preliminary report

Pelvic adhesions are one of the major factors which significantlyand adversely affect surgery outcome due to intra-and postoperativemorbidity and reduce future female fertility. Using a rodentmodel, we evaluated the efficacy of aspirin, a non-steroidalanti-inflammatory drug, in the prevention of adhesion formation.A total of 72 female Wistar rats received a standardized primarytraumatic lesion to the right uterine horn. They were randomlydivided into eight groups: group I (control) had no treatmentand group II received a single pre-operative 0.70 mg aspirin.All the succeeding groups (III-VIII) received aspirin in dosesof 0.35, 0.70, or 1.40 mg every 6 h for either 48 or 96 h inaddition to the pre-operative aspirin (0.70 mg). All animalswere killed 4 weeks later and adhesions were assessed usinga modified adhesion scoring scale. The lowest adhesion scorewas found in the group treated with 0.35 mg of aspirin for 96h, and the highest was found among the groups treated with either0.70 or 1.40 mg for 48–96 h respectively (P < 0.05).These results are in line with the hypothesis that administrationof a low dose of aspirin selectively inhibits the productionof thromboxane A₂, whereas basal prostacyclin biosynthesis ispreserved. This phenomenon might contribute to reducing postoperativeadhesion formation in a rat model. Thus, future studies intothe prevention of adhesion formation may require the additionaluse of a non-steroidal anti-inflammatory drug, for which aspirindeserves further attention, before extrapolation into humantherapy.     

Inhibition of chemokines prevents intraperitoneal adhesions in mice

BACKGROUND: The present study evaluates the efficacy of a broad-spectrumchemokine inhibitor, NR58-3.14.3, in the prevention of adhesionformation after i.p. surgery in mice. METHODS: A total of 110eight week old female Balb/c mice underwent laparotomy. Fortyanimals were randomly assigned to receive daily i.p. injectionsof either vehicle (control) or NR58-3.14.3. Time-course of adhesionformation was assessed. A titration of NR58-3.14.3 was conductedfor i.p. and s.c. administrations. The effectiveness of a singleintra-operative dose of NR58-3.14.3 was evaluated. Number, extent,location and type of adhesions were recorded. Immunohistochemistryof adhesions was done with leukocyte common antigen, CD45. RESULTS:Adhesion scores peaked on post-operative days 6–8. Onboth days 6 and 8, there were smaller adhesion size and lowercumulative adhesion scores in NR58-3.14.3-treated group. Moreover,on day 8, there were significantly fewer adhesions in NR58-3.14.3-treatedgroup compared to controls. The least effective dose for i.p.administration of NR58-3.14.3 was 0.45 mg/animal. Subcutaneousand single intra-operative i.p. administrations were also effectivein the prevention of i.p. adhesions. Although NR58-3.14.3 decreasedthe number of CD45⁺ inflammatory cells in the adhesions by 22.5%compared to control group, this was not significant. CONCLUSIONS:Our results show that this broad-spectrum chemokine inhibitorprevents post-operative adhesions in mice and may have a potentialclinical use.     

Postoperative adhesion prevention with low-dose aspirin: effect through the selective inhibition of thromboxane production

The aim of the present study was to evaluate the efficacy of low-dose versus high-dose aspirin in the prevention of postoperative adhesion formation. Forty New Zealand White rabbits were randomized into three groups: low-dose aspirin (1.7 mg/kg per day for 5 days starting on the day of surgery), high-dose aspirin (28.0 mg/kg per day), and controls. The rabbits underwent a standardized surgical injury on the ovary, uterine horn and abdominal wall on one side at laparotomy. On postoperative day 21, a second-look laparotomy was performed for the evaluation of postoperative adhesions. In five animals in each group, peritoneal fluid samples were collected at initial surgery, then through an additional 2 cm incision performed on postoperative day 3, and at second-look laparotomy. The peritoneal concentrations of thromboxane B2 and 6-keto-prostaglandin F1alpha (the stable hydrolysis product of prostacyclin) were measured by radioimmunoassay. At second- look laparotomy, the adhesion formation rate was 46% in the low-dose aspirin group, 77% in the high-dose group, and 100% in the control group. The adhesion score in the low-dose group was significantly lower (P < 0.01) than in the high-dose and control groups. Peritoneal thromboxane decreased significantly during treatment in both low-dose and high-dose aspirin groups, whereas prostacyclin decreased only in the high-dose group. Postoperative adhesion reduction observed in this study with low-dose aspirin treatment could be due to the selective inhibition of thromboxane over prostacyclin production.      

The effects of melatonin on postoperative intraabdominal adhesion formation

PURPOSE: Postoperative intraabdominal adhesion formation is a major clinical problem. No previous study was found, reporting the relationship between adhesion formation and melatonin administration, but melatonin, a strong antioxidant, is recognized to have certain effects on the progression of adhesion formation mechanism. It was therefore decided to investigate the effects of melatonin on postoperative adhesion formation. MATERIALS AND METHODS: A total number of 24 Sprague-Dawley rats were utilized. Three groups, described as: Group A, sham laparatomy (n=8), Group B, rats that underwent only ischemia-reperfusion (n=8) and Group C, rats that underwent ischemia- reperfusion and were given 10 mg/kg melatonin solution i.v. (n=8). For Groups B and C, the ileocolic vessels were clamped. Blood glutathione peroxidase levels of all study groups were assessed, then microscopic and macroscopic adhesion scores were evaluated. RESULTS: Glutathione peroxidase levels of the melatonin-treated group were significantly higher and fibroblast proliferation and macroscopic adhesion scores were significantly lower, than in the melatonin-free group. CONCLUSION: The results of this study supported the hypothesis, that melatonin administration may prevent intraabdominal adhesions resulting from surgery.     

丙酮酸对模型大鼠移植小肠细胞间黏附分子表达的影响

背景：小肠移植过程中移植肠不可避免地要受到缺血再灌注的损害,而小肠又对缺血再灌注损伤特别敏感。前期研究证实丙酮酸对小肠和移植小肠缺血再灌注损伤具有保护作用,并探讨了部分相关机制。 目的：在前期研究基础上,进一步证实探讨丙酮酸对大鼠移植小肠缺血再灌注损伤的保护作用与移植小肠组织中细胞间黏附分子表达的关系。 方法：选用近交系成年雄性SD大鼠,按随机数字表法分为3组：假手术组行剖腹、左侧肾切除作为对照;移植小肠缺血再灌注组和丙酮酸处理组均建立小肠移植缺血再灌注动物模型,分别于供体小肠阻断血流、灌洗前10 min向肠腔内注入10 mL含有多聚葡萄糖的营养液或含有分析纯丙酮酸的营养液。分别留取缺血45,90 min和再灌注30,180 min小肠组织标本,光镜下观察小肠组织损伤病理变化,免疫组化法检测小肠组织中细胞间黏附分子1的表达。 结果与结论：缺血再灌注不同时相移植小肠缺血再灌注组小肠组织损伤程度均重于其他2组,而丙酮酸处理组小肠组织损伤程度与假手术组相似。缺血期间小肠组织中细胞间黏附分子1的表达均不明显,呈弱阳性;再灌注后移植小肠缺血再灌注组细胞间黏附分子1的表达迅速增加,高于与假手术组及丙酮酸处理组(P < 0.01),而丙酮酸处理组细胞间黏附分子1的表达变化不明显(P > 0.05)。说明丙酮酸作用下大鼠移植小肠缺血再灌注过程中细胞间黏附分子1的表达减少,可能是丙酮酸保护大鼠移植小肠缺血再灌注损伤的重要环节之一。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

Effects of jnk inhibitor on inflammation and fibrosis in the ovary tissue of a rat model of polycystic ovary syndrome

Objective: In our study, we aimed to investigate the effects of Jun N-terminal kinase inhibitor (SP600125) on fibrosis and inflammation in rats with polycystic ovary syndrome (PCOS). Method: 50 Wistar-albino rats were divided into five groups (n=10 each): control group, sham group, PCOS group, SP600125+ PCOS group and SP600125 group. In the estradiol valerate (EV)-treated group in which PCOS was injected with a single 4 mg/kg i.p. of EV in 0.2 ml sesame oil and the rats were sacrificed on day 60. The estradiol valerate (EV)-treated + SP600125-treated group was injected with a single 4 mg/kg i.p. of EV in 0.2 ml sesame oil. As of day 60, the treatment group was additionally given 15 mg/kg i.p. of SP600125 once daily for 4 consecutive days and the rats were sacrificed on day 65. Histopathological findings (ovarian morphology, edema, inflammatory cell infiltration, vascular congestion and hyperemia) and collagen type IV immunoexpression were assessed. Results: The SP600125+ PCOS group showed a significant level of improvement in ovarian follicle morphology, edema, inflammatory infiltrate, vascular congestion and hyperemia as compared with the PCOS group. Furthermore, collagen type IV immunoexpression showed a significant reduction in staining intensity on the theca cell layer and ovary stroma as compared to the PCOS group. Conclusion: This study demonstrates the therapeutic effect of SP600125 in the prevention of PCOS in an experimental model.     

Reduction of adhesion formation in rabbits by intraperitoneal administration of lazaroid formulations

Adhesion formation is a major source of postoperative morbidity and mortality. In this study, the ability of a variety of lazaroid formulations [the antioxidant 21-aminosteroid PNU74006F (tirilazad) and the non-steroidal 2-methylaminochroman derivative PNU83,836E] to reduce i.p. adhesion formation in three rabbit models was examined. In initial studies, PNU83836E was administered via Alzet miniosmotic pump to the site of injury. In the sidewall and double uterine horn models, PNU83,836E was administered via Alzet miniosmotic pump for the entire postoperative interval. In the sidewall model, there was a dose- dependent reduction in the area of the sidewall injury that was involved in adhesions. In the double uterine horn model, PNU83,836E was administered via Alzet miniosmotic pump to the area of injury for 1, 2, 3 or 7 days. Administration for as little as 24 h after surgery significantly reduced the extent of adhesion formation and the reduction was increased if it was administered for longer. Further studies were conducted in which various lazaroid formulations were administered as a bolus at the end of surgery. In both the sidewall and double uterine horn models, administration of either PNU83,386E (in citrate buffer) or PNU74006F (in cyclodextrin or lipid emulsion vehicles) at the end of surgery reduced adhesion formation. Administration of a bolus of PNU74006F 10 min prior to initiation of surgery with or without additional treatment at the end of surgery further increased its efficacy in the reduction of adhesion formation. Administration of a minimum of 1.5 mg before and after surgery (3 mg total) was required for maximal efficacy. These studies demonstrate that pre- and postoperative administration of either a steroidal (PNU74006F) or non-steroidal (PNU83,836E) lazaroid intraperitoneally reduced the formation and reformation of postoperative adhesions in three animal models.      

Cross-linked hyaluronate hydrogel prevents adhesion formation and reformation in mouse uterine horn model

The aim of this study was to evaluate the efficacy of cross-linked hyaluronate hydrogel (HA gel) as an adjuvant for postoperative adhesion prevention, in a mouse uterine horn model. In experiment 1 uterine horns were abrased with iodine. HA gel was applied to the injured surface before closure in the treatment group. In experiment 2, after injuring the uterine horns, three stitches were placed at equal distances around the uterine horns to appose the injured medial surfaces of the two horns during healing. HA gel was inserted between the uterine horns in the treatment group. In experiment 3 prevention of adhesion reformation was assessed. After lysis of adhesions that were induced as in experiment 2, HA gel was introduced between the serosal surfaces of apposing uterine horns. Untreated animals served as controls in each experiment. Statistical analysis was carried out using Student's t-test. The adhesion score was significantly lower in the HA gel group on the 14th day compared with controls in all the experiments: in experiment 1, 0.3 +/- 0.4 versus 1.7 +/- 1.2; in experiment 2, 0.9 +/- 1.0 versus 2.6 +/- 0.5; and in experiment 3, 1.5 +/- 0.9 versus 2.2 +/- 0.6 respectively. Cross-linked HA gel significantly reduced de-novo adhesions (P< 0.03) and adhesion reformation (P < 0.03).     

Effect of Hypericum perforatum on intraperitoneal adhesion formation in rats

Introduction

The aim of this study was to evaluate the efficacy of Hypericum perforatum for prevention of adhesion formation in rats.

Material and methods

Twenty-four female wistar rats underwent left uterine horn adhesion model. Rats were randomised into 4 groups. Group 1 (Control): Closure of abdominal incision without any agent administration. Group 2: Closure of incision after administration of intraperitoneal (i.p.) Ringer''s lactate solution. Group 3: Closure of incision after administration of i.p. olive oil (diluent of H. perforatum). Group 4: Hypericum perforatum extract (Ecodab^®) was administered i.p. before the closure of incision. Fourteen days later, relaparatomy was performed and surgical adhesion scores, inflammation and fibrosis scores were noted. Groups were compared according to these scores.

Results

There was statistical significant difference between ringer''s lactate group and olive oil group according to surgical adhesion score (p = 0.009). However, groups were not different according to inflammation and fibrosis scores (p > 0.05).

Conclusions

Despite antiinflammatory, antioxidants and antimicrobial properties of H. perforatum, our results revealed no positive effect of H. perforatum on the prevention of intraperitoneal adhesion formation.     

Effect of temperature upon adhesion formation in a laparoscopic mouse model

BACKGROUND: Pneumoperitoneum can be a cofactor in adhesion formation. Pneumoperitoneum with non-humidified gas causes desiccation in the peritoneal cavity which decreases temperature. The effect of desiccation upon adhesion formation is widely accepted. The specific effect of the associated cooling upon adhesion formation remains unexplored, and was addressed specifically in our laparoscopic mouse model. METHODS: Adhesions were induced during laparoscopy and scored after 7 days during laparotomy. Pneumoperitoneum was performed using CO2 or CO2 with oxygen with or without humidification. Animals were placed at different environmental temperatures to modulate body and intraperitoneal temperature. RESULTS: Anaesthesia, environment with a lower temperature and pneumoperitoneum all independently decrease body temperature. A decrease in body temperature decreases adhesion formation (P=0.004). Therefore, at 37 degrees C, pneumoperitoneum-enhanced adhesion formation is more important than at room temperature (P=0.04). As was observed at room temperature, adhesion formation at 37 degrees C increases with the duration (P=0.01) of pneumoperitoneum and decreases with the addition of 3% of oxygen (P=0.03). CONCLUSIONS: Hypothermia reduces pneumoperitoneum-enhanced adhesion formation, which supports hypoxia as a driving mechanism, since hypothermia decreases the toxic effects of hypoxia and of the ischaemia-reperfusion process. These data could open up new possibilities for adhesion prevention in laparoscopic surgery.     

Reactive oxygen species and adhesion formation: clinical implications in adhesion prevention

Postoperative adhesion formation is a major clinical problem.It has been demonstrated that the pneumoperitoneum used duringlaparoscopy is a cofactor in adhesion formation. Reactive oxygenspecies (ROS) are produced in a hyperoxic environment and duringthe ischaemia/reperfusion process. ROS activity is deleteriousfor cells, which protect themselves by an antioxidant systemknown as ROS scavengers. ROS activity can increase by up-regulationof ROS themselves or by down-regulation of ROS scavengers. Recentdata also point to a role for ROS in adhesion formation sincethe administration of ROS scavengers decreases adhesion formationin several animal models. ROS activity increases during bothlaparotomy and laparoscopy. During laparoscopy, the pneumoperitoneumdetermines ischaemia at the time of insuflation and reperfusionat the time of deflation. During laparotomy, the environmenthas a 150 mmHg partial pressure of oxygen (pO₂), which is muchhigher than the intracellular pO₂ (5–40 mmHg). This canexplain the increase in ROS activity. The aim of this debateis to open a discussion about the importance of ROS activity,besides the known players and mechanisms involved, in adhesionformation and in adhesion prevention.     

Effects of five different barrier materials on postsurgical adhesion formation in the rat

Postsurgical adhesion formation is a significant clinical problem within every surgical specialism. Due to the problems that adhesions cause, a wide variety of adjunctive treatments to prevent the formation and reformation of adhesions have been proposed. One of the modalities that has been studied extensively and that has been showing the most promising results is the so-called barrier method. The purpose of the present study was to compare the efficacy of five of these barrier materials in the prevention of postsurgical adhesion formation in a standardized rat adhesion model. It was concluded that no beneficial effect of Ringer's lactate on adhesion formation was seen. Significant reductions (P < 0.0001) in adhesion percentages compared to control animals were seen with Polyactive((TM)), PRECLUDE Peritoneal Membrane((TM)), Seprafilm((TM)) and Tissucol((TM)), but only PRECLUDE Peritoneal Membrane and Seprafilm significantly reduced adhesions (P < 0.01) when the barrier-treated peritoneal defects were compared with contralateral control-side peritoneal defects. The results of our study suggest that Seprafilm and PRECLUDE Peritoneal Membrane are superior to Tissucol and Polyactive in preventing adhesion formation. When Polyactive was still attached to the site of application during the second laparotomy, similar results to Seprafilm and PRECLUDE Peritoneal Membrane were seen. Future studies on the efficacy of a material to decrease adhesion formation should always include a comparison of several control materials in the same model. Our study indicates that Seprafilm or PRECLUDE Peritoneal Membrane might be used as standards of control.     

Inhibitory effects of pentoxifylline on LPS-induced leukocyte adhesion and macromolecular extravasation in the microcirculation

Pentoxifylline (PTX) has been shown to combat effectively endotoxin induced symptoms of shock or inflammation by reducing both leukocyte activation and endogenous cytokine formation. With regard to blood perfusion, inflammation is defined as a local reaction to injury of the living microvasculature and its content. Leukocyte margination, rolling, adhesion, and emigration is mediated by adhesion molecules along the endothelium of postcapillary venules and is considered to be an important step in the inflammatory response. Changes in the vascular integrity can be estimated in terms of increased extravasation of macromolecules. Using intravital microscopy with the help of an analogous video image processing system we measured the effect of PTX on lipopolysaccharide (LPS, 15 mg/kg i.v.) induced leukocyte adhesion and extravasation of FITC-rat serum albumin (FITC-RSA) in rat mesenteric venules. The changes in vascular permeability correlates significantly (r=0.75) with a locally increased number of adherent leukocytes. PTX significantly inhibits both leukocyte adhesion and extravasation of FITC-RSA dose dependently. Our results indicate that PTX effectively preserves vascular integrity in the microcirculation by acting primarily on LPS-induced leukocyte adhesion.     

The influence of DHEA pretreatment on prepulse inhibition and the HPA-axis stress response in rat offspring exposed prenatally to polyriboinosinic-polyribocytidylic-acid (PIC)

Periventricular leukomalacia (PVL) is the dominant form of brain injury in premature infants and no specific treatment is currently available. Neotrofin, a neurotrophin agonist, has been shown to provide neuroprotection in several in vivo and in vitro studies. The aim of this study was to investigate the neuroprotective effect of neotrofin treatment after endotoxin induced PVL in a rat model. Wistar rat pups were divided into four groups as: (1) control, (2) lipopolysaccharide (LPS)-administered group, (3) LPS-administered and prenatal maternal neotrofin-treated group and (4) LPS-administered and postnatal neotrofin-treated group. Intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) was administered consecutively at the 18th and 19th embryonic days to establish endotoxin-induced PVL model. In the prenatal treatment group dams received an i.p. injection of neotrofin (60 mg/kg) following after the second LPS dose; and in the postnatal treatment group rat pups received i.p. injection of neotrofin (60 mg/kg) at birth. At P7, apoptosis and hypomyelination in periventricular white matter were evaluated by immunohistochemical assessments. The prenatal maternal neotrofin treatment significantly reduced the number of apoptotic cell death and greatly prevented LPS-stimulated loss of hypomyelinization. However, neotrofin treatment in the postnatal period was not as effective as intrauterine treatment. Given our results, neotrofin may be useful in reducing brain injury and possessing clinical relevance for the treatment of white matter injury in newborns.     

Effects of mebendazole onAngiostrongylus costaricensis in mice,with special reference to the timing of treatment

Mebendazole was given to mice infected withAngiostrongyls costaricensis at a single dose of 5 mg/kg at 6, 11, 16 or 21 days post-infection (p.i.) and in five successive doses at 5 mg/kg daily at 6, 11 or 16 days p.i. The effects were comparatively assessed by examining various parameters in host mice and worms. As a whole, the effects of mebendazole were caused more conspicuously by five successive treatments than by a single treatment. In both treatment modalities, the effects were more remarkable in earlier treatments, and nearly complete effects were caused by five successive treatments before 15 days p.i. These results suggest that the inhibition of egg formation and/or oviposition will inhibit the pathological changes caused in the disease byA. costaricensis, especially before the onset of the changes.     

几丁糖防治运动损伤后的肌腱粘连

背景：肌腱损伤是运动训练中的常见损伤,在肌腱损伤修复过程中易形成粘连,从而使肌腱原有的功能下降或丧失。目前受到国内外学者瞩目的防治肌腱粘连的方法是防粘连材料的应用,在众多材料中,几丁糖备受关注。 目的：综述了几丁糖防治运动损伤后的肌腱粘连。 方法：应用计算机检索CNKI和PubMed数据库中1990-01/2010-12关于几丁糖防治运动损伤后肌腱粘连的文章,在标题和摘要中以“几丁糖,肌腱,粘连,运动损伤”或“chitosan,tendon,adhesion,sports injury”为检索词进行检索。选择文章内容与几丁糖防治运动损伤肌腱粘连相关,同一领域文献则选择近期发表或发表在权威杂志文章。根据纳入标准选择29篇文章进行综述。 结果与结论：肌腱主要由胶原纤维组成,其生物力学特性与胶原纤维密切相关。肌腱损伤后的愈合过程通过外源性愈合和内源性愈合两条途径完成,外源性愈合是产生粘连的主要原因。动物实验及临床实验均表明几丁糖具有良好的预防肌腱粘连的效果,其作用机制主要有降低胶原纤维的产生、屏障隔离、加速止血、抗菌消炎等。因此几丁糖是一种较为理想的预防肌腱粘连的物质,但应用中仍发现一些问题有待解决。     

环孢菌素A对大鼠腹主动脉球囊损伤后内膜增生的抑制作用

目的: 探讨环孢菌素A对大鼠腹主动脉球囊损伤后内膜增生的影响。方法: 雄性SD大鼠36只,随机分为假手术组(n=12)、球囊损伤组(n=12)和环孢菌素治疗组(n=12)。环孢菌素组大鼠行腹主动脉球囊损伤术前3 d开始每天灌喂环孢菌素A 12.5 mg/kg,假手术组和球囊损伤组灌喂等容积的水,直至术后30 d。球囊损伤术后30 d取材,血管组织作HE染色、免疫组化检测钙调神经磷酸酶(CaN)在血管壁中的表达,光学显微镜观察病理学改变;rea1-time PCR技术检测血管壁组织中CaN和活化T细胞核因子3(NFATc3)的表达变化。结果: 球囊损伤后血管壁出现新生内膜,形成的新生内膜厚度不均。环孢菌素治疗组与球囊损伤组相比较,内膜增生减轻,内膜/中膜厚度明显降低(P<0.05)。免疫组化检测血管壁上CaN表达,环孢菌素治疗组明显低于球囊损伤组 (P<0.05)。大鼠腹主动脉损伤后,损伤血管壁组织CaN和NFATc3 mRNA表达升高,环孢菌素治疗组与球囊损伤组相比表达明显减少(P<0.05)。结论: 环孢菌素A可能通过抑制CaN-NFATc途径减轻球囊扩张术后动脉再狭窄。     

Clerodendron glandulosum.Coleb leaf extract attenuates in vitro macrophage differentiation and expression of VCAM-1 and P-selectin in thoracic aorta of atherogenic diet fed rats

Present inventory evaluates the anti-atherogenic potential of C. glandulosum.Coleb leaf extract (CG) using in vivo and in vitro experimental models. Serum markers of low density lipoprotein (LDL-C) oxidation, cholesterol, triglycerides, lipoproteins, auto-antibody titer, ex vivo LDL-C oxidation, LDL-C aggregation, aortic lipids, histopathological evaluations and immunolocalization of macrophage surface marker (F4/80), vascular cell adhesion molecule-1 (VCAM-1) and P-selectin were performed in CON [rats treated with single dose of saline (i.p.) and fed with laboratory chow], ATH [rats treated with single dose of vitamin D3 (600,000 IU, i.p) and fed with atherogenic diet] and ATH+CG [rats treated with single dose of vitamin D3 (600,000 IU, i.p.) and fed with atherogenic diet and simultaneously treated with 200?mg/kg CG extract, p.o.] for 8 weeks. CG extract supplementation to atherogenic diet fed rats significantly prevented increment in serum cholesterol, triglycerides, and lipoproteins, markers of LDL-C oxidation, auto-antibody titer and aortic lipids. Also, LDL-C isolated from ATH+CG rats recorded mimimal aggregation and susceptibility to undergo ex vivo LDL-C oxidation. Microscopic evaluation of thoracic aorta of ATH+CG rats reveled prevention of atheromatous plaque formation, accumulation of lipid laden macrophages, calcium deposition, distortion/defragmentation of elastin, accumulation of macrophages and, down regulation of cell adhesion molecules (VCAM-1 and P-selectin) expression. Further, in vitro monocyte to macrophage differentiation was significantly attenuated in presence of CG extract (200 μg/mL). It can be concluded from the present study that, CG extract is capable of controlling induction of experimental atherosclerosis and warrants further scrutiny at the clinical level as a possible therapeutic agent.