Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model

BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.     

Recipient hypertonic saline infusion prevents cardiac allograft dysfunction

Objective

Hypertonic saline (HTS) has potent immune and vascular effects. We assessed recipient pretreatment with HTS on allograft function in a porcine model of heart transplantation and hypothesized that HTS infusion would limit endothelial and left ventricular (LV) dysfunction following transplantation.

Regulation of fibroblast-induced collagen gel contraction by interleukin-1β

Fibroblasts incorporated within collagen gels induce a cell-mediated contraction of the gel to form a three-dimensional, tissue-like structure by a mechanism thought to mimic wound contraction in vivo . In this study a gel contraction model was used to investigate the ability of fibroblasts derived from adult gingiva, adult skin and fetal skin to organise a collagen matrix. In addition the effects of interleukin-1β (IL-1β) on the contraction process was also investigated. Over the concentration range 5-50 U/ml, IL-1β induced a statistically significant inhibition of gel contraction in all fibroblast cell types ( P <0.05), although fetal fibroblasts appeared least responsive and gingival fibroblasts most responsive to the inhibitory effects of this cytokine. Comparison of gel contraction by the different fibroblast strains indicated that fetal and gingival fibroblasts shared similar contraction kinetics. For the adult skin fibroblasts, three of five strains studied showed significantly diminished levels of gel contraction compared to fetal and gingival cells. This apparent difference in fibroblast phenotype may, at least in part, explain the fetal-like wound healing pattern seen in the oral mucosa.     

心肌和骨骼肌对低血钙不同反应性机理的初步研究

本实验采用枸椽酸钠等静脉输入复制家兔低血钙。实验动物血钙显著下降,同时出现骨骼肌抽搐和心肌收缩性下降。测定骨骼肌匀浆钙含量在低血钙前、后均比心肌匀浆高。认为这两种肌肉细胞内固有钙含量的差异,是低血钙时骨骼肌收缩亢进和心肌收缩性下降的原因之一,其次为神经肌肉的兴奋性改变。     

丹参酚酸B盐对内皮素诱导的人肝星状细胞收缩的抑制作用及机制研究

目的 以培养的人肝星状细胞（HSC）为研究对象，观察内皮素-1（ET-1）对HSC的收缩作用及丹参酚酸B盐（SA-B）对ET-1的抑制作用，并探讨SA B抑制HSC收缩的作用环节和可能作用机制。 方法 采用酶消化、Nycodenz密度梯度离心的方法分离人HSC，以胶原凝胶收缩法观察ET-1对于传代HSC的收缩作用，以及低、中、高3种剂量的SA B对其不同的干预作用；将ET-1、SA-B直接添加于传代HSC的无血清培养液中，以激光共聚焦显微镜技术观测HSC内钙离子浓度的变化。 结果 胶原凝胶收缩实验显示，ET-1可诱导HSC收缩（P<0.01）；3种剂量的SA-B可明显抑制ET-1诱导的HSC收缩（均P<0.01）；加入ET-1后，HSC形态学改变明显，细胞数量减少，但SA B对这些改变也有抑制。激光共聚焦显微镜下观察，ET-1可刺激细胞内钙离子短暂迅速增加，加入SA-B后，该作用被明显抑制。 结论 SA-B能显著抑制ET-1诱导的HSC收缩，其抑制收缩的机制与降低HSC内的钙离子浓度有关。SA-B的抑制HSC收缩作用可能是其抗肝纤维化及门脉高压的机制之一。     

等长收缩运动治疗单纯颈伸肌劳损的疗效观察

目的总结等长收缩运动治疗单纯颈伸肌劳损的疗效。方法随机将56例单纯颈伸肌劳损分为两组,一组应用等长收缩运动进行治疗,另一组应用手法治疗,对比两组患者疗效。结果治疗1周后,两组患者的总有效率均为100%（P〉0.05）。结论等长收缩运动治疗单纯颈伸肌劳损的疗效与手法治疗相近,但该法具有更安全、经济、且不受条件、时间限制,更有主动巩固疗效和积极预防的作用。     

Relaxin down-regulates renal fibroblast function and promotes matrix remodelling in vitro.

BACKGROUND: Renal fibroblasts are important effector cells in tubulointerstitial fibrosis, with experimental antifibrotic strategies focusing on the functional down-regulation of these cells. Several experimental models of fibrosis have provided evidence for the effectiveness of the polypeptide hormone relaxin as a potential antifibrotic agent. This study was conducted to further elucidate the antifibrotic mechanisms of relaxin on renal fibroblasts in vitro. METHODS: Rat cortical fibroblasts were obtained from outgrowth culture of renal tissue isolated from kidneys 3 days post-unilateral ureteric obstruction and constituted 100% of cells studied. A relaxin radio-receptor assay was used to establish binding of relaxin to renal fibroblasts in vitro. Functional studies then examined the effects of H2 relaxin (0, 1, 10 and 100 ng/ml) on fibroblast kinetics, expression of alpha-smooth muscle actin (alpha-SMA), total collagen synthesis, collagenase production and collagen-I lattice contraction. CTGF mRNA expression was also measured by northern analysis. RESULTS: H2 relaxin bound with high affinity to rat renal fibroblasts, but receptor numbers were low. Consistent with its previously reported bimodal effect, transforming growth factor (TGF-beta 1) reduced fibroblast proliferation, an effect abrogated by H2 relaxin. Fibroblasts exposed to H2 relaxin (100 ng/ml) for 24 h demonstrated decreased immunostaining for alpha-SMA and reduced alpha-SMA protein expression compared with controls. There was a trend for a relaxin-mediated reduction in total collagen synthesis and alpha 1(I) mRNA expression with large dose-related increases in collagenase protein expression being observed. TGF-beta 1-stimulated collagen-I lattice contraction was significantly inhibited following co-incubation with 100 ng/ml relaxin. Incremental doses of H2 relaxin had no significant effect on CTGF mRNA expression. CONCLUSIONS: The findings of this study suggest that the antifibrotic effects of relaxin involve down-regulation of fibroblast activity, increase in collagenase synthesis and restructuring of collagen-I lattices, which are consistent with its known physiological role of matrix remodelling. Although there appears to be an interaction between TGF-beta 1 and H2 relaxin, this does not appear to involve a reduction in CTGF mRNA expression.