蛴螬提取物对视网膜静脉阻塞兔内皮抑素表达的影响

目的 评价蛴螬提取物对兔视网膜静脉阻塞的治疗作用及其机制。方法 将40只兔随机分为4组：空白组、模型组、复方血栓通组、蛴螬组，每组10只兔20只眼，除空白组外，其余3组均用光化学动力法建立视网膜静脉阻塞（retinal vein occlusion，RVO）动物模型，于给药后1周、3周行FFA检查、HE染色、免疫组化观察内皮抑素表达。结果 FFA检查结果显示：给药后周1周，模型组中央静脉荧光渗漏、出血，复方血栓通组和蛴螬组渗漏、出血较模型组少；给药后3周，模型组渗漏、出血的静脉周围出现无灌注区，复方血栓通组渗漏、出血明显减小，蛴螬组渗漏、出血基本吸收。视网膜切片光镜观察结果显示：蛴螬组视网膜各层结构病理变化均轻于模型组、复方血栓通组。内皮抑素免疫组化结果显示：各造模组内皮抑素表达均下降，蛴螬组表达最强，模型组表达最弱，差异有统计学意义（P<0.05）。结论 蛴螬提取物能改善视网膜缺血缺氧的状态，促进RVO模型中内皮抑素的表达。     

Endostatin inhibits bradykinin-induced cardiac contraction

.Endogenous fragments of extracellular matrix are known to possess various biological effects. Levels of endostatin, a fragment of collagen type XVIII, increase in certain cardiac diseases, such as cardiac hypertrophy and myocardial infarction. However, the influence of endostatin on cardiac contraction has not been clarified. In the present study, we investigated the effects of endostatin on bradykinin-induced atrial contraction. Isometric contractile force of mouse isolated left atria induced by electrical current pulse was measured. Voltage-dependent calcium current of guinea pig ventricular myocytes was measured by a whole-cell patch-clamp technique. Endostatin (100–1,000 ng/ml) alone treatment had no influence on left atrial contraction. On the other hand, pretreatment with endostatin (300 ng/ml) significantly inhibited bradykinin (1 µM)-induced contraction and voltage-dependent calcium current. These data suggest that endostatin may decrease bradykinin-induced cardiac contraction perhaps through the inhibition of voltage-dependent calcium channel.     

Tumor Neoangiogenesis Inhibitors--Angiostatin and Endostatin Implication

Angiostatin and endostatin are two tumor neoangiogenesis inhibitors . They can suppress the growth of endothelial cell of the newly formed blood vessels in tumor , induce apoptosis and prevent tissue invasion,metastasis.Patients do not become resistant to angiostatin and endostatin despite continued treatment as chemotherapies proceed.The paper explains angiostatin and endostatin structure,fuction through schemic diagrams,and reviews their implications from the latest progress.     

Inhibitory effect of recombinant human endostatin on angiogenesis in atherosclerotic plaque of rats by regulating Dll4/Notch pathway

AIM: To observe the inhibitory effect of recombinant human endostatin (rhES) on plaque angiogenesis, and to explore the regulatory mechanism of Dll4/Notch pathway in the anti-angiogenic effect of rhES. METHODS: Male Wistar rats were randomized into 3 groups:normal control group (N group), atherosclerotic model group (AS group), and rhES treated group (AS+rhES group). The rats in N group were fed a normal diet, while the remaining 2 groups were established to atherosclerotic rat model via high-cholesterol diet, intraperitoneal injection of vitamin D₃ and aortic balloon injury. The rats in AS+rhES group received intraperitoneal injection of rhES. The blood total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), C-reactive protein (CRP), interleukin-1 (IL-1) and troponin I (TnI) were measured. The atherosclerotic abdominal aortas were taken for pathological observation. Immunohistochemical staining was used to measure the density of neovessels in the plaques, which were marked by CD31. The protein levels of Dll4 and Notch1 in the aortas were analyzed by Western blot. RESULTS: The levels of blood TC, TG, LDL-C, CRP and IL-1 in AS group and AS+rhES group were much higher than those in N group (P<0.05), and no statistical difference between AS group and AS+rhES group was observed. The expression of CD31 in AS group was the highest among all groups. Compared with AS group, the density of neovessels in the plaques of AS+rhES group decreased significantly (P<0.05). The protein expression of Dll4 and Notch1 in AS group was lower than that in N group (P<0.05). Compared with AS group, the protein expression of Dll4 and Notch1 increased significantly (P<0.05). CONCLUSION: rhES has the ability to inhibit plaque angiogenesis in rats. The activation of Dll4/Notch pathway may be the mechanism of rhES in inhibiting plaque angiogenesis.     

血管生成拮抗因子内皮抑素在急慢性白血病中的应用研究

应用vWF标记免疫组化法观察骨髓新生血管情况及ELISA法测定血浆内皮抑素(ES)含量，研究急慢性白血病患者骨髓新生血管情况及血浆血管生成拮抗因子ES的变化情况。结果表明：急性白血病(AL)和慢性白血病(CML)患者骨髓微血密度(MVD)较对照组极显著增高，治疗后获缓解者骨髓MVD显著降低，且接近正常水平；AL和CML血浆ES显著高于对照组，化疗后获完全缓解(CR)的AL和CML血浆ES含量均降至正常水平。说明初诊白血病患者存在骨髓新生血管及血管生成拮抗因子ES水平的增高，白血病患者体内ES的增加很可能对机体具有一种保护作用，其含量的变化可能与白血病患者的预后有关。     

Endostatin inhibits T-type Ca2+ channel current in guinea pig ventricular myocyte

Endostatin, a fragment of collagen XVIII, is known as an endogenous angiogenesis inhibitor, and its serum concentration increases in various cardiovascular diseases. T-type Ca²⁺ channel, low voltage-activated Ca²⁺ channel, is not expressed in adult ventricular myocytes. Re-expression of T-type Ca²⁺ channels in cardiac myocytes is thought to be involved in the development of cardiac hypertrophy. We examined the effects of endostatin on T-type Ca²⁺ channel current by whole-cell patch clamp technique in freshly isolated adult guinea pig ventricular myocytes, which exceptionally express T-type Ca²⁺ channels. Although endostatin 300 ng/ml had no effect on L-type Ca²⁺ current, it significantly inhibited T-type Ca²⁺ current. These data indicate that endostatin can be an endogenous inhibitor of T-type Ca²⁺ channels in the cardiac myocytes.