无机活性元素对大鼠慢性溃疡组织上皮细胞增殖的影响

目的测定无机活性元素(德莫林)对大鼠皮肤慢性溃疡组织细胞增殖的影响,并探讨其作用机制。方法制备SD大鼠慢性溃疡模型,实验组应用无机活性元素,对照组常规消毒换药。于用药第3、7天时取2组溃疡局部肉芽组织,应用流式细胞术检测细胞周期;RT-PCR技术对用药7d时2组肉芽组织增殖相关基因PCNA、CyclinD1、P27的表达进行检测。结果与对照组比较第3、7天时实验组G1期细胞比例明显低于对照组(P<0.05),而S期细胞比例则高于对照组(P<0.05);第7天时实验组CNA、Cy-clinD1mRNA表达均高于对照组(P<0.05),而P27mRNA表达低于对照组(P<0.05)。结论无机活性元素有促进慢性溃疡肉芽组织增殖的作用,其机制与该药物能促进PCNA、CyclinD1、P27表达有关。     

大蒜素对慢性肾衰大鼠肾脏组织纤维化抑制作用的研究

目的观察大蒜素(Allicin)对慢性肾功能衰竭(Chronic renal failure,CRF)大鼠肾脏组织纤维化的影响,研究大蒜素对CRF大鼠的保护作用机制。方法采用腺嘌呤溶液250 mg/(kg·d)灌胃21 d的方法建立CRF动物模型,将大鼠分为模型组(生理盐水),大蒜素低[5 mg/(kg·d)]、中[10 mg/(kg·d)]、高[20 mg/(kg·d)]剂量组,每组20只;另设正常对照组(生理盐水)20只。疗程为28 d。测定血清肾功能指标[尿素氮(BUN)、血肌酐(SCr)、尿酸(UA)、24 h尿蛋白量(Pro)],测定肾脏质量并计算肾脏指数,HE染色观察肾脏组织病理变化并进行病变评分。酶联免疫吸附法(ELISA)测定血清炎症因子[C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]含量水平,测定血清中层黏连蛋白(LN)、纤维联结蛋白(FN)、Ⅲ型前胶原(PC-Ⅲ)、Ⅳ型胶原(C-Ⅳ)含量;免疫组织化学法(IHC)检测肾组织中的Ⅰ型胶原(ColⅠ)、基质金属蛋白酶1(MMP-1)及纤溶酶原激活物抑制物1(PAI-1)表达。结果大蒜素中、高剂量组CRF大鼠血清BUN、SCr、UA含量和Pro降低(P<0.05或P<0.01),肾脏组织病变明显改善,体重增加(P<0.05),肾脏指数及肾脏组织病变评分降低(P<0.01)。CRF大鼠血清炎症因子(CRP、TNF-α)含量降低(P<0.05或P<0.01);血浆PC-Ⅲ、C-Ⅳ降低,FN提高(P<0.05或P<0.01);肾脏组织ColⅠ、PAI-1表达下调,MMP-1表达上调(P<0.05或P<0.01)。大蒜素高剂量组CRF大鼠血清IL-6含量和血浆LN水平降低(P<0.05)。结论大蒜素能够抑制肾脏组织纤维化,进而对CRF大鼠起到一定的保护作用。     

Distribution of inorganic elements in human autopsy tissue

In the practice of forensic medicine, we find many of cases of death where the actual cause is not determinable with autopsy, histological or toxicological examinations. In these cases of death, we can consider cardiac dysfunction of unknown origin, in the background of which such a physiologic cardiac insufficiency occurs that cannot be detected with the previously mentioned methods. The dysfunction is possibly associated with a significant change in certain inorganic elements, primarily in the conduction system of the heart. In the absence of published data, our goal was to determine the concentration of inorganic elements in the specialized rhythm determining muscle cell groups in the heart: sinus node (SN), atrioventricular node (AV), septum (SE), left ventricle anterior wall (LVAW). With microwave technology we destroyed the muscle tissue and measured the concentration of ions (Na, Mg, K, Ca, Mn, Fe, Cu, Zn, P, S) using Inductive Completed Plasma Atom Emission Spectrometry (ICP-AES) equipment. Of the 24 cases examined, the average ion concentrations in microgram/g were the following; Sinus: Na 2602 +/- 493, Mg 120 +/- 24, K 1787 +/- 347, Ca 244 +/- 41, Mn 0.129 +/- 0.011, Fe 58 +/- 12, Cu 2.171 +/- 0.46, Zn 10.4 +/- 2.027, P 1147 +/- 227, S 2301 +/- 245; Septum: Na 1452 +/- 315, Mg 243 +/- 56, K 3269 +/- 689, Ca 105 +/- 26, Mn 0.17 +/- 0.05, Fe 74 +/- 16, Cu 3.557 +/- 0.952, Zn 25.75 +/- 8.4, P 2764 +/- 494, S 3001 +/- 523; Av: Na 2614 +/- 517, Mg 242 +/- 40.2, K 2010 +/- 395, Ca 271 +/- 27.3, Mn 0.13 +/- 0.029, Fe 54 +/- 12, Cu 2.369 +/- 0.297, Zn 15 +/- 3.2, P 1625 +/- 291, S 2535 +/- 346; Lvaw: Na 1340 +/- 201, Mg 250 +/- 37, K 3659 +/- 532, Ca 88 +/- 22, Mn 0.175 +/- 0.05, Fe 76 +/- 19, Cu 3.62 +/- 0.58, Zn 27.13 +/- 3.1, P 3025 +/- 441, S 3140 +/- 440.     

异甘草酸镁对慢性髓细胞性白血病K562细胞系增殖的抑制作用

目的：观察异甘草酸镁对慢性髓细胞白血病K562细胞系增殖的抑制作用。方法：将异甘草酸镁以1640培养液倍比稀释成10,1,10-1,10-2,10-3,10-4,10-5,10-6g·L-1共8个浓度组,分别处理增殖期K562细胞,镜下观察不同时间点各浓度组细胞生长情况,应用CCK-8法检测细胞增殖能力,绘制生长曲线,计算抑制率和半数抑制浓度（IC50）。结果：在给药第3天,浓度大于10-3g·L-1的异甘草酸镁对K562细胞增殖具有抑制作用（P〈0.05）,细胞倍增时间为48h,并且具有时间和浓度依赖性。其中,10g·L-1和1g·L-1异甘草酸镁的抑制作用最强（P〈0.01）,IC50约为1.6g·L-1。结论：异甘草酸镁对K562细胞的增殖具有抑制作用,为临床应用异甘草酸镁预防和治疗白血病化疗相关肝损伤提供实验依据。     

基于ICP-MS研究断体地龙对大鼠创面无机元素含量的影响

目的 建立微波消解-ICP-MS法测定大鼠创面皮肤中无机元素含量,考察断体地龙促创面愈合作用与无机元素的关系。方法 采用HNO3体系-微波消解法对样品进行前处理,电感耦合等离子质谱法（ICP-MS）法对大鼠创面皮肤中钾、镁、钙、锰、铁、钴、镍、铜、锌、砷、硒、镉、碲、铅14 种无机元素进行测定和分析。结果 在优化的实验条件下,元素在0 μg?L-1 ~ 250 μg?L-1范围内回归方程系数r ≥ 0.999;方法的检出限(3σ,n = 10)为0.02 μg?L-1～13.04 μg?L-1;加样回收率(n = 6)为85.4%～ 119.0%。 断体地龙可明显提高创面组织中钾钙镁铜铁锌硒的含量,且未增加重金属元素的含量。 结论 该方法简便快速、灵敏度高、准确性好,可用于同时测定大鼠创面皮肤中多种无机元素的含量。断体地龙发挥促创面愈合作用与提高各无机元素含量有关,且具有较高的安全性。     

阿藿烯对大鼠抗血栓活性作用研究

目的:研究阿藿烯对大鼠血栓形成和凝血功能的影响,评价其抗血栓活性。方法:将SD大鼠随机分为空白对照组、血塞通阳性药组(50mg/kg)、阿藿烯低剂量组(25mg/kg)、中剂量组(50mg/kg)、高剂量组(75mg/kg),各组动物连续灌胃5d,末次给药2h后建立下腔静脉结扎模型、FeCl3致动脉血栓模型、断尾流血时间测定模型测定阿藿烯对血栓形成和凝血的影响;并测定各组大鼠给药前及给药后2h血浆凝血酶原时间(PT)、活化部分凝血酶时间(APTT)。结果:阿藿烯能抑制动静脉血栓的形成,使血栓重量降低,且高剂量阿霍烯对动静脉血栓形成的抑制率均大于40%;同时有效延长大鼠断尾流血时间,并能使大鼠血浆APTT、PT明显延长(P<0.05),且都具有剂量依赖关系。结论:阿藿烯有抗血栓活性。     

Changes in connective tissue components in ulcer tissue during the healing process of acetic acid ulcer in rats.

In order to elucidate the role of connective tissue components on the repair of ulcerated regions, quantitative changes in chemical components in ulcer tissue during the healing process were investigated in acetic acid-induced ulcer in rats. The ulcer index showed a peak on the 5th day after the operation, declined rapidly and maintained a slight level the 15th to the 60th days, without a complete recovery. In ulcer tissue, sialic acid and hexosamine remarkably increased in the early stages of healing, showing a peak on the 5th day. The patterns of time course of changes in both components ran almost parallel with those in the ulcer index. Uronic acid maintained slightly higher levels than normal levels the 5th to the 60th days. Hydroxyproline continued to increase with the time course from the 25th day. When acid mucopolysaccharides in ulcer tissue were isolated into various fractions, there were increases in hyaluronic acid on the 5th day, in chondroitin sulfate A and chondroitin sulfate C on the 30th day and chondroitin sulfate B on the 60th day, respectively. Significance of changes in these components in the healing process is discussed.     

蝎毒结肠靶向小球对幼鼠慢性内脏痛的抑制作用

目的:研究蝎毒结肠靶向小球对幼鼠慢性内脏痛的抑制作用。方法:选用新生SD大鼠,出生后8～14d内,每天固定时间给予一次60mm Hg结直肠扩张刺激,建立慢性内脏痛模型,对照大鼠除了不行结直肠扩张外,其他情况同模型大鼠。实验分组:对照组、对照空白小球组、对照蝎毒小球组、模型组、模型空白小球组、模型蝎毒小球低剂量组、模型蝎毒小球中剂量组、模型蝎毒小球高剂量组。大鼠第28天开始胃肠给药,连续给予蝎毒靶向制剂14d后,采用腹外斜肌放电来评估肠道痛觉的敏感性;进而采用离体脑片场电位的记录方法,观察慢性内脏痛幼鼠海马CAl区场电位LTP的变化。结果:模型幼鼠腹外斜肌放电明显增强,服用蝎毒靶向小球后,腹外斜肌放电幅值显著减少(P<0.05);记录离体海马场电位LTP显示,模型幼鼠场电位LTP较对照幼鼠的幅值显著增加(P<0.05),同时蝎毒结肠靶向小球可显著降低模型幼鼠海马场电位LTP的幅值(P<0.05),而对对照幼鼠的作用无统计学差异(P>0.05)。结论:蝎毒结肠靶向小球可抑制幼鼠慢性内脏痛觉敏感性。     

利洛司酮对大鼠异位子宫内膜的抑制作用(英文)

目的 :观察利洛司酮对大鼠异位子宫内膜的抑制作用。方法 :用外科自体移植术建立大鼠子宫内膜异位症模型。灌胃给药 ,qd× 2 1d ,测量给药前、后异位内膜体积 ,计算药物对异位内膜的抑制率。结果 :用药后对照组大鼠异位子宫内膜比用药前略增大 ;给予利洛司酮 2 0 ,80mg·kg- 1和米非司酮 50mg·kg- 1后 ,异位内膜的体积比用药前明显缩小 ,抑制率依次为 (80± 2 7) % ,(88± 2 2 ) %和 (82± 31) %。结论 :利洛司酮和米非司酮一样明显抑制大鼠异位子宫内膜的生长     

依普利酮抑制细胞增殖拮抗急性环孢素A肾损伤的研究

目的探讨盐皮质激素受体阻断剂依普利酮抑制细胞增殖拮抗环孢素A肾损伤的作用。方法经口灌服环孢素A(100 mg.kg-1.d-1),诱导小鼠急性肾脏损伤,给以依普利酮100 mg.kg-1.d-1治疗,d 10采血、摘取肾脏。放免法检测血清醛固酮水平,免疫组化检测增殖细胞核抗原(PC-NA)、纤连蛋白表达;RT-PCR、Western blot检测PCNA、FN、TGF-β1表达。结果血清醛固酮水平检测显示环孢素A组(318.83±95.72)ng.L-1较空白对照组(82.05±23.04)ng.L-1升高,依普利酮可明显抑制其分泌(149.50±36.20)ng.L-1。环孢素A组肾脏PCNA阳性细胞增多,纤连蛋白表达增强;PCNA、FN、TGF-β1蛋白及mRNA表达较空白对照组明显上调,依普利酮可抑制其表达。结论依普利酮可以抑制醛固酮的分泌、抑制细胞增殖,减轻环孢素A诱导的肾脏损伤。     

沙棘原花青素对应激性胃溃疡大鼠上皮细胞凋亡与增殖的影响

目的探讨沙棘原花青素对应激性胃溃疡大鼠上皮细胞凋亡与增殖的影响及其可能的机制。方法60只♂W ist-ar大鼠随机分为6组:正常组,对照组,低、中、高剂量组及雷尼替丁阳性对照组。采用束缚-浸水应激的方式造应激性胃溃疡模型,造模前灌胃不同剂量的SBPC或阳性药物。测定溃疡指数、大鼠血浆EGF及NO的水平;大鼠血浆NOS及iNOS的活性;免疫组化的方法测定胃粘膜组织中iNOS、EG-FR及PCNA的表达;采用原位末端标记法检测胃粘膜上皮细胞的凋亡。结果与对照组相比,高剂量组SBPC(150 mg.kg-1)的溃疡指数明显降低(P<0.01);血浆EGF的水平升高(P<0.05),血浆NO的浓度(P<0.01)降低;NOS及iNOS的活力降低(P<0.05);粘膜中的iNOS的表达降低(P<0.01),EGFR的表达增强((P<0.01),PCNA的表达增强(P<0.05),凋亡指数降低(P<0.05)。结论SBPC可能通过调节EGF和NO促进大鼠的细胞增殖抑制细胞凋亡,从而对应激性胃溃疡的发生起保护作用。     

Inhibitory effect of statins on the proliferation of human breast cancer cells

OBJECTIVE: Long-term hormone therapy in the postmenopause is associated with a moderate increase in cardiovascular and breast cancer risk. Of great concern, therefore, is the question of how women with menopausal symptoms and enhanced cardiovascular risk can be treated. Evidence is growing that an estrogen/statin combination may be a good choice, since this combination seems to elicit additive beneficial effects on the lipid profile and on the vasculature. METHODS: In the present study, the effect of two statins on the proliferation of breast cancer cells in the presence and absence of estradiol was investigated. RESULTS: Atorvastatin and fluvastatin were able to inhibit the proliferation of MCF-7 cells in the absence of estradiol. This effect seems to depend on an apoptotic statin effect which may be mediated by the down-regulation of the anti-apoptotic protein Bcl-2 rather than up-regulation of Fas-L or p53. However, in the presence of estradiol the inhibitory effect of the statins was less pronounced. CONCLUSIONS: The present data indicate that statins may possess anticancerogenic properties concerning the development of breast cancer in postmenopausal women. Clinical trials are necessary to prove a beneficial statin effect on breast cancer risk when combined with long-term hormone therapy.     

Inhibitory effect of pentalenolactone on vascular smooth muscle cell proliferation

The effect of pentalenolactone, an inhibitor of glyceraldehyde-3-phosphate dehydrogenase, on rat vascular smooth muscle cell proliferation was studied. Addition of pentalenolactone together with serum to quiescent cells dose-dependently inhibited cell proliferation and DNA synthesis. This inhibition was not associated with cell death. When quiescent cells were stimulated with serum and then treated with pentalenolactone, the inhibitory effect on the DNA synthesis declined gradually. A similar result was obtained when PD 98059 (2'-amino-3'-methoxyflavone), an inhibitor of extracellular signal-regulated kinase1/2 (ERK1/2) kinase (MEK1/2), was added to the cells after serum stimulation. Pentalenolactone inhibited serum or protein kinase C activator (phorbol 12,13-dibutyrate)-induced phosphorylation of ERK1/2 and MEK1/2. In contrast, pentalenolactone had little effect on platelet-derived growth factor receptor autophosphorylation. Taken together, these results indicate that pentalenolactone inhibits vascular smooth muscle cell proliferation, and that this inhibition appears to be mediated by inhibition of the ERK1/2 cascade.     

银杏内酯B对慢性炎症血管生成的抑制作用

目的研究银杏内酯B对慢性炎症血管生成的作用及部分作用机制。方法比色法测定小鼠慢性肉芽肿气囊模型血管生成指数，组织形态学方法检测气囊病理变化；放射免疫方法测定白介素-1β(IL-1β)含量；L929生物测定法测定肿瘤坏死因子(TNF-α)含量；RT-PCR法检测IL-1β和TNF-α mRNA的表达。结果银杏内酯B可显著抑制模型小鼠的血管指数，与病理观察结果相符；银杏内酯B可显著抑制模型小鼠血清中IL-1和TNF-α的分泌；能显著抑制PMA诱导的U937细胞IL-1β和TNF-α的分泌及其mRNA的表达。结论银杏内酯B能抑制小鼠慢性炎症性血管生成模型的血管生成，能抑制促血管生成细胞因子IL-1β和TNF-α的转录及表达，这可能是其抑制慢性炎症血管生成的机制之一。     

中华眼镜蛇毒活性组分抑制微血管形成研究

目的探讨中华眼镜蛇毒活性组分(CCVAF)抗血管生成的作用。方法采用原代培养牛肺主动脉内皮细胞克隆形成实验、Transwell小室趋化实验及大鼠胸主动脉环体外无血清培养微血管样结构形成实验,分别观察CCVAF对内皮细胞克隆形成、细胞迁移及大鼠动脉环微血管生成的影响。结果 CCVAF浓度为1.25,2.5,5.0μg/mL时,其对内皮细胞克隆形成抑制率分别为17.7%,40.3%,62.9%,呈浓度依赖性(r=0.982,P<0.05),而对内皮细胞迁移抑制率分别为20.5%,59.0%,73.5%,呈浓度依赖性(r=0.902,P<0.05);大鼠动脉环培养至第13天,CCVAF组较溶剂对照组微血管生成率下降了86.5%,CCVAF+VEGF组较VEGF对照组微血管生成率下降了88.1%。结论 CCVAF能够抑制内皮细胞克隆的形成、Hela细胞诱导的内皮细胞迁移和大鼠动脉环微血管的生成。     

Inhibitory effect of rhodamine B on the proliferation of human lip fibroblasts in culture

The effect of the cosmetic dye rhodamine B on the proliferation of human lip fibroblasts (KD cells) was investigated in a culture system. Rhodamine B at 25 micrograms/ml and above significantly decreased the number of the cells after a 72 h culture. A time course study revealed that 50 micrograms/ml of rhodamine B-induced decrease in the cell number occurred after 48 h and longer, suggesting that the dye inhibited cell proliferation without a decrease in cell attachment. The detachment of [3H]thymidine-labeled cells from the monolayer was unaffected by rhodamine B at 100 micrograms/ml and below. The incorporation of [3H]thymidine and [14C]leucine into the acid-insoluble fraction of the cell layer was significantly inhibited by 50 micrograms/ml rhodamine B treatment. Histologically, the damage of KD cells was not marked, however, a degenerative change of nuclei and an irregular shape of the cells as well as a decrease in the cell number were caused by 50 micrograms/ml rhodamine B. Rhodamine 6G caused a severe damage of the cells, and rhodamine B significantly decreased the cell number; rhodamine 123 had no significant effect; rhodamine 116 significantly increased the cell number. Furthermore, rhodamine B decreased the number of both vascular endothelial cells from bovine aorta and vascular smooth muscle cells from murine aorta after a 72 h culture. It is concluded that rhodamine B inhibits the proliferation of human lip fibroblasts. This rhodamine B effect may be a warning sign for the dye toxicity.     

大黄素抑制肾代偿性肥大的作用

利用单侧肾切除的方法．观察了大黄素对术后对侧肾代偿性肥大的影响。结果表明．手术初期对侧肾即可出现肾重量增加．肾重／体重比和肾代偿性肥大率升高；但是．随着实验进展．尽管肾脏仍明显增大．而肾重／体重比保持不变。大鼠经大黄素治疗后．肾重量明显低于非治疗组．而且其肾重／体重比值和肾代偿性肥大率均低于非治疗组。同时．单侧肾切除后．尿表皮生长因子（ＥＧＦ）排泄量增加．而大黄素能明显减少其尿ＥＧＦ的排泄量。研究还证实．经大黄素治疗后的大鼠，其菊粉清除率明显低于非治疗组。故推测．肾脏代偿性肥大发生于肾切除初期．大黄素能明显抑制肾脏代偿性肥大。肾组织ＥＧＦ参与了其代偿性肥大．大黄素的作用与其减少尿ＥＧＦ排泄量有关。     

Inhibitory effect of somatostatin on gastric acid secretion in rats

Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 microgram/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 micrograms/kg/min) also dose-dependently inhibited the bethanechol-induced gastric acid secretion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 microgram/kg/min for vagally stimulated acid secretion and 2.5 micrograms/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentolamine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitory effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adrenoceptor-mediated mechanisms.     

Inhibitory effect of cycloheximide on gastric secretion in rats.

Cycloheximide administered to rats in non-toxic doses immediately after pyloric ligation results in a lower incidence of experimental gastric ulcers. The effect is paralleled by an impaired secretion of hydrochloric acid (more than 90 per cent inhibition). Simultaneously the activity of pepsin in gastric juice and in homogenates of gastric mucosa was reduced by 60 per cent and mucoproteins were lowered by 30 per cent. The basal and pentagastrin-stimulated secretion were inhibited by cycloheximide to the same extent.