加减下瘀血汤对人肾小球系膜细胞清道夫受体表达的影响

目的 :探讨加减下瘀血汤对人肾小球系膜细胞 (HMC)表面清道夫受体A(SR -A)表达的影响。方法 :通过采用体外培养HMC ,在佛波酯 (PMA)刺激SR -A上调后 ,用加减下瘀血汤含药血清对其进行干预 ,观察加减下瘀血汤对HMC表面SR -AmRNA表达水平及SR -A与配体结合能力的影响。结果 :(1)体外培养的HMC在PMA的刺激下SR -AmRNA水平明显增高 ,摄取乙酰化低密度脂蛋白 (AC -LDL)能力增强 ,其作用随药物浓度增加而增强 (P <0 .0 5 ) ;(2 )中、高浓度的加减下瘀血汤含药血清能下调PMA诱导SR -AmRNA水平的上调 ,低浓度含药血清作用不明显。且该作用随着药物浓度的增加、作用时间的延长而增强 (P <0 .0 5 )。结论 :加减下瘀血汤治疗肾病的机理之一 ,可能是通过抑制病理状态下HMC表面SR -A的高表达。     

氯沙坦对血管紧张素Ⅱ诱导人足细胞分泌VEGF的影响

目的：研究血管紧张素Ⅱ（AngⅡ）对人足细胞分泌血管内皮细胞生长因子（VEGF）的影响及氯沙坦的保护作用。方法：将人足细胞与干预药物共培养。（1）按AngⅡ浓度梯度0、1、10、100nm和时间梯度0、3、6、12、24h分组培养,用RT-PCR检测VEGF的mRNA表达水平;（2）用100nm AngⅡ刺激足细胞,并按不同浓度氯沙坦干预分组培养,用RT-PCR检测VEGF的mRNA表达水平。结果：AngⅡ可以剂量和时间依赖性的诱导足细胞表达VEGF增高,而氯沙坦可以剂量依赖性的阻断VEGF表达增高。结论：AngⅡ对VEGF基因表达的增高呈剂量和时间依赖性,氯沙坦可拮抗AngⅡ诱导人足细胞表达VEGF增高。     

积雪排毒汤含药血清对人肾小管上皮细胞转分化的影响

目的观察经验方积雪排毒汤含药血清对转化生长因子β1（TGF-β1）所诱导的肾小管上皮细胞（TECs）转分化的影响；初步探讨其延缓肾小管间质纤维化的作用机制。方法给予实验家兔积雪排毒汤灌胃3d后制备积雪排毒汤含药兔血清，应用含药血清处理经TGF-β1诱导活化的HK-2细胞，用RT-PCR法测定其α-平滑肌肌动蛋白（α-SMA）mRNA、钙黏蛋白（E-cadherin）mRNA表达的变化。结果含药兔血清能抑制TGF-β1诱导活化的HK-2细胞α-SMA的表达，上调其E-Cadherin mRNA的表达。结论积雪排毒汤可能是通过抑制TECs转分化而对防治肾小管间质纤维化发挥作用。     

糖肾汤对大鼠肾小球系膜细胞分泌细胞外基质的影响

目的:研究糖肾汤对高糖培养下大鼠肾小球系膜细胞外基质的影响.方法:在体外高糖培养的大鼠肾小球系膜细胞中,加入糖肾汤含药血清进行干预,用酶联免疫吸附法检测培养上清中纤维连接蛋白(FN)、层黏连蛋白(LN)、Ⅳ型胶原(ColⅣ)的含量.结果:高糖可刺激肾小球系膜细胞分泌LN,糖肾汤对此无对抗影响;但能抑制高糖环境下肾小球系膜细胞高分泌Ⅳ型胶原、纤维连接蛋白的作用,且有一定的量效依赖关系,优于开搏通对照组.结论:糖肾汤能抑制高糖环境下肾小球系膜细胞高分泌Ⅳ型胶原,纤维连接蛋白的作用,具有一定的量效依赖关系.     

丹参多酚酸盐对实验性小鼠草酸钙结晶生成的影响

目的 观察中药丹参多酚酸盐对小鼠肾脏草酸钙结晶生成的干预效果,并探讨其可能的作用机制.方法 24只8周龄雄性C56BL/6小鼠根据丹参多酚酸盐干预与否以及干预浓度（80mg/kg、160 mg/kg）进行分组,每组8只.各组小鼠均给予腹腔注射乙醛酸盐（100 mg/kg）造模,丹参多酚酸盐干预组在乙醛酸盐诱导结晶肾损伤基础上加用不同浓度的丹参多酚酸盐注射液,均为1次/d,连续给药7d后,收集肾脏组织标本.光镜下观察各组小鼠肾组织中草酸钙结晶生成情况;检测肾组织中钙含量、脂质过氧化丙二醛（malondialdehyde,MDA）、谷胱甘肽（glutathione,GSH）、过氧化氢酶（catalase,CAT）及超氧化物歧化酶（superoxide dismutase,SOD）活性.结果 与模型组相比,给予丹参多酚酸盐注射液后的小鼠肾组织SOD、GSH和CAT显著升高,而MDA和肾组织钙含量显著下降（P＜0.05）,但丹参多酚酸盐两种浓度间未见明显的量效关系.结论 丹参多酚酸盐能有效的抑制由乙醛酸盐诱导的小鼠草酸钙结晶的生成.     

加味当归补血汤对肾小管上皮细胞TGF-β1／SMADs信号转导通路的影响

目的：观察加味当归补血汤对转化生长因子β1（TGF-β1）刺激的小鼠肾小管上皮细胞Smad3、Smad4、Smad7信号通路的影响，探讨该方防治肾间质纤维化的细胞分子生物学机制。方法：原代培养BalB／C小鼠肾小管上皮细胞．用TGF-β（1ng／ml）刺激24h，加味当归补血汤及洛汀新含药血清干预。共分6组：正常组、模型组、加味当归补血汤低中高剂量组（含药血清浓度分别为2．5％、5％、10％）、洛汀新组，观察各组细胞形态学变化，检测细胞Smad3、Smad4、Smad7的mRNA和蛋白质表达情况（PT—PCR、Western-Blotting）。结果：（1）TGF-β1刺激后，肾小管上皮细胞部分形态发生变大，伸长，呈梭形，经中药加味当归补血汤和洛汀新干预后，细胞形态又恢复正常；（2）TGF-β1刺激肾小管上皮细胞后，Smad3、Smad4 mRNA和蛋白质表达显著增加，Smad7 mRNA和蛋白质则显著减少（P〈0、05～0、01）；（3）各浓度加味当归补血汤能显著下调异常增高的Smad3，上调Smad7的基因和蛋白质表达水平（P〈0．05～0．01），能显著下调Smad4基因表达。结论：加味当归补血汤防治肾间质纤维化可能与调控肾小管上皮细胞TGF-β1／Smads信号转导途径相关。     

OX-LDL诱导活化的巨噬细胞对肾小球系膜细胞TGF-β与Fn基因表达的影响及水蛭素的干预作用

目的：研究氧化低密度脂蛋白（OX—LDL）诱导活化的巨噬细胞对肾小球系膜细胞转化生长因子（TGF-β）、纤连蛋白（Fn）基因表达的影响以及水蛭素的干预作用，探讨炎症状态下肾硬化发生的病理机制和水蛭素的有效作用。方法：体外培养大鼠肾小球系膜细胞，将OX—LDL诱导活化的大鼠腹腔巨噬细胞转入细胞培养小室，或采集其条件培养基与肾小球系膜细胞共培养；水蛭素干预组在分层共培养系统的培养有系膜细胞的下层培养液中加入水蛭素。浓度分别为2.5U／ml、5．0U／ml、10U/ml。逆转录-聚合酶链扩增反应（RT—PCR）检测肾小球系膜细胞TGF-β、Fn的基因表达。结果：OX—LDL刺激后，大鼠腹腔巨噬细胞上清液中IL-1浓度明显升高；无论是活化的巨噬细胞还是其奈件培养基均能上调TGF-β和Fn mRNA的表达，但以分层共培养作用最为显著；水蛭素在一定浓度下可显著下调T（再一p和Fn的基因表达。结论：（1）在分层共培养条件下，OX—LDL诱导活化的巨噬细胞与系膜细胞处于一个整体系统中，巨噬细胞不仅可通过分泌细胞因子等病理产物，而且两种细胞还可能通过相互作用增强对系膜细胞增殖和TGF-β和Fn分泌等的促进作用。（2）水蛭素可能通过抑制病理条件下硬化因子和细胞外基质的基因表达起到干预肾硬化的作用。     

补肾活血中药含药血清对滑膜细胞分泌TNF-α、IL-1β水平的影响

目的:探讨补肾活血中药是否可以抑制兔滑膜细胞分泌TNF-α、IL-1β等炎性因子。方法:制作补肾活血方含药血清,体外分离并培养兔滑膜细胞,并鉴定、传代。实验分含空白血清对照组、含10%西乐葆血清组、含5%、10%、20%中药血清组等5组。以西乐葆含药血清作为对照,将不同浓度的中西药血清加入培养传代的第3代滑膜细胞,继续培养。观察药物对滑膜细胞分泌TNF-α、IL-1β水平的影响。结果:补肾活血方含药血清具有和西乐葆含药血清类似的抑制滑膜细胞分泌TNF-α、IL-1β的作用,其抑制TNF-α分泌的作用随药物浓度的增加作用增强。结论:补肾活血中药可抑制滑膜细胞分泌TNF-α、IL-1β等炎性因子。     

复方鳖甲软肝片方对TGF-β1诱导的肾间质成纤维细胞增殖及分泌细胞外基质的影响

目的：观察中药“复方鳖甲软肝片方”对TGF-β1诱导的肾间质成纤维细胞（NRK-49F）增殖及分泌细胞外基质的影响。方法：以2 ng/ml hTGF -β1诱导 NRK -49F 细胞,并以软肝片方大、中、小剂量（分别以7g/kg、3.5 g/kg、1.75 g/kg）药物血清进行干预,分别应用MTT法、ELISA、免疫细胞化学方法,观察肾间质成纤维细胞增殖、细胞上清FN浓度及ColⅠ、ColⅢ的表达。结果：软肝方含药血清对hTGF-β1诱导的细胞增殖无影响;但大、中剂量软肝方能不同程度地降低FN的分泌及ColⅠ、ColⅢ的表达,软肝方大剂量组作用最强（P〈0.01）。结论：复方鳖甲软肝片方在一定程度上抑制TGF-β1诱导的肾间质成纤维细胞ColⅠ或ColⅢ的表达,大剂量软肝方作用最强。     

独活寄生汤含药血清对兔退变软骨细胞“caveolin-p38MAPK”信号通路调控作用的影响

目的:观察独活寄生汤含药血清对兔退变软骨细胞"caveolin-p38MAPK"信号通路的调控作用,探讨独活寄生汤治疗骨关节炎的作用机制。方法:将20只3月龄新西兰兔随机分为生理盐水组(空白血清组)和独活寄生汤组(含药血清组),每组10只。分别在24 h、36 h、48 h不同采血时间点采集独活寄生汤含药血清和空白血清,将5%、10%、15%、20%不同浓度两种血清作用于体外培养第2代软骨细胞,确定含药血清最佳干预条件;建立体外退变软骨细胞模型,分别给予独活寄生汤含药血清(含药血清组)和空白血清(空白血清组)干预36 h,收集软骨细胞,运用Western Blot法检测血清干预后退变软骨细胞caveolin-1、p38、p-p38蛋白表达,RT-PCR法检测血清干预后退变软骨细胞白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、基质金属蛋白酶(MMP)-3、MMP-13、caveolin-1 m RNA表达。结果:浓度为15%的36 h采血时间点含药血清的促增殖作用最明显;退变软骨细胞中存在"caveolin-p38MAPK"信号通路的激活,独活寄生汤含药血清可抑制caveolin-1、p-p38蛋白表达及IL-1β、TNF-α、MMP-3、MMP-13、caveolin-1 m RNA的表达,差异有统计学意义(P0.05)。结论:独活寄生汤能通过抑制"caveolin-p38MAPK"信号通路的激活及其下游效应分子,从而有效抑制软骨细胞凋亡。     

Oxidized LDL leads to podocyte injury through PTEN/SR-A pathway

Objective To evaluate the effect of oxidized LDL (Ox-LDL) on scavenger receptor A (SR-A) expression in mouse podocytes and to explore the possible mechanism. Methods The conditionally immortalized mouse podocyte cell line was cultured in vitro and exposed to Ox-LDL of different concentrations for 24 h, or 20 mg/L Ox-LDL for different hours. Cell cholesterol accumulation was examined. Real-time quantity PCR and Western blotting were used to analyze the expression level of PTEN, SR-A and nephrin. Podocytes were incubated with DiI labeled Ox-LDL for 4 h and immunofluorescence was used to analyze lipid uptaking. To further confirm the relationship between PTEN and SR-A, PTEN inhibitor bpv (hOpic) [dipotassium bisperoxo (5-hydroxypyridine-2-carboxyl) oxovanadate (V) ], PTEN siRNA and PTEN adenovirus (adPTEN) were used to dual-directional regulate PTEN expression, so as to observe the change of SR-A, nephrin, cell cholesterol accumulation and lipid uptake. Results SR-A was expressed on mouse podocyte and mediated podocyte lipid uptake. Compared with control group, Ox-LDL increased cell cholesterol accumulation, and up-regulated SR-A expression along with inhibited expression of PTEN and nephrin (P＜0.05), which were correlate with dose and exposure time of Ox-LDL. Expression of PTEN significantly inhibits the expression level of SR-A and lipid uptake induced by Ox-LDL (P＜0.05), thereby decreasing cell cholesterol accumulation, but up-regulating nephrin level (P＜0.05). However, down-regulation of PTEN could cause opposite effect. Conclusion Ox-LDL up-regulates SR-A through decreasing the expression of PTEN, and contributes to podocyte injury.     

银杏叶提取物治疗实验性肾病综合征的实验研究

目的:观察银杏叶提取物761(EGB761)对实验性肾病综合征的疗效,并探讨其可能机制.方法:实验大鼠复制成阿霉素(ADR)肾病(NS)模型,分为正常组、模型组、模型 EGB761组(EGB761组).结果:(1)EGB761组尿蛋白量下降幅度显著高于模型组(P＜0.05).(2)实验8周末,EGB761组血清总蛋白(TP)、白蛋白(Alb)升高幅度显著高于模型组(P＜0.05);EGB761组血清总胆固醇(TC)、总甘油三酯(TG)、低密度脂蛋白(LDL)下降水平均显著高于模型组(P＜0.05).(3)模型组血清总超氧化物歧化酶(SOD)显著低于正常组;丙二醛(MDA)显著高于正常组(P＜0.05);EGB761组总SOD升高水平及MDA下降水平均显著高于模型组.(4)24 h尿蛋白量与血清总SOD呈直线负相关,r=-0.923(P＜0.01);24 h尿蛋白量与血清MDA呈直线正相关,r=0.774(P＜0.01).结论:EGB761能显著改善NS大鼠临床指标,其减轻尿蛋白的作用与清除氧自由基、降血脂有关.     

内毒素对人巨噬细胞系U937生物学性状和生长因子分泌能力的影响

目的　探讨不同浓度的内毒素 /脂多糖 (LPS)对人巨噬细胞系U937生物学性状和生长因子分泌能力的影响。　方法　分别以 0 .0、0 .1、1.0、10 .0、5 0 .0、10 0 .0 μg/ml的LPS刺激体外培养的U937,作用 2 4h后运用四氮噻唑蓝 (MTT)法测定细胞增殖活力 ,应用流式细胞仪测定细胞凋亡率 ,并用酶联免疫吸附测定法检测细胞培养上清中转化生长因子 β1(TGF β1)和血管内皮生长因子(VEGF)浓度的变化。　 结果　与LPS为 0 .0 μg/ml时比较 ,当其浓度为 0 .1～ 10 0 .0 μg/ml时可刺激U937细胞凋亡、促进其分泌TGF β1(P <0.0 5～ 0.0 1),其中低浓度 (0 .1～ 10 .0 μg/ml)的LPS可促进U937增殖 (P <0.0 5～ 0.0 1),但对VEGF的分泌无明显影响 (P >0.0 5);高浓度 (5 0 .0、10 0 .0μg/ml)的LPS对U937的增殖无促进作用 (P >0.0 5 ),但能提高VEGF的分泌能力 (P <0.0 1)。结论　LPS可激活U937并促使其分泌TGF β1,刺激浓度以 0 .1～ 10 .0 μg/ml为宜 ;LPS仅在较高浓度时能促进U937细胞分泌VEGF。     

Low–Density Lipoprotein Adsorption for Arteriosclerotic Patients

Abstract: A wide variety of treatments is now available for arteriosclerosis obliterans (ASO) patients, not very successful in some cases. Low—density lipoprotein (LDL) apheresis using an extracorporeal adsorption column containing dextran sulfate cellulose beads was applied to control lipid levels intensively in ASO patients with accompanying drug—resistant hyperlipidemia. A series of the apheresis procedures had a remarkable impact on clinical symptoms and physiological findings with improvement in intermittent claudication observed in more than 80% of the patients. Improvements in plethysmogram and thermogram readings suggested an increased circulation in lower extremities in more than 80% of patients. In addition, the treatment improved blood rheology, as evidenced by a reduction in blood viscosity. In a follow—up study made by sending a questionnaire to previously treated patients, it was revealed that improvements in clinical symptoms were well maintained even after cessation of the treatment. In conclusion, LDL apheresis proved to be a useful therapeutic tool in ASO patients having elevated lipid levels     

Treatment of Homozygous Familial Hypercholesterolemia with Low Density Lipoprotein Apheresis: A 4 Year Follow-Up Study

Abstract: Hypercholesterolemia and elevated lipoprotein (a) (Lp[a]) levels are considered to be risk factors for the development and progression of premature atherosclerosis. The purpose of our report is to describe the effects of low density lipoprotein (LDL) apheresis (Liposorber system, Kanegafuchi Chemical Industrial Company LTD, Osaka, Japan) on serum lipoprotein concentrations and the clinical status in 2 male patients with homozygous familial hypercholesterolemia. Compared with pretreatment values, the posttreatment concentrations of total cholesterol, LDL cholesterol, and Lp(a) were significantly reduced by 50–60% (p < 0.0001). The concentration of high density lipoprotein (HDL) cholesterol was slightly affected. After one treatment session, LDL cholesterol and Lp(a) were decreased on average by 65% and then increased to reach about 70–75% of the pretreatment values before the next session. Prior to the treatment with LDL apheresis, each patient had suffered one myocardial infarction and had had 2 coronary angiographies. After treatment with LDL apheresis, neither cardiac complaints nor myocardial infarction were observed. The xanthomas were much decreased during the treatment or disappeared. We conclude that LDL apheresis can be continued safely and without major technical problems for several years. Apheresis effectively lowers the serum levels of total and LDL cholesterol. Furthermore, it reduces Lp(a), which is not influenced by lipid-lowering drugs. The reduction of LDL cholesterol and Lp(a) may delay the progression of the atherosclerotic process, thereby helping to reduce the risk of new episodes of coronary heart disease and thus extending the life expectancy in these patients.     

Attenuation of Chloroquine‐Induced Renal Damage by α‐Lipoic Acid: Possible Antioxidant Mechanism

The toxic effect of chloroquine (CQ) has been attributed to oxidative stress with the consequences of lipid peroxidation. This study investigates the effects of α‐lipoic acid (LA) on CQ‐induced nephrotoxicity in rats. A single oral administration of CQ (970 mg/kg)‐induced nephrotoxicity, manifested biochemically by a significant increase in serum creatinine and blood urea nitrogen concentrations. In addition, renal tissue from CQ‐treated rats showed a significant increase in lipid peroxides measured as thiobarbituric acid reactive substances and hydroperoxides, along with significant decrease in nonenzymic antioxidants (vitamin C, vitamin E, and reduced glutathione) and enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione‐S‐transferase) levels. Oral administration of LA (10, 30, or 100 mg/kg) in different doses for 10 days produced a significant protection against nephrotoxicity induced by CQ. Treatment with LA markedly reduced the elevated lipid peroxidation, restored the depleted renal antioxidant defense system. LA at 100 mg /kg was effective when compared with other doses (10 and 30 mg/kg). This was accompanied by the histopathological observations in kidney tissue. The results suggest that LA ameliorate the lipid peroxidation and the loss of cellular antioxidants, thereby protecting the CQ‐induced oxidative damage in kidney.     

Low–Density Lipoprotein Apheresis Versus Lipid Lowering Drugs in the Treatment of Severe Hypercholesterolemia: Four Years' Experience

Abstract: Elevated lipoprotein concentrations seem to be linked strongly in a dose dependent manner to an increased incidence of atherosclerosis. A total of 47 patients suffering from severe hyperlipidemia were matched to treatment with LDL apheresis (Baxter, Kaneka, Li–popak; 24 patients, aged 50.2 ±11.5 years), diet, and/or lipid–lowering drugs or with diet and lipid–lowering drugs only (23 patients, aged 48.8 ±11.8 years). After treatment periods of 49.8 ±13.4 months (apheresis group, 2,396 treatment sessions) and 38.6 ± 15.1 months (drug group), the ensuing results revealed significant differences (p <0.0001): –47.3% versus –12.1% for total cholesterol, –46.9% versus –21.8% for LDL, +8.4% versus +0.9% for HDL, –52.0% versus – 13.1% for the LDL/HDL ratio, –36.4% versus –16.2% for triglycerides, and –25.9% versus + 1.5% for lipoprotein (a). In the apheresis group, one patient died of myocardial infarction; in the drug group, there was one nonfatal myocardial infarction and the manifestation of coronary heart disease in 3 cases. There were no severe side effects in either group. All patients in the apheresis group responded to therapy. The present trial suggests that a continuing reduction in serum lipid concentrations may lower, in a dose dependent manner, the risk for development and progression of coronary heart disease. Regarding clinical and laboratory results, LDL apheresis seems to be safe, effective therapy for treatment of severe hyperlipidemia.     

低分子肝素对血液透析患者脂质代谢影响的临床研究

目的 探讨长期应用低分子肝素抗凝对尿毒症血液透析患者脂质代谢的影响。方法 采用为期１年的长期开放、随机对照的方法,选择３５例无明显出血倾向尿毒症患者,随机分成普通肝素（ＵＦＨ）组（１３例）及低分子肝素（ＬＭＷＨ）组（２２）例,于透前分别按个体剂量给予普通肝素及低分子肝素钠动脉血路端注射,并在治疗前、治疗后６月及１２月检测血脂、脂蛋白、载脂蛋白水平及脂酶活性。结果 （１）两治疗组透析前血甘油三酯（Ｔ     

Attenuation of chloroquine-induced renal damage by alpha-lipoic acid: possible antioxidant mechanism

The toxic effect of chloroquine (CQ) has been attributed to oxidative stress with the consequences of lipid peroxidation. This study investigates the effects of alpha-lipoic acid (LA) on CQ-induced nephrotoxicity in rats. A single oral administration of CQ (970 mg/kg)-induced nephrotoxicity, manifested biochemically by a significant increase in serum creatinine and blood urea nitrogen concentrations. In addition, renal tissue from CQ-treated rats showed a significant increase in lipid peroxides measured as thiobarbituric acid reactive substances and hydroperoxides, along with significant decrease in nonenzymic antioxidants (vitamin C, vitamin E, and reduced glutathione) and enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) levels. Oral administration of LA (10, 30, or 100 mg/kg) in different doses for 10 days produced a significant protection against nephrotoxicity induced by CQ. Treatment with LA markedly reduced the elevated lipid peroxidation, restored the depleted renal antioxidant defense system. LA at 100 mg/kg was effective when compared with other doses (10 and 30 mg/kg). This was accompanied by the histopathological observations in kidney tissue. The results suggest that LA ameliorate the lipid peroxidation and the loss of cellular antioxidants, thereby protecting the CQ-induced oxidative damage in kidney.     

化痰通络方含药血清对血管内皮生长因子诱导的脐静脉内皮细胞增殖的影响及其机制研究

目的:观察化痰通络方含药血清对血管内皮生长因子(VEGF)诱导的脐静脉内皮细胞(HUVEC)增殖的影响及其机制。方法:将20只新西兰兔随机分为化痰通络方高(HTTL-h)、中(HTTL-m)、低(HTTL-l)剂量组,雷公藤多苷组(TG组),生理盐水组(Sal组),每组4只。分离鉴定健康新生儿HUVEC,siRNA敲降VEGFR2、PLCG1以及MAPK1,并采用RT-PCR和及Western Blot检测VEGFR2、PLCG1和MAPK1 mRNA及蛋白水平的表达。MTT法检测经VEGF诱导的HUVEC增殖情况。结果:与Sal组比较,VEGF可显著促进HUVEC增殖,而TG或HTTL-l均可显著抑制VEGF诱导的HUVEC增殖;siRNA敲降VEGFR2后,VEGF则不能促进HUVEC增殖,同时TG也失去了对HUVEC增殖的抑制能力;siRNA敲降PLCG1后,VEGF依然可以显著促进HUVEC增殖,此时TG对VEGF刺激的HUVEC增殖失去了抑制效应,但HTTL-m和HTTL-l依然对VEGF刺激的HUVEC增殖具有显著抑制效应;siRNA敲降MAPK1后,VEGF也可显著促进HUVEC增殖,TG对VEGF刺激的HUVEC增殖具有抑制效应,同时HTTL-l也对VEGF刺激的HUVEC增殖具有显著抑制效应。结论:化痰通络方含药血清对VEGF诱导的HUVEC增殖具有抑制作用。TG抑制VEGF诱导的HUVEC增殖依赖于VEGFR2和PLCG1表达,而化痰通络方对VEGF刺激的HUVEC增殖的抑制效应则不依赖VEGF/VEGFR2/PLCG1/MAPK1信号通路。