Role of reactive oxygen species in triptolide-induced apoptosis of renal tubular cells and renal injury in rats

This study investigated the role of reactive oxygen species(ROS) in the pathogenesis of triptolide-induced renal injury in vivo.Rats were randomly divided into 4 groups(n=5 in each):triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8;control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8;vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8;triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days,and then to the same treatment as the triptolide group on day 8.All the rats were sacrificed on day 10.Blood samples were collected for detection of plasma creatinine(Pcr) and plasma urea nitrogen(PUN) concentrations.Both kidneys were removed.The histological changes were measured by haematoxylin-eosin(HE) staining.The production of ROS was determined by detecting the fluorescent intensity of the oxida-tion-sensitive probe rhodamine 123 in renal tissue.Renal malondialdehyde(MDA) content was meas-ured to evaluate lipid peroxidation level in renal tissue.TUNEL staining was performed to assess apop-tosis of renal tubular cells.Renal expression of apoptosis-related proteins Bcl-2,Bax,Bid,Bad,Fas and FasL,as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR.The results showed that triptolide treatment promoted the generation of a great amount of ROS,up-regulated the expression of Bax,Bid,Bad,Fas and FasL at both protein and mRNA levels,as well as the ratio of Bax to Bcl-2,and caused the apoptosis of renal tubular cells and renal injury.However,pretreatment with an antioxidant,vitamin C,significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury.It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury.The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.     

The effects on cell growth of tea polyphenols acting as a strong anti-peroxidatant and an inhibitor of apoptosis in primary cultured rat skin cells

Studies during the past few years have indicated an inhibitory effect of green tea or tea polyphenols on tumorigenesis in animal and even in human.The purpose of this study was to observe the possible effects of tea polyphenols on skin cell growth and on apoptosis in rat priary cultured keratinocytes and fibroblasts.The release of a cell plasma enzyma enzyme(LDH),lipid peroxidation products (MDA production),and GSH-Px(glutathione peroxidase)into the medium in cultrued cells was determined after treatment with tea polyphenols in a primary culture of skin cells,The percentage of cells in each cell cycle phase and in apoptosis were assayed by flow cytometry(FCM),Tea polyphenols may have a beneficial effect on skin cells at concentrations from 0.05% to 0.1%,showing a dose-dependent decrease in LDH,MDA(malondialdehyde)production,and a significant dose -de -pendent increase in GSH-Px and cell number,These effects were more obvious after exposure for 24h than after 12h,The results indicate that tea polyphenols may stabliize and protect the cell membrane against the release of cell plasma enzyme LDH,and its anti-peroxidation effect is also important for cell growth,FCM analysis revealed that treatment with 0.01% to 0.1% tea polyphenols dereased the percentage of cells in the G1/G0(quiescent)phase from 81.32%to 74.38%,and increased the percentage of cells in S and G2/M phase from 9.87% to 15.26%,and from 6.51% to 10.36%,respectively,Tea polyphenols also increased the value of PI(proliferation index) from 18.17 to 25.62,At the same time it decreased the percentage of apoptosis from 27.10% to 17.97%,which indicates that green tea stimulates cell growth and inhibits the occureeence of apoptosis,Our results indicate that tea polyphenols are effective anti-oxidants and also inhibit apoptosis ,which may improve the proliferative capacity of primary skin cells in vitro.     

Interventions to improve chronic cyclosporine A nephrotoxicity through inhibiting renal cell apoptosis: a systematic review

Objective To reveal interventions for chronic cyclosporine A nephrotoxicity （CCN） and provide new targets for further studies,we analyzed all relevant studies about interventions in renal cell apoptosis.Data sources We collected all relevant studies about interventions for cyclosporine A （CsA）-induced renal cell apoptosis in Medline （1966 to July 2010）,Embase （1980 to July 2010） and ISI （1986 to July 2010）,evaluated their quality,extracted data following PICOS principles and synthesized the data.Study selection We included all relevant studies about interventions in CsA-induced renal cell apoptosis no limitation of research design and language） and excluded the duplicated articles,meeting abstracts and reviews without specific data.Results There were three kinds of intervention,include anti-oxidant （sulfated polysaccharides,tea polyphenols,apigenin,curcumin,spirulina,etc）,biologics （recombinant human erythropoietin （rhEPO）,a murine pan-specific transforming growth factor （TGF）-beta-neutralizing monoclonal antibody1D11,cartilage oligomeric matrix protein （COMP）-angiopoietin-1 and hepatocyte growth factor （HGF） gene）,and other drugs （spironolactone,rosiglitazone,pirfenidone and colchicine）.These interventions significantly improved the CCN,renal cell apoptosis and renal dysfunction through intervening in four apoptotic pathways in animals or protected renal cells from apoptosis induced by CsA and increased cell survival through respectively four pathways in vitro.Conclusions There are three group interventions for CCN.Especially anti-oxidant drugs can significantly improve CCN,renal cell apoptosis and renal dysfunction.Many drugs can improve CCN through intervening in Fas/Fas ligand or mitochondrial pathway with sufficient evidences.Angiotensin Ⅱ,nitric oxide （NO） and endoplasmic reticulum （ER） pathways will be new targets for CCN.     

Changes of Apoptosis in Rats of Acute Ischemic Renal Injury under Treatment of Tetrandrine

Objective To elucidate the effect of tetrandrine on acute ischemic renal injury and its relation with apoptosis.Methods A model for bilateral post-ischemic renal injury in rats was developed by clamping renal pedicles for 45 min.Renal tissular DNA fragmentation analysis and renal tissular HE staining were used.Also quantitative analysis of apoptosis in injured renal tubular epithelium was carried out by using TdT-mediated dUTP nick and labeling(TUNEL).Results Apoptosis of renal tubular epithelium increased in acute ischemic renal injury.Tetrandrine could remarkably decrease the level of apoptosis in injured renal tubule while protecting renal tissue against the ischemic injuries.Conclusion Tetrandrine could adjust the level of apoptosis in renal tubular epithelium and alleviate renal tissular injury.     

Caspase-3在缺氧和内毒素致肾小管损伤的肾组织表达

目的 为了建立缺氧和内毒素致肾小管损伤模型,观察Caspase-3在肾组织的表达,以探讨其肾小管的损伤机制.方法 以SD大鼠为实验动物,予麻醉及机械通气,同时予阴茎静脉注射伤寒杆菌脂多糖,吸入氧浓度从21%降至5%的氧,通气至180rain结束.取肾组织作HE染色病理切片检查及用Caspase-3免疫组化S-P法染色观察模型肾组织的病理改变及肾组织中Caspase-3的表达.结果 (1)病理组织学所见:大部分肾小球充血,内皮及系膜细胞轻度肿胀,肾近曲小管上皮明显肿胀,呈浊样改变;大部分远曲小管镜下未见明显改变,部分上皮细胞肿胀,浊样变性在;整个肾间质呈充血现象.无炎性细胞浸润,(2)免疫组化结果:Caspase-3染色位于胞浆,大部分远曲小管上皮呈Caspase-3阳性反应,以外髓远曲小管为明显;近曲小管偶见Caspase-3阳性细胞,肾小球Caspase-3染色阴性.结论 (1)缺氧及内毒素可致肾小管损伤,且以近曲小管为著,远曲小管及内髓部损伤相对较轻,(2)Caspase-3在远曲小管明显表达,提示在缺氧及内毒素致肾小管损伤中,同时存在细胞变性坏死及细胞凋亡,近曲小管以细胞变性坏死为著,而远曲小管细胞凋亡明显.

Abstract：

Objectives To observe the expression of caspase-3 in the kidney of a rat model of renal tubular damage induced by endotoxin and hypoxia and explore the mechanism of renal tubular damage. Methods Ten rats were anesthetized with artificial ventilation and received 2 mg/kg lipopolysaccharide (LPS) injection through the penile vein. The FiO_2 was reduced 90 min later from 21% to 5%, and the ventilation was withdrawn after another 90 min. Immediately after ventilation withdrawal, the kidney of the rats were obtained for immunocytochemistry and HE staining. Results HE staining showed obvious hyperemia in most of the glomeruli, mild swelling of the endothelial and mesangial cells, severe swelling and turbidity in the proximal tubular epithelial cells without obvious changes in most of the distal proximal tubules. A small portion of the interstitial epithelial cells showed swelling and turbidity, and the entire renal interstitium appeared hyperemic but without inflammatory cell infiltration. Immunocytochemistry detected the presence of caspase-3 in the cytoplasm, and most of the distal renal tubule cells were positive for caspase-3, while only occasional cells showed caspase-3 positivity in the proximal tubular epithelial cells. Most of the proximal tubular epithelial and glomerulus cells were negative for caspase-3. Conclusions Endotoxin and hyoxia can induce renal damage, particularly in the proximal renal tubule cells, and the distal tubular epithelial cells sustain relatively light damage. Caspase-3 is strongly expressed in the distal renal tubular cells, suggesting that in renal tubular damage induced by endotoxin and hypoxia, cell degeneration, necrosis and apoptosis coexist in the tubular epithelial cells; degeneration and necrosis occur primarily in the proximal tubular epithelial cells, while apoptosis is obvious in the distal renal cells.     

Effects of Chinese Herbal Medicine Serum on the Apoptosis of Sinoatrial Node Cells Induced by Simulated Ischemia-reperfusion

Objective:To study the effect of Chinese herbal medicine Kangxin Fumai Granule(康心复脉颗粒 Granule for heart diseases) serum on the primary cultured sinoatrial node(SAN) cell apoptosis induced by simulated ischemia-reperfusion(IR).Methods:The SAN cells removed from SAN tissue of neonatal Wistar rats were cultured and purified with differential attachment and 5’-bromodeoxyuridine(BrdU) treatment.Simulated IR model was adopted.The obtained cells were morphologically observed with inverted microscopy.By using the method of serum pharmacology,the cell apoptosis was measured with TUNEL staining qualitatively and with flow cytometry quantitatively.Results:Three kinds of cells were observed in the cultured SAN cells:spindle,triangle and irregular.The spindle cells comprised the greatest proportion.The SAN cells in the model group showed moderate positive brown staining in the nucleus,and the apoptosis rate increased significantly compared to that in the control group(P<0.01).While the SAN cells in the Kangxin Fumai Granule high-dose group did not demonstrated positive staining in the nucleus,and the apoptosis rate decreased significantly compared to that in the model group(P<0.05).Conclusion:Of the cells cultured from SAN,the spindle cells were pacemaker cells of SAN in rats.Blockade and/or inhibition of the SAN cell apoptosis might be one of the important mechanisms of Kangxin Fumai Granule in preventing and treating sinoatrial injury induced by simulated IR.     

Effects of Selenium and Zinc on Renal Oxidative Stress and Apoptosis Induced by Fluoride in Rats

To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. Methods Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4·7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4·7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry. Results NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urineγ-glutamyl transpeptidase (γ-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly. Conclusion Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.     

The p53-mediated Apoptosis in Hypercholesterolemia-induced Renal Injury of Rats

Summary： The apoptosis and the expression of tumor suppressor gene p53 in hypercholesterolemia （HC）-induced renal injury were investigated in rats. A high cholesterol diet （HCD）-induced HC rat model was made and serum lipid, urinary protein excretion （UPE） and N-aceto-β-D-glucosidase （NAG） were measured. The levels of malondialdehyde （MDA）, as an index of lipid peroxidation, in renal cortex and serum were compared between the two diet groups. Apoptosis and p53 expression were determined by TUNEL and immunohistochemistry, respectively. In the HCD-induced HC group, serum total cholesterol （TC）, low density lipoprotein cholesterol （LDL-C） as well as triglyceride （TG） were significantly increased, while the level of high density lipoprotein cholesterol （HDL-C） decreased. Meanwhile, increased excretions of UPE and NAG in urine were observed, which were accompanied with a decrease in urinary creatinine clearance （Ccr） and indicated both glomerular and tubular damages. In addition, apoptotic cell death coexisted in the kidney, as revealed by increased TUNEL positive cells. Finally, an increase in p53 expression was observed in tubuli, but not in glomeruli. Both TUNEL positive cells and p53 expression were found to be correlated to the level of renal cortical MDA （r=0. 817, P〈0.01 and r=0.547, P〈0.01, respectively）. The major manifestation of HCD-induced renal injury is apoptosis. The lipid peroxidation is a critical event to induce DNA damage and p53 is involved in the pathogenesis of lipid-induced renal injury.     

汉防己甲素体外辅助多柔比星杀伤胃癌细胞及机制研究

目的探讨中药活性成分汉防己甲素是否能在体外辅助多柔比星杀伤胃癌细胞并研究其机制。方法噻唑蓝(MTT)法检测胃癌细胞系MGC-803相对细胞活力。Western blot实验检测MGC-803细胞中小窝蛋白-1(caveolin-1)表达水平、蛋白激酶B(AKT)和B淋巴细胞瘤-2蛋白(Bcl-2)相关细胞死亡激动子(Bad)磷酸化水平、半胱天冬酶-9(caspase-9)和半胱天冬酶-3(caspase-3)活化水平。免疫共沉淀法检测Bad与大分子B淋巴细胞瘤蛋白(Bcl-xl)及Bcl-2相互作用。流式细胞术检测MGC-803细胞的凋亡。结果汉防己甲素+多柔比星组MGC-803相对细胞活力(0.34±0.03)显著低于多柔比星(0.79±0.06)(P0.05),汉防己甲素+多柔比星组MGC-803的细胞凋亡率显著高于多柔比星组[(40.32±3.51)%比(12.23±1.13)%,P0.05]。汉防己甲素+多柔比星组MGC-803细胞的caveolin-1表达水平、AKT和Bad的磷酸化水平均低于多柔比星组,而汉防己甲素+多柔比星组MGC-803细胞的Bad与Bcl-xl及Bcl-2结合水平、caspase-9和caspase-3活化水平均高于多柔比星组。汉防己甲素+多柔比星+caveolin-1质粒组MGC-803相对细胞活力显著高于汉防己甲素+多柔比星组[(0.71±0.06)比(0.34±0.03),P0.05],而其细胞凋亡率显著低于汉防己甲素+多柔比星组[(15.94±1.22)%比(40.32±3.51)%,P0.05]。结论汉防己甲素可能通过caveolin-1/AKT/Bad途径增强多柔比星对胃癌细胞的凋亡诱导活性。     

Survey: Chinese children get inadequate sleep

Background The identification of vulnerable plaques before rupture is an important clinical goal. The purpose of the present study was to assess the difference in plaque composition among patients with acute coronary syndrome （ACS） and stable coronary artery disease （SCAD） by intravascular ultrasound virtual histologic analysis. Methods One hundred and thirty-nine patients were divided into ACS group and SCAD group according to clinical presentation. A total of 229 de novo lesions with 〉50% stenosis in native coronary arteries with diameters 〉2.5 mm were studied with intravascular ultrasonography. Geometric and compositional data were obtained using intravascular ultrasound virtual histology software. Results There were no significant differences in overall lesions for fibrous （（52.0±11.9）% vs （54.3±8.5）%, P〉0.05）, fibrolipidic （（12.3±10.1）% vs （13.8±9.5）%,P〈0.05）, calcium （（14.0±9.1）% vs （19.3±13.1）%, P〉0.05）, or necrotic core （（22.0±11.1）% vs （19.7±5.4）%, P〉0.05） percentages in ACS and SCAD patients, respectively. There were also no significant differences in culprit lesions for fibrous （（46.4±12.0）% vs （53.6±8.8）%, P〉0.05）, fibrolipidic （（9.1±9.0）% vs （12.9±9.7）%, P〉0.05）, calcium （（16.6±9.7）% vs （21.8±26.3）%, P〉0.05）, or necrotic core （（28.0±12.6）% vs （20.6±5.2）%, P〉0.05） percentages in ACS and SCAD patients, respectively. High density lipoprotein-cholesterol levels 〉1.04 mmol/L were associated with more fibrolipidic （（14.5±10.4）% vs （7.1±6.5）%, P〈0.05） and less necrotic core （（20.6±9.7）% vs （27.9±12.6）%,P〈0.05） percentages in the cohort with ACS. Conclusions In this study, coronary plaque composition assessed by intravascular ultrasound virtual histologic analysis was not significantly different between ACS and SCAD patients. The anatomic relationship of the specific plaque components to the lumen of the vessel was more important than th     

Predictors of left atrial appendage stunning after electrical cardioversion of non-valvular atrial fibrillation

Atrialfibrillation (AF)isthemostcommon persistentarrhythmia,leadingtoembolismsfrequently 1Restorationofsinusrhythmimprovescardiacfunctionalcapacity,alleviatespalpitation ,andreducestheriskofembolisms Direct currentcardioversionhastheadvantageofimmediaterestorationofsinusrhythm ,butitisfrequentlyassociatedwithtransientatrialmechanicaldysfunction ,i e “atrialstunning” ,whichmayincreasetheriskofsubsequentthromboembolicevents 2 　Withtheadventoftransesophagealechocardiography (TEE) ,leftatrial…     

Decreased small arterial compliance with increased serum vascular endothelial growth factor-A and circulating endothelial progenitor cell in dilated cardiomyopathy

Background Evidence showed that both myocardium and blood vessels were damaged in dilated cardiomyopathy （DCM）. However, the changes in arterial compliance, serum cytokines and circulating endothelial progenitor cells （EPC）, and their correlations remain unknown.
Methods Sixty-five DCM patients and 49 healthy volunteers were studied. Both large artery compliance （C1） and small artery compliance （C2） were measured with the CVProfUor DO-2020. Quantitative enzyme-linked immunosorbent assays （ELISAs） were used to measure the levels of vascular endothelial growth factor-A （VEGF-A） and VEGF receptor 2 （VEGF-R2）. Circulating EPC was assessed by EPC colony-forming assays and flow cytometry （CD133^＋/CD34^＋cells）. Phagocytized Dil-acLDL and binded FITC-UEA-I were used to analyze endothelial lineage marker expression by immunofluorescence.
Results Although C2 was markedly lower in DCM patients than in control group （（3.8±1.8） ml/mmHg × 100 vs （5.0±2.2） ml/mmHg × 100, P〈0.0001）, there was no statistically significant difference in C1 between the two groups （P〉0.05）. Levels of VEGF-A, the numbers of colony-forming units （CFU） and the fractions of EPC were obviously higher in DCM patients than in control group （（127.6±139.5） pg/ml vs （58.8±42.9） pg/ml, P〈0.0001; （2.5±1.5）% vs （0.5±0.3）%, P〈0.05; 23.5±12.8 vs 10.8±7.4, P〈0.01, respectively） and however, there was no significant difference in VEGF-R2 between two groups （P〉0.05）. LgVEGF-A was positively correlated with the number of EPC-CFU （r=-0.435; P〈0.05） and inversely correlated with C2 （r=-0.543; P〈0.001） in DCM patients. Conclusions The reduction of C2, a sensitive marker reflecting endothelial dysfunction, was observed in DCM patients and closely related to the increase in serum VEGF-A.     

Connective tissue growth factor is associated with the early renal hypertrophy in uninephrectomized diabetic rats

Structural remodeling in diabetic kidney ischaracterized by the early appearance ofhypertrophy in glomerular and tubular components, subsequently developing the thickness of glomerular and tubular basement membranes, and the progressive accumulation of extracellular matrix components.1 Recent studies have demonstrated that early renal hypertrophy is detrimental to the kidney in the long term and is a precursor of development of renal fibrosis.2,3 However, the exact mechanism of renal hypertrop…     

槲皮素通过SIRT1/ROS/DR5途径发挥对TRAIL的协同抗前列腺癌活性

目的: 探讨中药活性成分槲皮素是否对TRAIL有协同抗前列腺癌效应并研究其机制。方法: MTT实验检测前列腺癌细胞系PC3的细胞活力;流式细胞术检测PC3细胞的凋亡和ROS的产生;western blot实验检测PC3细胞中SIRT1、DR5的表达水平及caspase-8、caspase-3的活化水平。结果: TRAIL联合槲皮素对PC3的细胞活力抑制率(64.7±5.2)和凋亡诱导率(34.7±2.6)显著高于TRAIL单治疗组的细胞活力抑制率(16.9±1.4,P<0.05)和凋亡诱导率(9.1±0.8,P<0.05)。TRAIL联合槲皮素治疗组的SIRT1表达水平显著低于TRAIL单治疗组,同时TRAIL联合槲皮素治疗组的DR5表达水平、ROS产生水平及caspase-8、caspase-3活化水平均显著高于TRAIL单治疗组。另外,TRAIL+槲皮素+SIRT1质粒组PC3的细胞活力抑制率(23.4±1.9)和凋亡诱导率(12.5±1.2)及TRAIL+槲皮素+NAC组PC3的细胞活力抑制率(21.5±1.8)和凋亡诱导率(11.3±1.1)均显著低于TRAIL联合槲皮素组PC3的细胞活力抑制率(64.7±5.2,P<0.05)和凋亡诱导率(34.7±2.6,P<0.05)。结论: 槲皮素通过SIRT1/ROS/DR5途径发挥对TRAIL的协同抗前列腺癌活性。     

黄芩素通过SIRT1/p53途径提高宫颈癌细胞对顺铂的敏感性

目的: 探讨中药活性成分黄芩素是否对顺铂有协同抗宫颈癌效应并研究其机制。方法: MTT实验检测宫颈癌细胞系Hela的细胞活力;流式细胞术检测Hela细胞的凋亡;western blot实验检测Hela细胞中SIRT1、p53、乙酰化p53、Puma的表达水平及caspase-3的活化水平。结果: 顺铂联合黄芩素对Hela的细胞活力抑制率(66.3±5.7)和凋亡诱导率(38.4±3.2)显著高于顺铂单治疗组的的细胞活力抑制率(18.1±1.4,P<0.05)和凋亡诱导率(10.4±0.9,P<0.05)。顺铂联合黄芩素治疗组的SIRT1表达水平显著低于顺铂单治疗组,同时顺铂联合黄芩素治疗组的p53乙酰化水平和表达水平、Puma表达水平及caspase-3活化水平均显著高于顺铂单治疗组。另外,顺铂+黄芩素+SIRT1质粒组Hela的细胞活力抑制率(25.7±2.1)和凋亡诱导率(14.5±1.1)显著低于顺铂联合黄芩素组Hela的细胞活力抑制率(66.3±5.7,P<0.05)和凋亡诱导率(38.4±3.2,P<0.05)。结论: 黄芩素通过SIRT1/p53途径增强顺铂对宫颈癌细胞的杀伤活性。     

Monocyte chemoattractant protein-1 expression in renal tissue is associated with monocyte recruitment and tubulo-interstitial lesions in patients with lupus nephritis

目的　观察狼疮性肾炎 (LN)患者肾组织中单核细胞趋化因子 (MCP 1)的分布及其与肾间质单核细胞浸润和间质病变的关系 ,探讨其在LN患者肾小管间质病变中的作用。方法　采用PAP四层法对 18例LN患者肾组织MCP 1,CD68 ,CD4 ,及CD8 进行免疫组化染色。同时取 8例微小病变型肾病患者作为对照。结果　 18例患者肾组织中均有不同程度的MCP 1染色阳性。其主要位于肾小管基侧膜 (16/ 18例 )及间质小血管壁 (9/ 18例 )上。对照组MCP 1阳性的小管明显低于狼疮性肾炎患者 (7 4± 6 2 %vs 2 6 7± 2 2 8% ,P <0 0 1)。LN患者肾间质中CD4 ,CD8 及CD68 细胞数明显高于对照。其MCP 1阳性小管数与间质CD68 细胞浸润及间质病变的程度明显相关。而与CD4 ,CD8 细胞浸润程度及患者尿蛋白的多少无相关性。结论　LN患者肾小管MCP 1表达增加可能是导致间质单核细胞浸润及肾小管间质损伤的一个重要原因     

Electrical remodeling of membrane ionic channels of hypertrophied ventricular myocytes from spontaneously hypertensive rats

Ｍｅｔｈｏｄｓ　Ｍｅｍｂｒａｎｅｉｏｎｉｃｃｈａｎｎｅｌｓｗｅｒｅｓｔｕｄｉｅｄｉｎｅｎｚｙｍａｔｉｃａｌｌｙｄｉｓｐｅｒｓｅｄｓｐｏｎｔａｎｅｏｕｓｌｙｈｙｐｅｒｔｅｎｓｉｖｅｒａｔｓ (ＳＨＲｓ)ｌｅｆｔｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓｕｓｉｎｇｔｈｅｗｈｏｌｅ ｃｅｌｌｃｏｎｆｉｇｕｒａｔｉｏｎｏｆｐａｔｃｈ ｃｌａｍｐｔｅｃｈｎｉｑｕｅ ,ｗｉｔｈｎｏｒｍａｌＷｉｓｔａｒｒａｔｓｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓａｓｃｏｎｔｒｏｌｓ Ｗｅｏｂｓｅｒｖｅｄｄｅｐｏｌａｒｉｚｉｎｇｃｕｒｒ…     

The role of calcineurin in the lung fibroblasts proliferation and collagen synthesis induced by basic fibroblast growth factor

Objective To investigate the role of calcineurin (CaN) in the lung fibroblast proliferation and collagen synthesis induced by basic fibroblast growth factor (bFGF).Methods We used Western blot and immunohistochemical methods for investigating the content and distribution of calcineurin in the lung tissue. Calcineurin activity in different tissues was measured using 32P-labelled substrate. In the primary culture of lung fibroblasts, 3H-thymidine (3H-TdR) and 3H-proline incorporation methods were used to study the effect of cyclosporin A (CsA), an inhibitor of calcineurin, on the lung fibroblast DMA and collagen synthesis stimulated by bFGF.Results We found that calcineurin was expressed in lung tissue and has phosphatase activity (7.1±2.0 pmol Pi/mg pr/min). CsA (10~(-8)-10~(-6) mol/L) inhibited lung fibroblast 3H-TdR incorporation induced by bFGF in a dose-dependent manner, with the inhibitory rates by 20% , 46% and 66% (P< 0.01). CsA (10~(-7) -10~(-6) mol/L) inhibited 3H-proline incorporation in lung