Biomedical subjects

Li Yao

Publications and source records attributed to Li Yao.

At least 37 records · Page 2Linked to original sources

PubMed2005

[Mechanism of differentiation and apoptosis in leukemia cells induced by tributyrin].

To elucidate the possible mechanism of differentiation and/or apoptosis in NB4, K562 cells induced by tributyrin (TB), a histone deacetylase inhibitor (HDACi), the level of acetylated histone H3 was detected by Western blot, p21(WAF1) expression was detected by semi-quantitative RT-PCR. The results showed that histone H3 hyperacetylation was detected in NB4 (or K562) cells after treatment with TB 0.1 mmol/L (or TB 0.5 mmol/L) for 16 hours in a dose-dependent manner. p21(WAF1) dose-dependently increased at RNA level in these two cell lines treated by TB 0.1 mmol/L. The level of p21(WAF1) mRNA increased at 2 hours after TB treatment, reaching peak at 16 hours, and maintaining for 48 hours. In conclusion, the mechanism of differentiation and apoptosis in NB4, K562 cells induced by tributyrin may associate with its up-regulation of acetylated histone and p21(WAF1) mRNA level.

Acetylation↗

PubMed2005

[The significance of microvessel density and CD34 expression in nasal polyps].

OBJECTIVE: To study the clinicopathologic significance of microvessel density (MVD) and the expression of CD34 in human nasal polyps. METHOD: Using Elivision Plus immunohistochemistry method. Thirty cases of normal inferior turbinate, 60 cases of nasal polyps were stain with CD34. RESULT: MVD of CD34 marker showed higher in the group of nasal polyps than in the group of normal inferior turbinate (P <0.01). MVD in nasal polyps type II phase 3 and type III was higher than that in the nasal polyps type II phase (P < 0.01). CONCLUSION: MVD is closely related with the formation edema and development of nasal polyps. Angiogenesis may play an important role in the development of nasal polyps.

Adolescent↗

PubMed2005

Comparative study of expressions of cytoplasmic CD79a and other B-lymphoid immunomarkers in acute leukemic cells.

To evaluate the expression of cytoplasmic CD79a (CyCD79a) and other commonly used B-lymphoid immunomarkers including cytoplasmic CD22 (CyCD22), CD19, CD20 and CD10 in various acute leukemia cells and to define the most sensitive and specific markers in the diagnosis of precursor B-cell acute lymphoblastic leukemia (pB-ALL), the immunophenotypic data from 221 de novo adult and pediatric acute leukemia patients as studied using multi-parameter flow cytometry in addition to routine morphologic and enzyme cytochemical assay, were retrospectively analyzed. Cytogenetic and/or molecular biological data in all 45 cases of acute promyelocytic leukemia (APL) and 13 cases of acute leukemia suspected as AML with the fusion genes such as AML1/ETO and CBFbeta/MYH11 were investigated. The results showed that CyCD79a and CyCD22 were the most sensitive and specific markers respectively for pB-ALL. Expression of CyCD79a was seen in 100% of 58 cases of pB-ALL. At the same time, none (0%) of all 147 cases of acute myeloid leukemia (AML) and 15 cases of precursor T-cell acute leukemia (pT-ALL) was positive for CyCD22. The conclusion is made that united detection of CyCD79a and CyCD22 is the optimal immune combination for the diagnosis pB-ALL and the distinguishing pB-ALL with AML and pT-ALL.

Acute Disease↗

PubMed2004

Effect of rat serum containing Biejiajian oral liquid on proliferation of rat hepatic stellate cells.

AIM: Liver fibrosis is a common pathological process of chronic liver diseases. Activation of hepatic stellate cells (HSCs) is the key issue in the occurrence of liver fibrosis. In this study, we observed the inhibitory action of rat serum containing Biejiajian oral liquid (BOL), a decoction of turtle shell, on proliferation of rat HSCs, and to explore the anti-hepatofibrotic mechanisms of BOL. METHODS: A rat model of hepatic fibrosis was induced by subcutaneous injection of CCl(4). Serum containing low, medium and high dosages of BOL was prepared respectively. Normal and fibrotic HSCs were isolated and cultured. The effect of sera containing BOL on proliferation of HSCs was determined by (3)H-TdR incorporation. RESULTS: The inhibitory rate of normal rat HSC proliferation caused by 100 mL/mL sera containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group: 34.56+/-4.21% vs 29.12+/-2.85%, P<0.01; high dosage group: 37.82+/-1.32% vs 29.12+/-2.85%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L serum containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group: 51.31+/-3.14% vs 38.32+/-2.65%, P<0.01; high dosage group: 60.15+/-5.36% vs 38.32+/-2.65%, P<0.01). The inhibitory rate of normal rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group: 69.02+/-9.96% vs 50.82+/-9.28%, P<0.05; 200 mL/L group: 81.78+/-8.92% vs 50.82+/-9.28%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group: 72.19+/-10.96% vs 61.38+/-7.16%, P<0.05; 200 mL/L group: 87.16+/-8.54% vs 61.38+/-7.16%, P<0.01). CONCLUSION: Rat serum containing BOL can inhibit proliferation of rat HSCs, and the inhibition depends on the dosage and concentration of BOL. The inhibitory effect on HSC proliferation is one of the main anti-hepatofibrotic mechanisms of BOL.

Animals↗

PubMed2004

Possible contributions of reactive oxygen species and mitogen-activated protein kinase to renal injury in aldosterone/salt-induced hypertensive rats.

Studies were performed to test the hypothesis that reactive oxygen species (ROS) and mitogen-activated protein kinase (MAPK) contribute to the pathogenesis of aldosterone/salt-induced renal injury. Rats were given 1% NaCl to drink and were treated with one of the following combinations for 6 weeks: vehicle (0.5% ethanol, SC, n=6); aldosterone (0.75 microg/H, SC, n=8); aldosterone plus a selective mineralocorticoid receptor antagonist; eplerenone (0.125% in chow, n=8); aldosterone plus an antioxidant; and tempol (3 mmol/L in drinking solution, n=8). The activities of MAPKs, including extracellular signal-regulated kinases (ERK)1/2, c-Jun-NH2-terminal kinases (JNK), p38MAPK, and big-MAPK-1 (BMK1) in renal cortical tissues were measured by Western blot analysis. Aldosterone-infused rats showed higher systolic blood pressure (165+/-5 mm Hg) and urinary excretion of protein (106+/-24 mg/d) than vehicle-infused rats (118+/-3 mm Hg and 10+/-3 mg/d). Renal cortical mRNA expression of p22phox, Nox-4, and gp91phox, measured by real-time polymerase chain reaction, was increased in aldosterone-infused rats by 2.3, 4.3, and 3.0-fold, respectively. Thiobarbituric acid-reactive substances (TBARS) content in renal cortex was also higher in aldosterone (0.23+/-0.02) than vehicle-infused rats (0.09+/-0.01 nmol/mg protein). ERK1/2, JNK, and BMK1 activities were significantly elevated in aldosterone-infused rats by 3.3, 2.3, and 3.0-fold, respectively, whereas p38MAPK activity was not changed. Concurrent administration of eplerenone or tempol to aldosterone-infused rats prevented the development of hypertension (127+/-2 and 125+/-5 mm Hg), and the elevations of urinary excretion of protein (10+/-2 and 9+/-2 mg/day) or TBARS contents (0.08+/-0.01 and 0.11+/-0.01 nmol/mg protein). Furthermore, eplerenone and tempol treatments normalized the activities of ERK1/2, JNK, and BMK1. These data suggest that ROS and MAPK play a role in the progression of renal injury induced by chronic elevations in aldosterone.

Aldosterone↗

PubMed2004

Radial distributions of temperature pressure and velocities for pulsatile blood flow in an axisymmetrical stiff tube.

Using perturbation theory with the assumption that the pulsatile blood flow in an axisymmetrical stiff tube is the first-order term to solve the linear equations of continuity, motion and heat conduction, the equations of the pulsatile flow, including temperature, are derived, and the instantaneous radial distribution of temperature, pressure and velocities for one frequency component are obtained. Using the published geometrical and physiological parameters of a large artery, a numerical analysis of the distribution relationship between the axial velocity and temperature is carried out. The primary studies show that the amplitude of temperature fluctuation in the tube is inversely proportional to the pulsatile frequency, the temperature and velocities gradients are mainly restricted in the near-wall layers with the increase of pulsatile frequency, and there is a close similarity of the radial pulsating distribution between temperature and axial velocity, which indicates that the blood flux in the artery as well as the motion function of heart can be indirectly described by the measurement of temperature fluctuation.

Animals↗

PubMed2004

Time-dependent transition of tempol-sensitive reduction of blood pressure in angiotensin II-induced hypertension.

OBJECTIVE: Reactive oxygen species (ROS) participate in the intracellular signalling of angiotensin II. However, the mechanisms of the interaction of ROS with hypertension and mitogen-activated protein kinase (MAPK) in vivo have remained unclear. Angiotensin II infusion provokes sustained hypertension accompanied with enhancement of ROS production; initially hypertension is non-sensitive to ROS, but thereafter becomes sensitive. We examined the time-dependent transition of ROS-sensitive vasoconstriction during angiotensin II infusion and also ROS sensitivity to cardiovascular MAPK activation in acutely and chronically angiotensin II-infused rats. METHODS AND RESULTS: During infusion of a pressor dose of angiotensin II to conscious Sprague-Dawley rats, tempol, a superoxide dismutase mimetic, was administered at 10 min, some 1, 3, 6, 12 and 24 h after the start of infusion. The magnitude of the reduction in blood pressure by tempol was initially negligible, but gradually enlarged, and reached a maximum of 96% of delta increase by angiotensin II at 12 h. However, even after sensitization to tempol, superimposed angiotensin II enabled an increase of blood pressure under tempol treatment. In chronically angiotensin II-infused rats, superimposed angiotensin II exhibited tempol quenchable MAPK activation. CONCLUSIONS: These results indicate that the mechanisms of angiotensin II-induced vasoconstriction may shift from being non-sensitive to ROS to sensitive within 12 h; nevertheless, both ROS non-sensitive vasoconstriction and ROS-sensitive MAPK activation by angiotensin II, which are both seen in the acute phase of infusion, are restored in the late maintaining phase of prolonged angiotensin II infusion.

Angiotensin II↗

PubMed2004

Effects of AT1 receptor blockade on renal injury and mitogen-activated protein activity in Dahl salt-sensitive rats.

BACKGROUND: The mitogen-activated protein kinase (MAPK) cascade is an important intracellular mediator of angiotensin II (Ang II)-induced cell growth and differentiation. Here, we examined the effect of angiotensin II type 1 receptor (AT1) receptor blockade on renal injury and MAPK activity in Dahl salt-sensitive (DS) rats. METHODS: DS rats were maintained on a high (H: 8.0%NaCl, N= 8) or low (L: 0.3%NaCl, N= 7) salt diet, or H + candesartan cilexetil (10 to 15 mg/kg/day, N= 8). Urinary protein excretion (UproteinV), renal cortical collagen content, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined after 4-week treatments. Plasma and kidney Ang II levels were measured by radioimmunoassay. Protein levels of AT1 and AT2 receptors in the renal cortical tissues were analyzed by Western-blotting analyses. MAPKs activities, including extracellular signal-regulated kinases (ERK)1/2, c-Jun NH2-terminal kinases (JNK), p38 MAPK, and Big-MAPK-1 (BMK1), were measured by Western-blotting analyses or in vitro kinase assays. RESULTS: DS/H rats showed higher mean blood pressure (MBP), UproteinV, and renal cortical collagen content than DS/L rats. Increased ERK1/2, JNK, and BMK1 activities were observed in renal cortical tissues of DS/H rats (approximately 6.3-, 4.5-, and 2.5-fold, respectively), whereas p38 MAPK activity was unchanged. Plasma Ang II levels were significantly reduced in DS/H rats compared with DS/L rats, whereas kidney Ang II contents and AT1 receptor protein levels were similar. Candesartan did not alter MBP, but significantly reduced UproteinV and collagen content, and ameliorated progressive sclerotic and proliferative glomerular changes. Furthermore, candesartan decreased renal tissue Ang II contents (from 216 +/- 19 to 46 +/- 3 fmol/mL) and ERK1/2, JNK, and BMK1 activities (-45%, -60%, and -70%, respectively) in DS/H rats. CONCLUSION: In DS hypertensive rats, some of the renoprotective effects of AT1 receptor blockade are accompanied by reductions in intrarenal Ang II contents and MAPK activity, which might not be mediated through arterial pressure changes.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2004

Olmesartan improves endothelin-induced hypertension and oxidative stress in rats.

Recent studies have indicated that both endothelin (ET) and angiotensin (Ang) II stimulate oxidative stress, which contributes to the development of hypertension. Here, we examined the effects of Ang II type 1 (AT1) receptor blockade on reactive oxygen species (ROS) formation in ET-dependent hypertension. Chronic ET-1 infusion (2.5 pmol/kg/min, i.v., n=7) into rats for 14 days increased systolic blood pressure from 113+/-1 to 141+/-2 mmHg. ET-1-infused rats showed greater plasma renin activity (8.1+/-0.8 Ang I/ml/h), and greater Ang I (122+/-28 fmol/ml) and Ang II levels (94+/-13 fmol/ml) than vehicle (0.9% NaCl)-infused rats (3.1+/-0.6 Ang I/ml/h, 45+/-8 and 47+/-7 fmol/ml, respectively, n=6). Angiotensin converting enzyme and AT1 receptor expression in aortic tissues were similar between the vehicle- and ET-1-infused rats. Vascular superoxide anion (O2-) production and plasma thiobarbituric acid-reactive substance (TBARS) levels were greater in ET-1-infused rats (27+/-1 counts per minutes [CPM]/mg dry tissue weight and 8.9+/-0.8 micromol/l, respectively) than vehicle-infused rats (16+/-1 CPM/mg and 5.1+/-0.1 micromol/l, respectively). The ET-1-induced hypertension was prevented by simultaneous treatment with a new AT1 receptor antagonist, olmesartan (0.01% in chow, 117+/-5 mmHg, n =7), or hydralazine (15 mg/kg/day in drinking water, 118+/-4 mmHg, n=6). Olmesartan prevented ET-1-induced increases in vascular O2- production (15+/-1 CPM/mg) and plasma TBARS (5.0+/-0.1 micromol/l). Vascular O2- production and plasma TBARS were also decreased by hydralazine (21+/-1 CPM/mg and 7.0+/-0.3 micromol/l, respectively), but these levels were significantly higher than in vehicle-infused rats. These data suggest that ET-dependent hypertension is associated with augmentation of Ang II levels and ROS formation. The combined effects of the elevations in circulating ET-1 and Ang II, as well as the associated ROS production, may contribute to the development of hypertension induced by chronic ET-1 infusion.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2004

[In vitro effects of mevastatin on the proliferation and apoptosis in human multiple myeloma cell line U266].

In order to investigate the anti-tumor activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and the mechanism underlying the cell proliferation and apoptosis modulated in myeloma cells, the effects of mevastatin, an HMG-CoA reductase inhibitor, on cell growth, cell cycle progression and apoptosis in U266 human multiple myeloma (MM) cell line in vitro were explored by MTT colorimetric assay, morphologic observation, flow cytometry, DNA gel electrophoresis, and RT-PCR. The results demonstrated that mevastatin inhibited the growth of U266 cells in time- and dose-dependent manners. Cell cycle analysis showed that U266 cells underwent G(0)/G(1) arrest under exposure to mevastatin, but it did not affect p27 expression at both mRNA and protein level. Morphologic observations revealed cytoplasm shrinkage, nuclear condensation and fragmentation in mevastatin-treated cells, and fraction of annexin V(+)PI(-) cells increased significantly in the presence of the agent as determined by flow cytometric assay. In addition, mevastatin caused the collapse of mitochondrial transmembrane potential (Deltapsim), induced DNA fragmentation, and down-regulated the mRNA expression of bcl-2. The growth-inhibitory, cell cycle arresting, and proapoptotic effects of mevastatin in U266 cells could be effectively reversed by the addition of mevalonate (MVA), the immediate endproduct of the reaction catalyzed by HMG-CoA reductase. It is concluded that mevastatin suppresses proliferation by inducing G(0)/G(1) phase arrest and triggering apoptosis via down-regulation of bcl-2 and reduction of Deltapsim, which may be attributed to the inhibition of MVA pathway by mevastatin. Statins including mevastatin may find their future application in the treatment of MM.

Apoptosis↗

PubMed2004

[The expression of CXCR4 on acute leukemia cells and its implication for extramedullary infiltration].

OBJECTIVE: To study the expression of CXCR4 in acute leukemic cells and its clinical significance. METHOD: Bone marrow samples from 73 acute leukemia patients and leukemic cell lines were investigated by flow cytometry (FCM), the expression of SDF-1 in human marrow stromal cells and meninges were studied by using reverse transcription polymerase chain reaction (RT-PCR). Adhesion, migration and invasion of U937, NB4 and K562 cells were studied in vitro. RESULTS: The expression rates of CXCR4 in ALL and AML patients was 65.6% and 17.1%, respectively. And it was 0.2%, 41.0% and 52.0% in K562, U937 and NB4 cells, respectively. The extramedullary infiltration rates were 61.9% and 18.2% for CXCR4 positive and negative groups of ALL, respectively (P < 0.05); while in AML, the number of peripheral white blood cells in CXCR4 positive group was lower than that in CXCR4 negative group (P < 0.05). SDF-1alpha could enhance the adhesion, migration and invasion capacity of leukemic cells in vitro. CONCLUSION: Overexpression of CXCR4 in AL cells might be the molecular mechanism of extramedullary infiltration in leukemia.

Acute Disease↗

PubMed2004

[Establishment and characterization of leukemic cell line U937 stably expressing exogenous RbAp46].

To establish leukemic cell lines stably transfected by RbAp46 gene, electroporation was performed after optimizing the transfection condition for suspended cells. Under conditions of low voltage and high capacitance, RbAp46 was transfected into U937 by electroporation. Individual clones selected with G418 for 3 weeks were isolated. The integration and the protein levels of the exogenous RbAp46 in transfectants were determined by PCR and Western blot analysis, respectively. The subclone expressing high level of RbAp46 was then established. Viability of transfected cells was assayed by trypan blue exclusion. Cell number was counted daily to determine the growth rate. The results showed that growth rate of U937 cell lines expressing exogenous RbAp46 was about 50% lower than that in control. It is concluded that leukemic cell lines stably expressing exogenous RbAp46 were established and overexpression of RbAp46 inhibits the growth of U937 leukemic cells.

Blotting, Western↗

PubMed2004

[Growth inhibition of human hepatocellular carcinoma xenograft in nude mice by combined treatment with human cytokine-induced killer cells and chemotherapy].

OBJECTIVE: To compare the inhibitory effects of cytokine-induced killer (CIK) cells alone, chemotherapeutic drug alone, and CIK cells combined with chemotherapeutic drug on the growth of hepatocellular carcinoma (HCC) cells transplanted in nude mice. METHODS: Peripheral blood mononuclear cells (PBMC) collected from five healthy donors by blood cell separator were incubated in vitro to induce CIK cells in the presence of interferon-gamma (IFN-gamma), IL-2 and anti-CD3 monoclonal antibody (mAb). The phenotype of CIK cells was characterized by flow cytometric analysis. BEL-7402 HCC cells were inoculated subcutaneously to nude mice. On day 5, at the inoculation site were injected normal saline (group 1), CIK cells (3 x 10(7) and 6 x 10(7), group 2 and 3), mitomycin-C (MMC 80 microg in 0.2 ml, group 4), and CIK cells combined with MMC (group 5), respectively. RESULTS: The percentage of CD3(+), CD3(+)CD8(+), CD3(+)CD56(+), CD25(+) cells increased from 64.0%, 28.0%, 7.8%, and 9.1% to 94.7%, 67.7%, 61.3%, and 84.0% respectively after cytokine induction. The percentage of CD3(+) and CD3(+)CD8(+) cells remained at high levels during incubation period, but that of CD25(+) and CD3(+)CD56(+) cells peaked respectively on day 7 and 13 and then declined. During the 90-day observation, the tumor formation rates were 100%, 70.0%, 80.0%, 70.0% and 66.7%; and the mouse survival rates were 10.0%, 60.0%, 40.0%, 50.0% and 75.0%, respectively from group 1 to group 5. Compared to the other groups, in the combined therapy group of mice, not only the tumor grew slowly and but also showed more marked tissue necrosis. CONCLUSION: The growth inhibitory effect on human HCC transplanted in nude mice of combined CIK cells and MMC treatment is more potent than that of CIK cells or MMC alone.

Animals↗

PubMed2004

[Maxillary sinus polyp and cyst excised by endoscopes surgery in chronic sinusitis and significance].

OBJECTIVE: To look for a simple and convenient surgical method to treat the maxillary sinus polyp and cyst. METHOD: By means of Rudolf 4.5 mm cannula paracentetic needle trough inferior nasal meatus the polyp and cyst were be cut by cutter. RESULT: For half a year, 50 cases were followed and no relapse was found by X-ray or CT. CONCLUSION: Maxillary sinus polyp and cyst can be excised by endoscope surgery through inferior canal, and it is a minimally invasive operation. The effective is positive.

Adolescent↗

PubMed2003

[Long term follow up of patients with knee osteoarthritis after high tibial osteotomy].

OBJECTIVE: To investigate the clinical result of knee osteoarthritis after high tibial osteotomy (HTO) in long term follow-up. METHODS: 107 patients of knee joint osteoarthritis performed with high tibial osteoarthritis between 1983 and 2000 was followed up. Standing anteroposterior radiograph of knee were taken for every patient. RESULTS: The clinical results of 137 knees (88%) were rated as good at 1 to 5 years follow-up. 21 knees were good at 5 to 10 years follow-up. And 5 knees were good at lest 10 years follow-up. Only one patient was done TKA 8 year after HTO. CONCLUSIONS: The patients done HTO show excellent clinical results in short time follow-up. And the results of most patients was maintained in intermediate and long-term follow-up. The internal fixition allow patients early activity and recover quickly.

Adult↗

PubMed2003

Role of angiotensin II and reactive oxygen species in cyclosporine A-dependent hypertension.

Treatment with cyclosporine A (CysA), a potent immunosuppressive agent, is associated with systemic and renal vasoconstriction, leading to hypertension. The present study was conducted to elucidate the contribution of angiotensin II (Ang II) to CysA-induced hypertension and reactive oxygen species (ROS) generation. CysA (30 mg/kg per day SC), given for 3 weeks in rats, increased systolic blood pressure (SBP) from 119+/-2 to 145+/-3 mm Hg (n=7). Plasma and kidney Ang II levels were significantly higher in CysA-treated rats (136+/-10 fmol/mL and 516+/-70 fmol/g) than in vehicle-treated (1 mL olive oil) rats (76+/-10 fmol/mL and 222+/-21 fmol/g, n=7). CysA treatment increased AT1 receptor protein expression in the aorta (by 251+/-35%), whereas it was reduced in the kidney (by -32+/-4%). Superoxide anion production in aortic segments and kidney thiobarbituric acid-reactive substance (TBARS) contents were higher in CysA-treated rats (26+/-2 counts/min per milligram and 37+/-3 nmol/g) than in vehicle-treated rats (17+/-1 counts/min per milligram and 24+/-3 nmol/g). Concurrent administration of an AT1 receptor antagonist, valsartan (30 mg/kg per day, in drinking water), to CysA-treated rats (n=7) significantly decreased SBP (113+/-4 mm Hg) and prevented increases in vascular superoxide (16+/-2 counts/min per milligram) and kidney TBARS contents (21+/-3 nmol/g). Similarly, treatment with a superoxide dismutase mimetic, 4-hydroxy-2,2,6,6,-tetramethylpiperidine-N-oxyl (Tempol; 3 mmol/L in drinking water, n=7), prevented CysA-induced increases in SBP (115+/-3 mm Hg), vascular superoxide (16+/-1 counts/min per milligram), and kidney TBARS contents (19+/-2 nmol/g). These data suggest that ROS generation induced by augmented Ang II levels contributes to the development of CysA-induced hypertension.

Angiotensin II↗

PubMed2003

[Effects of aminophylline on proliferation and apoptosis in Raji lympho-blastoid cell line].

The aim of this study was to investigate whether and how phosphodiesterase (PDE) inhibitors modulate the proliferation, cell cycle and apoptosis in lymphoma cells. The effects of aminophylline (AM), a non-specific PDE inhibitor, on Raji cells were explored in vitro. MTT assay, light and transmission electron microscopy and annexin V staining were used to observe cell proliferation, morphologic changes and apoptosis rate in AM-treated cells, and FCM and RT-PCR techniques were adopted to detect the effect on cell cycle, the expression of cyclin B1 and Bcl-2 and mitochondrial transmembrane potential in AM-treated cells. The results showed that AM inhibited the growth of Raji cells in a concentration-dependent manner. Morphologic observations showed apoptosis changes in AM-treated cells, including cytoplamic shrinkage, cytoplasmic bubbling, karyopyknosis and nuclear fragmentation. FCM and RT-PCR detection showed that AM intervention increased the fraction of annexin V(+) cells, reduced the value of mitochondrial transmembrane potential, induced S phase arrest, and down-regulated the expression of Bcl-2 at both mRNA and protein level and cyclin B1 protein in a concentration-dependent manner. It is concluded that PDE inhibitor aminophylline may induce Raji cell growth inhibition, S phase arrest, apoptosis via down-regulation of Bcl-2 and reduction of mitochondrial transmembrane potential.

Aminophylline↗

PubMed2003

[Effects of bcl-2 antisense oligodeoxynucleotide on proliferation and apoptosis of Raji cells].

OBJECTIVE: To study the in vitro antitumor activity of bcl-2 fully phosporothioated antisense oligodeoxynucleotide (bcl-2 ASODN) to malignant lymphoblastic cells. METHODS: Proliferation and apoptosis of Raji cells incubated with bcl-2 ASODN were evaluated by MTT assay, flow cytometry (FCM) and electron microscopy, and the level of bcl-2 protein and mRNA expression were assessed by FCM and RT-PCR, respectively. RESULTS: MTT assay demonstrated that bcl-2 ASODN could partially inhibit the growth of Raji cells. After incubated with ASODN for 48 hours, Raji cells exhibited characteristic morphologic changes of apoptosis, including cytoplasm membrane blebbing, chromatin condensation crescents formation and nuclear fragmentation. The apoptosis rate of Raji cells treated with 20 micromol/L bcl-2 ASON for 72 hrs was 43.86% which is significantly higher than that of control (10.05%). The bcl-2 ASODN induced apoptosis of Raji cells was accompanied by declined expression of bcl-2 mRNA, which decreased to 0.88% at 72 hrs and was significantly lower than that of control (79.54%). CONCLUSION: bcl-2 ASODN induced Raji cells apoptosis by downregulating bcl-2 protein.

Apoptosis↗