Metallothionein inhibits homocysteine-induced proliferation of rat vascular smooth muscle cells

AIM:To investigate the effect of metallothionein(MT) on proliferation of rat vascular smooth muscle cells (VSMCs) stimulated by homocysteine and its mechanism. METHODS:VSMCs proliferation was measured by [³-H]-TdR incorporation, mitogen-activated protein kinase(MAPK)activity were determined by immunoprecipitation method, the intracellular contents of MT and malondialdehyde (MDA)were assayed by -hemoglobin saturation method and TBA reaction, respectively, and lactate dehydrogenase (LDH) leakage was measured by NADH oxidation. RESULTS:Hcy(10^-6-10^-4 mmol/L) stimulated [³-H]-TdR incorporation by the VSMCs in a concentration-dependent manner. Compared with control, [³-H]-TdR incorporation in VSMCs treated with 0.1 mmol/L Hcy was increased by 4.2 fold (P＜0.01). Meanwhile, Hcy enhanced MAPK activity, MDA formation and LDH release (P＜0.01)in a concentration-dependent manner. Treatment of VSMCs with MT alone did not change above parameters, compared with control. However, MT (10^-6-10^-4 mol/L)attenuated significantly Hcy-stimulated proliferation of VSMCs (P＜0.01)in a concentration-dependent manner. And MT inhibited obviously Hcy-induced activation of MAPK activity, MDA formation and LDH release. Preincubation of VSMCs with 0.5 mmol/L ZnCl₂ for 6 h induced an increase cellular MT content by 5.7-fold (P＜0.01). The MT-overexpressed VSMCs resisted Hcy-stimulating action on MAPK activity, MDA formation and LDH leakage (P＜0.01). CONCLUSION:These results show that MT has an inhibitory effect on Hcy-induced VSMCs proliferation, and that MT could inhibit Hcy-stimulated MAPK activity and lipid peroxidation.     

Changes of myocardial glycogen content and right ventricular function in hypoxia swimming rats

AIM: To investigate the changes of myocardium glycogen content and the relation ship between changes of the myocardial glycogen content and the myocardial function. METHODS: Male Wistar rats were placed in (hypoxia rats) and made to swim in (hypoxia swimming rats) a hypobaxic chamber simulating an altitude of 5 000 m above sea level. The content of myocardium glycogens was determined by colorimetry. RESULTS: The myocardium
glycogen content of rats significantly reduced along with the prolongation of hypoxic exposure and approached to control level in hypoxia swimming rats. The myocardial function of right ventricule was improved significantly compared with control group.CONCLUSION: Moderate exercise (swimming) is beneficial to hypoxic adaptation of rats under the condition of chronic hypoxia.     

纳米微粒材料生物学活性研究进展

综述了纳米微粒的生物学效应及其免疫调节、抗菌、抗肿瘤等多种生物学活性.     

甘肃东方蜜蜂的形态特征研究

通过测定甘肃2个不同样点的4群东方蜜蜂发现,甘肃蜜蜂种群内遗传变异丰富,种群中许多形态性状特征表现出较明显的地理变异性;蜜蜂个体增大、体色变深,具体是:前翅长、前翅宽、背板3,4宽;后腿长、蜡镜长、蜡镜宽、蜡镜间距、腹片3,6的长和宽逐渐增加;背板3,4、小盾片的色素度逐渐加深。这些均具有生态适应意义。     

Antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes

AIM: To observe the antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes. METHODS: Rat thymus lymphocytes were separated by Ficoll-Urografin density gradient centrifugation. Lipofectin was used to introduce antisense, sense and mismatched oligonucleotides for c-myc to rat thymus lymphocytes. The antiproliferative effect was assayed by incorporation of [³H]-TdR and MTS cell proliferation assay. TR-PCR was used to detect the expression of c-myc mRNA. RESULTS: c-myc antisense oligonucleotide inhibited ratthymus lymphocytes proliferation[(0.14±0.03)A vs(0.32±0.16)A,P<0.05],but this ef ect had no relationship with the concentration of c-myc antisense oligonucleot ide.c-myc antisense oligonucleotide decreased the expression of c-myc mRNA in rat thymus lymphocytes. CONCLUSION: c-myc antisense oligonucleotide inhibited rat thymus lymphocyte proliferation.     

Taurine reduced oxygen free radical production induced by homocysteine in electron transport chain and homocysteine inhibites taurine transporter in mitochondria membrane

AIM: To observe effects of homocysteine and antagonized effects of taurine on electronic leakage and free radical production in myocardial mitochondria. METHODS: Myocardial mitochondria of rat heart was isolated, and was broken by supersonic wave to prepare submitochondria. Recombinant of succinic acid cytochrome c reductase was prepared with mitochondria of porcine heart. They were co-incubated with homocysteine and/or taurine with various concentration. The H₂O₂ and O₂^- were determined by chemiluminescence methods. The taurine transporter of heart mitochondria and its propert, and effects of homocysteine on its function were studied with glass filter. RESULTS: Homocysteine stimulated oxygen free radical production in heart mitochondria, submitochondria, and succinic acid cytochrome c in a concentration-dependent manner. Although taurine itself did not affect oxygen free radical production, taurine did inhibit oxygen free radical production in mitochondria, submitochondria and succinic acid cytochrome c in a concentration-dependent manner. Taurine transporters of Na⁺-dependent were existed in mitochondria membrane. Homocysteine inhibited taurine transtport in mitochondria in a concentration-dependent manner. CONCLUSIONS: Taurine inhibited electronic leakage and oxygen free radical production induced by homocysteine in electron transport chain. There were taurine transporters in mitochondria membrane, and transport functions of taurine transporter were inhibited by homocysteine.     

Effects of glycine on intracellular of free calcium and tumor necrosis factor-α of cardiomyocytes during hypoxia/reoxygenation

AIM: To observe the influence of glycine on intracellular free calcium, the concentration of tumor necrosis factor-α and the survival rate of myocardial cells during hypoxia/reoxygenation (H/R). METHODS: The simulated model of myocardial ischemia-reperfusion with the primary cultured cardiomyocytes of neonatal rats was established, and the cultured cardiomyocytes were divided into seven groups, control group, hypoxia/reoxygenation group, glycine (0.5 mmol/L) plus hypoxia/reoxygenation group, glycine (1.0 mmol/L) plus hypoxia/reoxygenation group, glycine (2.0 mmol/L) plus hypoxia/reoxygenation group, glycine (4.0 mmol/L) plus hypoxia/reoxygenation group, 4.0 mmol/L glycine group. RESULTS: Within certain concentration (0.5-2.0 mmol/L), the glycine could inhibit the calcium overload resulting from hypoxia/reoxygenation injury in cells in a dose-dependent manner with the optimal inhibitory effect at 2.0 mmol/L. Glycine inhibited the secretion of tumor necrosis factor-α from myocardial cells and increased the survival rate of myocardial cells. CONCLUSION: Glycine has a protective effect on hypoxia/reoxygenation myocardial cells, which may be related to inhibiting calcium overload and decreasing the production of tumor necrosis factor-α.     

The molecular mechanism of inhibition of murine Lewis lung carcinoma metastasis by weimaining in vivo

AIM: To investigate the anti-metastasis effect of weimaining, extracted from fragopyrum cymosum meissn, a Chinese medicine, on murine Lewis lung carcinoma (3LL). METHODS: The anti-metastasis effect of weimaining in vivo was detected in the grafting lung metastasis model of murine Lewis lung carcinoma. The effects of the drug on the expression of CD34 and E-cadherin were investigated by immunohistochemical staining and RT-PCR. RESULTS: Weimaining effectively inhibited the lung metastasis of 3LL at a concentration of 250 mg·kg^-1·d^-1, significantly suppressed the expression of CD34 and increased the expression levels of E-cadherin protein and mRNA in 3LL cells. CONCLUSIONS: Weimaining inhibits the metastasis of murine Lewis lung carcinoma (3LL) in vivo via increasing the expression of E-cadherin and decreasing microvessel density of tumor tissue.     

Effect of atrial natriuretic peptide on acute lung injury induced by lipopolysaccharide

AIM: To investigate effect of atrial natriuretic peptide (ANP) on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rat. METHODS: Mean arterial blood pressure (MAP) was recorded with model 6280 physiology intelligentialize grapher, nitric oxide (NO) and endothelin (ET) concentrations in plasma were measured after lipopolysaccharide (LPS) or following LPS ,ANP was injected into vein in rats. After experiment,lung water as well as pulmonary histopathological changes was measured and observed, respectively. RESULTS: Administration of LPS elicited a persistence decrease in MAP (8.1 kPa±2.6 kPa,at 4 h,P<0.01 vs control); NO and ET concentration in plasma was evident higher than that in control group, respectively (P<0.01); Wet-dry ratio of lung was higher than that in control group (5.15±0.43,at 4 h) (P<0.05); Alveolus detelectasis was observed and pulmonary mesenchyme was thicker than that in control group. No erythrocyte and leukocytes in alveolus,which show an interstitial pulmonary edema, was observed in LPS+ANP group, ANP maintained MAP at higher levels (13.35 kPa±2.93 kPa, at 4 h, P<0.05 vs LPS) after an transient decline when LPS was injected; NO and ET concentration of plasma had all significantly decrease, respectively (P<0.05 vs LPS, at 4 h); Wet-dry ratio of lung was lower than LPS group (4.57±0.35, P<0.05). Compared with control group the ratio was not evident difference (P>0.05); The histopathological of lung displayed markedly improved. CONCLUSION: ANP attenuates ALI induced by LPS in the rat. The effect of ANP may be via decreasing secretion of ET,NO and regulation arterial blood pressure.     

Effects of fosinopril,captopril and valsartan on the expressionof tissue factor in human monocytes

AIM: To investigate the effects of angiotensin-converting enzyme inhibitors (ACEI), fosinopril, captopril and angiotensin II AT₁ antagonists, valsartan on tissue factor (TF) expression on monocytes induced by lipopolysaccharide (LPS). METHODS: Mononuclear leukocytes from normal delivered female umbilical veins were incubated with bacterial LPS in presence or absence of different ACE inhibitors .At the end of incubation, the cells were disrupted by 3 freeze-thaw cycles. TF procoagulant activity was assessed by a one-stage clotting assay. RT-PCR was used to check TF mRNA expression, and GAPDH mRNA was used for parallel assay. RESULTS and CONCLUSION: The results showed that increased expression of TF mRNA induced by LPS was inhibited by fosinopril, captopril and valsartan, respectively, and the procoagualant activity of monocytes was also reduced.