Angiotensin II up-regulates expression of inducible nitric oxide synthase in human umbilical endothelial cells: roles of AT1 and AT2 / 中华心血管病杂志

<p><b>OBJECTIVE</b>Angiotensin II is an important pro inflammation factor in the cardiovascular system. This experiment is aimed to study the effects of angiotensin II on inducible nitric oxide synthase expression in human umbilical endothelial cells.</p><p><b>METHODS</b>Human umbilical endothelial cells were cultured in vitro and treated with angiotensin II alone or in combination with AT1, AT2 and NF-kappaB inhibitors respectively. The inducible nitric oxide synthase expressions at protein and mRNA levels were measured with Western blot and reverse transcription-polymerase chain reaction (RT-PCR), and the activity of NF-kappaB was analyzed with EMSA.</p><p><b>RESULTS</b>Angiotensin II up-regulated inducible nitric oxide synthase expressions at the protein and mRNA levels at 5 h (P < 0.05), the activity of NF-kappaB was enhanced at 2 h (P < 0.05). These effects could be blocked by AT1 and NF-kappaB inhibitors but not by AT2 inhibitor.</p><p><b>CONCLUSION</b>Angiotensin II can upregulate the expression of inducible nitric oxide synthase through NF-kappaB pathway in human umbilical endothelial cells. AT1, other than AT2, play a key role in this process.</p>

Changes of mitochondrial genes expressed in the brain tissue of rat in stroke-like episodes rats / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>Stroke is a complex disorder caused by a combination of genetic and environmental factors. Epidemiological studies have provided evidence of genetic influence on the development of human stroke. However, genetic changes which contribute to the development of stroke are not well known. This study was designed to gain a deep insight into that aspect.</p><p><b>METHODS</b>Using cold-stimuli plus high-salt intake as environmental risk factors, the authors established a hypertension model in rats, which produced a complication of stroke. Then, they used the suppression subtractive hybridization(SSH) technique to identify the differential genes that specifically expressed in total cerebrum tissue of the rats in stroke group. A comparison was made between two populations, namely the control group and stroke group.</p><p><b>RESULTS</b>By the use of SSH approach, a total of 576 clones were generated in this study from two subtractive libraries, among them 456 clones were usable and were analyzed. Genes for metabolism transcripts in stroke group were shown to be up-regulated (P<0.01). Mitochondrial transcripts were observed in a high rate of 26.5%.</p><p><b>CONCLUSION</b>The findings suggested that mitochondrial genes should induce an increased sensitivity to stroke through the changes of gene expressions. Mitochondrial genes probably play important roles in the causes and effects of stroke.</p>

Relationship of the expressions of PPAR-?mRNA and MMP-9 with coronary artery lesions in patients with coronary heart disease / 中华老年医学杂志

Objective To investigate the relationship of the levels of peroxisome proliferator- activated receptor-?(PPAR-?)mRNA,MMP-9 with the severity of coronary artery lesions in patients with coronary heart disease(CHD).Methods One hundred and fifty three patients with CHD who underwent coronary angiography were admitted.The expression of PPAR-?mRNA in lymphocytes of peripheral blood was detected by using RT-PCR,the level of MMP-9 enzyme was measured by enzyme-linked immunosorent assay,and the severity of coronary artery lesions were analyzed. Results As compared with control(0.624-0.13),PPAR-?mRNA expression was significantly lower in CHD patients(0.4+0.12).Negative correlation was found between PPAR-?mRNA and the classification(r=-0.56,P＜0.01)of coronary artery lesions,so was the number of coronary artery lesions(r=-0.42,P＜0.01).MMP-9 level was significantly higher in CHD patients(1.27?0.16)?g/L than that in controls(1.21?0.05)?g/L.Positive correlation was found between MMP-9 level and the classification(r=0.36,P＜0.01)of coronary artery lesions,so was the number of coronary artery lesions(r=0.30,P＜0.01).Negative correlation was also found between PPAR-?mRNA expression and MMP-9 level.Conclusions PPAR-?is a negative regulator of coronary artery lesions and PPAR-?inhibits the activation of MMP-9.It may be a valuable method for protecting patients from the incident of coronary artery disease to activate the expression of PPAR-?and decrease the level of MMP-9.