Effects of genistein and folic acid on neuronal membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35 / 中华预防医学杂志

<p><b>OBJECTIVE</b>To observe the neuro-protective effects of genistein (Gen) and folic acid (FA) on neurons membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35 (Aβ31-35).</p><p><b>METHODS</b>The primary cultured rat cerebral cortical neurons were randomly divided into DMEM (control), Aβ31-35 (25 µmol/L), Gen (Gen 27 µg/ml), FA (FA 40 µg/ml) and Gen + FA (Gen 27 µg/ml + FA 40 µg/ml). Gen and/or FA were added two hours before Aβ31-35 addition. After twenty four hours, MTT assay was performed to measure the viability of cultured neurons. Fluorescence polarization was performed to observe the neuron cell membrane fluidity. The mitochondrial membrane potential (MMP) was determined to investigate the alteration of mitochondrial structure and function of neurons by laser scanning confocal microscope and a flow cytometer was used to investigate the activation of mitochondrial permeability transition pore (MPTP). Each experiment was repeated three times.</p><p><b>RESULTS</b>Compared with group Aβ31-35 (0.845 ± 0.050, F = 4.931, P < 0.05), the absorbance was significantly higher in group Gen (0.982 ± 0.110, t = 3.523, P < 0.01), FA (0.947 ± 0.061, t = 2.745, P < 0.01) and Gen + FA (0.996 ± 0.090, t = 3.966, P < 0.01). The viscosity of cell neuron membrane in group Gen (1.75 ± 0.28, t = 2.085, P < 0.05), FA (1.66 ± 0.37, t = 2.357, P < 0.05) and Gen + FA (1.50 ± 0.20, t = 3.784, P < 0.05) was significantly lower than that in group Aβ31-35 (2.11 ± 0.44, F = 5.529, P < 0.01), which indicated the cell membrane fluidity was significantly higher in group Gen and/or FA than that in group Aβ31-35. MMP was significantly decreased by Aβ31-35 (3.364 ± 1.140, t = 3.949, P < 0.01) when comparing to control group (6.383 ± 1.683), while it was significantly increased by Gen (5.286 ± 1.792, t = 2.406, P < 0.05), FA (5.884 ± 2.022, t = 2.887, P < 0.01) and Gen + FA (6.120 ± 2.124, t = 3.304, P < 0.01) when comparing to group Aβ31-35 (F = 7.585, P < 0.01). MPTP was activated by Aβ31-35 and Gen and/or FA could reverse this progress.</p><p><b>CONCLUSION</b>Gen and/or FA could protect the neuronal and mitochondrial membrane from the impairment induced by Aβ31-35.</p>

Neurotoxicity of beta-amyloid peptide 31-35 and 25-35 to cultured rat cortical neurons / 中华预防医学杂志

<p><b>OBJECTIVE</b>To compare the toxicity of mechanism beta amyloid peptide (Abeta) 25-35 and 31-35 to cultured rat cortical neurons.</p><p><b>METHODS</b>The primary rat cerebral cortical neurons of rat were cultured 48 hours and randomly divided into control, Abeta25-35 (25 micromol/L)and Abeta31-35 (25 micromol/L) treated groups. After twenty four hours culturing, the cells were collected MTT assay was performed to measure the viability of cultured neurons. The mitochondrial membrane potential was determined to investigate the alteration of mitochondrial structure and function of neurons by laser scanning confocal microscope. The DNA damage of neurons was measured by single cell gel electrophoresis. The expressions of Bcl-2, Bax and p53 gene were measured by reverse transcriptase polymerase chain reaction (RT-PCR). Each experiment was repeated three times.</p><p><b>RESULTS</b>The absorbance (0.746 +/- 0.071, 0.811 +/- 0.083) and fluorescence intensity (3.050 +/- 0.240, 2.806 +/- 0.203) of neurons in Abeta25-35 and 31-35 treated group were significantly lower (t(A) were 4.023 and 5.401, t(fluorescence intensity) were 9.524 and 7.589 respectively, P < 0.01) than those in control group (1.038 +/- 0.125 and 4.280 +/- 0.358 respectively). The percentage of comet cells (59.0%, 48.5%) and tail length (57.3 +/- 4.7, 54.2 +/- 6.8) microm in Abeta25-35 and 31-35 treated group were significantly higher (chi(2)(comet cell) were 99.397 and 137.071, t(tail length) were 19.058 and 29.173 respectively, P < 0.01) than those in control group (4.5% and (5.2 +/- 1.1) microm respectively). Compared with control group (Bax/Bcl-2 ratio 0.2090 +/- 0.0991, p53/beta-actin ratio 1.6560 +/- 0.0853), the Bax/Bcl-2 ratio (t value were 2.429 and 2.356 respectively, P < 0.05) and expressions of p53 (t value were 2.366 and 2.503 respectively, P < 0.05) gene were significantly increased (P < 0.05) in Abeta25-35 (Bax/Bcl-2 ratio 1.2774 +/- 0.0762, p53/beta-actin ratio 2.0284 +/- 0.2223) and Abeta31-35 (Bax/Bcl-2 ratio 1.0330 +/- 0.0683, p53/beta-actin ratio 1.9505 +/- 0.2725) treated group.</p><p><b>CONCLUSIONS</b>Neurotoxicity-induced by Abeta31-35 in cortical neurons is similar to that induced by Abeta25-35, which is possibly related to its direct neurotoxic and apoptotic effects to neurons.</p>

Relationships between Serum Lipid,Apolipoproteins and Angiocardiopathy in Obese Children / 实用儿科临床杂志

Objective To analyze obese children serum lipid level in order to understand the relationship between serum lipid and cardiovascular disease in obese children.Methods One hundred and fifty-three children(109 male and 44 female)aged 4-16 years old with obesity who attended the outpatient clinic of Beijing Children′s Hospital were collected.Percentage body fat (%BF),body fat (BF),fat-free mass (FFM) was estimated by using bioelectrical impedance analysis (BIA) and calculate.Waist and hip circumference,waist-to-hip ratio (WHR) was estimated by soft tape measure and calculate.Skinfold thickness of scapular bone below (S) and triceps muscle (T),S/T rate was estimated by skin fold meter and calculate.Serum total cholesterol (TC),triglyceride(TG),high density lipoprotein(HDL-C),low density lipoprotein(LDL-C),apolipoprotein(Apo) AI and Apo B levels were also measured.SPSS 11.0 software was used to analyzed the data.Results The cardiovascular disease related was the prevalence of high TC levels(3.3%)or high LDL-C level(6.0%) and high TG level(24.7%) was rather low.HDL-C level was reduced in 31.3% of obese children.In children over 10 years old,%BW and %BF showed a weak correlation with HDL-C(r=-0.202,-0.211).Conclusions In obese children,serum lipid as well as Apo level should be exa-mined in order to evaluate angiocardiopathy.