Acta biochimica et biophysica Sinica
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Acta Biochim. Biophys. Sin. (Shanghai) · Apr 2006
Neuroprotection of insulin against oxidative stress-induced apoptosis in cultured retinal neurons: involvement of phosphoinositide 3-kinase/Akt signal pathway.
In order to investigate the neuroprotection of insulin in retinal neurons, we used retinal neuronal culture as a model system to study the protective effects of insulin against H2O2-induced cytotoxicity and apoptotic death. Primary retinal neuronal cultures were grown from retinas of 0-2-day old Sprague-Dawley rats. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. ⋯ Pretreatment with LY294002, a specific PI3K inhibitor, abolished the cytoprotective effect of insulin. Insulin also strongly activated both PI3K and the downstream effector Akt. These results suggest that insulin protects retinal neurons from oxidative stress-induced apoptosis and that the PI3K/Akt signal pathway is involved in insulin-mediated retinal neuroprotection.
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Acta Biochim. Biophys. Sin. (Shanghai) · Nov 2004
Accumulation of pathogenesis-related type-5 like proteins in phytoplasma-infected garland chrysanthemum Chrysanthemum coronarium.
Soluble proteins extracted from leaves, apical shoots, axillary shoots, and stems of garland chrysanthemum plants infected by onion yellows phytoplasma were analyzed by two-dimensional gel electrophoresis. Computerized matching analysis revealed that at least six soluble proteins were accumulated specifically in phytoplasma-infected garland chrysanthemum. ⋯ Accumulation of these six proteins was also found in garland chrysanthemum plants infected by other phytoplasmas. These results demonstrate that phytoplasmal infection induces the accumulation of PR-5 like proteins in garland chrysanthemum plants.
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Acta Biochim. Biophys. Sin. (Shanghai) · Feb 2004
Hypoxia inducible factor-1 alpha correlates the expression of heme oxygenase 1 gene in pulmonary arteries of rat with hypoxia-induced pulmonary hypertension.
To test the hypothesis that hypoxia inducible factor-1 alpha (HIF-1alpha) up-regulated the expression of heme oxygenase-1 (HO-1) gene in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension, 8 male Wistar rats in each of 5 groups were exposed to hypoxia for 0, 3, 7, 14 or 21 d, respectively. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricle hypertrophy index were measured. Lungs were inflation fixed for immunohistochemistry, in situ hybridization; frozen for later measurement of HO-1 enzyme activity. mPAP increased significantly after 7 d of hypoxia [(18.4 +/- 0.4) mmHg, P<0.05], reaching its peak after 14 d of hypoxia, then remained stable. ⋯ HIF-1alpha protein (tunica intima) was conversely correlated with HIF-1alpha mRNA (r=0.921,P<0.01), HO-1 protein was conversely correlated with HIF-1alpha protein (tunica intima) (r=0.821, P<0.01). HIF-1alpha and HO-1 were both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rat. Hypoxia inducible factor-1 alpha correlated the expression of heme oxygenase 1 gene in pulmonary arteries of rat with hypoxia-induced pulmonary hypertension.
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Acta Biochim. Biophys. Sin. (Shanghai) · Jan 2004
Clinical Trial Controlled Clinical TrialA novel missense mutation (L296 Q) in cholesteryl ester transfer protein gene related to coronary heart disease.
Cholesteryl ester transfer protein (CETP) is a key participant in the reverse transport of cholesterol from the peripheral tissues to the liver. To understand further the role that CETP gene plays in the pathogenesis of coronary heart disease (CHD), the promoter region, all 16 exons and adjacent intronic regions of CETP gene were screened for single nucleotide polymorphisms (SNPs) in 203 CHD patients and 209 healthy volunteers by the combination of PCR, denaturing high performance liquid chromatography (DHPLC), molecular cloning, and DNA sequencing. A novel missense mutation in the CETP gene was identified. ⋯ Further studies found that there was a significant increase in the mutant allele frequency in the CHD patients compared with that in the controls (0.160 vs. 0.091,cgr;(2) = 9.014, P = 0.003), and the odds ratio to develop CHD was 1.83 for the (296)Q allele carriers vs. (296)LL homozygotes. Statistical analyses also demonstrated that the mutant (296)Q allele carrier patients displayed significantly higher total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) concentrations than noncarrier patients. All these results suggest that the Q(296) mutation in CETP gene was closely related to CHD, and the identification of new mutations in the CETP gene will afford the opportunity to investigate the relationship between CETP gene and CHD.