[Effect of HSP72 on acute injury of neonatal cardiomyocytes induced by oxidative stress].

OBJECTIVE: To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress. METHODS: Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.5 mmol/L (final concentration) H2O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyocytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats. RESULTS: Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP7-2 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2. CONCLUSION: HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.

[Effect of heat shock response on the cleavage of nucleolin induced by oxidative stress].

OBJECTIVE: To observe the cleavage of nucleolin (C23) during apoptosis induced by oxidative stress and to clarify the effect of heat shock response (HSR) on the cleavage of nucleolin and its possible molecular mechanism. METHODS: We added 0.5 mmol/L peroxide hydrogen (H2O2 ) into cultured cells to mimic oxidative stress. Apoptosis and cleavage of C23 were detected using caspase-3 colorimetric assay and Western blotting respectively. HSR was performed to observe the effect of HSR on cleavage of C23 induced by oxidative stress, and over-expressions of HSP70 and HSP25 were detected by Western blotting. RESULTS: Activity of caspase-3 increased significantly after 2 hours of 0.5 mmol/L H2O2 treatment, and reached the peak after 12 hours. The cleavage of C23 appeared 30 minutes to 1 hour after the treatment of H2O2 as indicated by a cleaved fragmentation of 80 kD, which was significantly inhibited by HSR. Moreover, HSR could induce HSP70 and HSP25 over-expressions. CONCLUSION: Oxidative stress can induce the activation of caspase-3, cleavage of C23, and apoptosis. HSR can significantly inhibit the cleavage of C23 induced by oxidative stress, which is related to the over-expressions of HSP70, HSP25, and other stress proteins.

[Cerebrospinal fluid levels of beta-amyloid protein 1-42 in Alzhemier disease].

OBJECTIVE: To study the role of beta-amyloid protein 1-42 (A beta 1-42) content in the cerebrospinal fluid (CSF) of Alzheimer disease (AD) patients. METHODS: A beta 1-42 levels were measured with the ELISA method in AD (n = 30), non-AD (NAD, n = 25) and non-dementia (ND, n = 21). RESULTS: The A beta 1-42 mean value for AD was (109.91 +/- 58.78) fmol.L-1. In ND, the A beta 1-42 mean value was (242.40 +/- 142.58) fmol.L-1. The mean value for AD was significantly lower than that of ND. In NAD, the A beta 1-42 mean value was (231.70 +/- 143.94) fmol.L-1, and it was not significantly different from the mean value for ND. The A beta 1-42 level was positively correlated with the severity of AD symptoms, but not with the duration. A beta 1-42 levels in CSF of AD were significantly lower than that of ND, and they decreased as the severity of disease increased. CONCLUSION: Cerebrospinal fluid beta-amyloid 1-42 analyses may be of value in the clinical diagnosis of Alzheimer's disease, especially in the earlier course of the disease, when drug therapy may have the greatest effect but clinical diagnosis is particularly difficult.