2000•Unpublished venueRequires access

Regulatory Effects of Dexamethasone on the Expression of HSP 70 mRNA in Neonatal Rats Following Cerebral Hypoxia-ischemia

Wu Sheng

Open publisher page 0 citations

Abstract

Objective To investigate the expression of HSP70 gene in the brain of neonatal rats following cerebral hypoxia ischemia (HI) and the effect of dexamethasone (DEX) on the expression of HSP70 mRNA. Methods Rapid competitive reverse transcriptase PCR was used to semi quantitatively analyze the expression of HSP70 mRNA in the ipsilateral cerebral hemisphere in a neonatal rat model of hypoxia ischemia. Groups were divided into those pre treated with DEX prior to hypoxia ischemia, those treated with DEX immediately following hypoxia ischemia, those pre treated with DEX prior to sham, and normal controls, respectively. Results Cerebral HI increased HSP70 mRNA expression. The peak time of overexpression was 12 h after HI(3.868±1.421), and maintained at a higher level during 12~48 h(3.186±0.803, 2.568±0.709). The intensity of HSP70 mRNA expression was greatly decreased or almost abolished completely by the pretreatment with DEX. At 12 h, 24 h and 48 h after this treatment, HSP 70 mRNA expression were 0.526±0.593, 0.492±0.450 and 0.434±0.428, respectively, while the treatment with DEX after the insults had no evident effect on the expression of HSP70 mRNA. AT 12 h, 24 h and 48 h, HSP 70 mRNA expression were 3.460± 1.309 , 3.020±0.565 and 2.242±0.504, respectively. Conclusions DEX prophylaxis could suppress the overexpression of HSP70 mRNA following cerebral HI. Inhibition of HSP70 mRNA expression by DEX prophylaxis could be related to the suppression of overexcitation of neurons. [

About this research paper

What this paper is about

Objective To investigate the expression of HSP70 gene in the brain of neonatal rats following cerebral hypoxia ischemia (HI) and the effect of dexamethasone (DEX) on the expression of HSP70 mRNA. Methods Rapid competitive reverse transcriptase PCR was used to semi quantitatively analyze the expression of HSP70 mRNA in the ipsilateral cerebral hemisphere in a neonatal rat model of hypoxia ischemia. Groups were divided into those pre treated with DEX prior to hypoxia ischemia, those treated with DEX immediately following hypoxia ischemia, those pre treated with DEX prior to sham, and normal controls, respectively. Results Cerebral HI increased HSP70 mRNA expression. The peak time of overexpression was 12 h after HI(3.868±1.421), and maintained at a higher level during 12~48 h(3.186±0.803, 2.568±0.709). The intensity of HSP70 mRNA expression was greatly decreased or almost abolished completely by the pretreatment with DEX. At 12 h, 24 h and 48 h after this treatment, HSP 70 mRNA expression were 0.526±0.593, 0.492±0.450 and 0.434±0.428, respectively, while the treatment with DEX after the insults had no evident effect on the expression of HSP70 mRNA. AT 12 h, 24 h and 48 h, HSP 70 mRNA expression were 3.460± 1.309 , 3.020±0.565 and 2.242±0.504, respectively. Conclusions DEX prophylaxis could suppress the overexpression of HSP70 mRNA following cerebral HI. Inhibition of HSP70 mRNA expression by DEX prophylaxis could be related to the suppression of overexcitation of neurons. [

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the expression of HSP70 gene in the brain of neonatal rats following cerebral hypoxia ischemia (HI) and the effect of dexamethasone (DEX) on the expression of HSP70 mRNA. Methods Rapid competitive reverse transcriptase PCR was used to semi quantitatively analyze the expression of HSP70 mRNA in the ipsilateral cerebral hemisphere in a neonatal rat model of hypoxia ischemia. Groups were divided into those pre treated with DEX prior to hypoxia ischemia, those treated with DEX immediately following hypoxia ischemia, those pre treated with DEX prior to sham, and normal controls, respectively. Results Cerebral HI increased HSP70 mRNA expression. The peak time of overexpression was 12 h after HI(3.868±1.421), and maintained at a higher level during 12~48 h(3.186±0.803, 2.568±0.709). The intensity of HSP70 mRNA expression was greatly decreased or almost abolished completely by the pretreatment with DEX. At 12 h, 24 h and 48 h after this treatment, HSP 70 mRNA expression were 0.526±0.593, 0.492±0.450 and 0.434±0.428, respectively, while the treatment with DEX after the insults had no evident effect on the expression of HSP70 mRNA. AT 12 h, 24 h and 48 h, HSP 70 mRNA expression were 3.460± 1.309 , 3.020±0.565 and 2.242±0.504, respectively. Conclusions DEX prophylaxis could suppress the overexpression of HSP70 mRNA following cerebral HI. Inhibition of HSP70 mRNA expression by DEX prophylaxis could be related to the suppression of overexcitation of neurons. [

Key concepts: Dexamethasone, Hypoxia (environmental), Messenger RNA, Hsp70, Ischemia, Gene expression, Endocrinology, Internal medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Regulatory Effects of Dexamethasone on the Expression of HSP 70 mRNA in Neonatal Rats Following Cerebral Hypoxia-ischemia — Research Paper | ScholarLens