2015Military Medical Journal of Southeast ChinaRequires access

Dexamethasone pretreatment reduces isoproterenol-induced myocardial injury and the expression of TNF-α

Yan Zhang

Open publisher page 0 citations

Abstract

Objective To investigate potential protective effect of glucocorticoid receptor( GR) agonist dexamethasone on isoproterenol-induced myocardial injury and the possible mechanism. Methods The sixteen mice were randomly divided into control( CON) group( n = 4),ISO group( n = 4),Dexamethasone pretreatment( DEX-pre) group( n = 4) and Dexamethasone treatment( DEX) group( n = 4). The mice in CON group and ISO group were given the same amount of 0. 9% sodium chloride and DEX-pre group given dexamethasone( 1. 25 mg / kg) injection by intraperitoneal injection as a pretreatment before treatment 30 minutes. CON group was given the same amount of 0. 9% sodium chloride injection by intraperitoneal injection. ISO group,DEX-pre group and DEX group received 5 mg / kg isoproterenol hydrochloride with daily intraperitoneal injection and continuous 3 days. At the two and three days,dexamethasone( 1. 25 mg / kg) was given after ISO injected 30 minutes in DEX group. Observe the serum ASL,LDH,CK,and CK-MP. Myocardial tissue injury was assessed by HE staining. The expression of TNF-α on serum was detected by ELISA. Results1 Compared with control group,the levels of ASL,LDH and CK was significantly increased; the degree of myocardial injury were greatly deteriorated in ISO group( P 0. 01). The expression of TNF-α on serum was greatly increased( P 0. 05) in ISO group.The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 2 Compared with ISO group,the levels of ASL and CK was significantly reduced( P 0. 01) and the levels of LDH and CK-MP was reduced( P 0. 05). The degree of myocardial injury were greatly improved( P 0. 01) in DEX-pre group. The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 3 Compared with ISO group,the levels of ASL,LDH,CK,CK-MP and the degree of myocardial injury weren't significantly difference in DEX group( P 0. 05). The expression of TNF-α on serum was significantly increased( P 0. 01)in DEX group. Conclusion DEX pretreatment has protective effect against ISO-induced myocardial injury. The mechanism might be the changes of inflammatory cytokinesthe.

About this research paper

What this paper is about

Objective To investigate potential protective effect of glucocorticoid receptor( GR) agonist dexamethasone on isoproterenol-induced myocardial injury and the possible mechanism. Methods The sixteen mice were randomly divided into control( CON) group( n = 4),ISO group( n = 4),Dexamethasone pretreatment( DEX-pre) group( n = 4) and Dexamethasone treatment( DEX) group( n = 4). The mice in CON group and ISO group were given the same amount of 0. 9% sodium chloride and DEX-pre group given dexamethasone( 1. 25 mg / kg) injection by intraperitoneal injection as a pretreatment before treatment 30 minutes. CON group was given the same amount of 0. 9% sodium chloride injection by intraperitoneal injection. ISO group,DEX-pre group and DEX group received 5 mg / kg isoproterenol hydrochloride with daily intraperitoneal injection and continuous 3 days. At the two and three days,dexamethasone( 1. 25 mg / kg) was given after ISO injected 30 minutes in DEX group. Observe the serum ASL,LDH,CK,and CK-MP. Myocardial tissue injury was assessed by HE staining. The expression of TNF-α on serum was detected by ELISA. Results1 Compared with control group,the levels of ASL,LDH and CK was significantly increased; the degree of myocardial injury were greatly deteriorated in ISO group( P 0. 01). The expression of TNF-α on serum was greatly increased( P 0. 05) in ISO group.The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 2 Compared with ISO group,the levels of ASL and CK was significantly reduced( P 0. 01) and the levels of LDH and CK-MP was reduced( P 0. 05). The degree of myocardial injury were greatly improved( P 0. 01) in DEX-pre group. The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 3 Compared with ISO group,the levels of ASL,LDH,CK,CK-MP and the degree of myocardial injury weren't significantly difference in DEX group( P 0. 05). The expression of TNF-α on serum was significantly increased( P 0. 01)in DEX group. Conclusion DEX pretreatment has protective effect against ISO-induced myocardial injury. The mechanism might be the changes of inflammatory cytokinesthe.

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 potential protective effect of glucocorticoid receptor( GR) agonist dexamethasone on isoproterenol-induced myocardial injury and the possible mechanism. Methods The sixteen mice were randomly divided into control( CON) group( n = 4),ISO group( n = 4),Dexamethasone pretreatment( DEX-pre) group( n = 4) and Dexamethasone treatment( DEX) group( n = 4). The mice in CON group and ISO group were given the same amount of 0. 9% sodium chloride and DEX-pre group given dexamethasone( 1. 25 mg / kg) injection by intraperitoneal injection as a pretreatment before treatment 30 minutes. CON group was given the same amount of 0. 9% sodium chloride injection by intraperitoneal injection. ISO group,DEX-pre group and DEX group received 5 mg / kg isoproterenol hydrochloride with daily intraperitoneal injection and continuous 3 days. At the two and three days,dexamethasone( 1. 25 mg / kg) was given after ISO injected 30 minutes in DEX group. Observe the serum ASL,LDH,CK,and CK-MP. Myocardial tissue injury was assessed by HE staining. The expression of TNF-α on serum was detected by ELISA. Results1 Compared with control group,the levels of ASL,LDH and CK was significantly increased; the degree of myocardial injury were greatly deteriorated in ISO group( P 0. 01). The expression of TNF-α on serum was greatly increased( P 0. 05) in ISO group.The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 2 Compared with ISO group,the levels of ASL and CK was significantly reduced( P 0. 01) and the levels of LDH and CK-MP was reduced( P 0. 05). The degree of myocardial injury were greatly improved( P 0. 01) in DEX-pre group. The expression of TNF-α on serum was significantly reduced( P 0. 01) in DEX-pre group. 3 Compared with ISO group,the levels of ASL,LDH,CK,CK-MP and the degree of myocardial injury weren't significantly difference in DEX group( P 0. 05). The expression of TNF-α on serum was significantly increased( P 0. 01)in DEX group. Conclusion DEX pretreatment has protective effect against ISO-induced myocardial injury. The mechanism might be the changes of inflammatory cytokinesthe.

Key concepts: Dexamethasone, Medicine, Intraperitoneal injection, Internal medicine, Endocrinology, Glucocorticoid, Corticosteroid, Agonist

Related papers

Back to paper searchBrowse research topicsOriginal source
Dexamethasone pretreatment reduces isoproterenol-induced myocardial injury and the expression of TNF-α — Research Paper | ScholarLens