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Expression of Macrophage Migration Inhibitory Factor in Neonatal Rats with Hypoxic-Ischemic Brain Damage

Ying Xiong

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Abstract

Objective To explore the role and pathomechanism of macrophage migration inhibitory factor(MIF) in neonatal rats with hypoxic-ischemic brain damage(HIBD).Methods Seven-day newborn SD rats were randomly divided into 3 groups:sham operation group(n=40),HIBD group(n=40) and intervention group with anti-MIF(n=40,5 mg·kg-1,intraperitoneal injection).The rats were sacrificed at 6 h,12 h,24 h,3 d and 7 d after hypoxic-ischemic(HI),and brain tissues were collected,immunohistochemistry was used to detect the expression of MIF and nuclear factor-kappa B(NF-κB) protein in the pallium,and the content of TNF-α in ischemic cerebral brain was detected by enzyme-linked immunosorbent assay(ELISA).Results Compared to the sham control group,the expression of MIF and TNF-α in palliumal cells in HIBD group were significantly increased at 6 hours after HI,peaked at 24 hours(Pa0.01),but no significant difference at 7 days(P0.05);The expression of NF-κB increased at 6 hours after HI,peaked at 24 hours and maintained until the 3rd day(Pa0.01),but no signifficant difference at 7 days(P0.05).However the concentrations of MIF,NF-κB,TNF-α were significantly down-regulated in anti-MIF intervention group compared with those in HIBD group(Pa0.01).Conclusion Perhaps MIF is involved in the immune reaction of HIBD by controlling NF-κB pathway that can change the content of TNF-α.

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What this paper is about

Objective To explore the role and pathomechanism of macrophage migration inhibitory factor(MIF) in neonatal rats with hypoxic-ischemic brain damage(HIBD).Methods Seven-day newborn SD rats were randomly divided into 3 groups:sham operation group(n=40),HIBD group(n=40) and intervention group with anti-MIF(n=40,5 mg·kg-1,intraperitoneal injection).The rats were sacrificed at 6 h,12 h,24 h,3 d and 7 d after hypoxic-ischemic(HI),and brain tissues were collected,immunohistochemistry was used to detect the expression of MIF and nuclear factor-kappa B(NF-κB) protein in the pallium,and the content of TNF-α in ischemic cerebral brain was detected by enzyme-linked immunosorbent assay(ELISA).Results Compared to the sham control group,the expression of MIF and TNF-α in palliumal cells in HIBD group were significantly increased at 6 hours after HI,peaked at 24 hours(Pa0.01),but no significant difference at 7 days(P0.05);The expression of NF-κB increased at 6 hours after HI,peaked at 24 hours and maintained until the 3rd day(Pa0.01),but no signifficant difference at 7 days(P0.05).However the concentrations of MIF,NF-κB,TNF-α were significantly down-regulated in anti-MIF intervention group compared with those in HIBD group(Pa0.01).Conclusion Perhaps MIF is involved in the immune reaction of HIBD by controlling NF-κB pathway that can change the content of TNF-α.

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Available abstract

Objective To explore the role and pathomechanism of macrophage migration inhibitory factor(MIF) in neonatal rats with hypoxic-ischemic brain damage(HIBD).Methods Seven-day newborn SD rats were randomly divided into 3 groups:sham operation group(n=40),HIBD group(n=40) and intervention group with anti-MIF(n=40,5 mg·kg-1,intraperitoneal injection).The rats were sacrificed at 6 h,12 h,24 h,3 d and 7 d after hypoxic-ischemic(HI),and brain tissues were collected,immunohistochemistry was used to detect the expression of MIF and nuclear factor-kappa B(NF-κB) protein in the pallium,and the content of TNF-α in ischemic cerebral brain was detected by enzyme-linked immunosorbent assay(ELISA).Results Compared to the sham control group,the expression of MIF and TNF-α in palliumal cells in HIBD group were significantly increased at 6 hours after HI,peaked at 24 hours(Pa0.01),but no significant difference at 7 days(P0.05);The expression of NF-κB increased at 6 hours after HI,peaked at 24 hours and maintained until the 3rd day(Pa0.01),but no signifficant difference at 7 days(P0.05).However the concentrations of MIF,NF-κB,TNF-α were significantly down-regulated in anti-MIF intervention group compared with those in HIBD group(Pa0.01).Conclusion Perhaps MIF is involved in the immune reaction of HIBD by controlling NF-κB pathway that can change the content of TNF-α.

Key concepts: Macrophage migration inhibitory factor, Brain damage, Immunohistochemistry, Intraperitoneal injection, Endocrinology, Tumor necrosis factor alpha, Internal medicine, Medicine

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