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Objective To discuss whether Omega-3 fish oil fat emulsion has the potential protective mechanism for 7-day-old rats with hypoxic-ischemic brain damage (HIBD).Methods One hundred and sixty-eight 7-day-old SD rats were randomly divided into 4 groups:group A (sham group),group B (Omega-3 fish oil fat emulsion group),group C (normal fat emulsion group),group D (model group),and there were 42 cases in each group.Neonatal HIBD was induced by the method of Rice.Rats were sacrificed at 1 d,3 d and 7 d after the surgery.Hippocampus was removed for Real-time PCR and Western blot test to detect Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) mRNA and protein expression.TUNEL staining comparison was done among different groups to observe the number of cellular apoptosis.Results HE staining of hippocampus CA1 area in 3 d showed that brain tissues in group A maintained normal structures;those in group D had much more brain cells with severe edema than other groups;TLR4 and NF-κB mRNA and protein expression levels in group D were higher than those in group A in 1 d (all P ＜0.05);TLR4 and NF-κB expression levels of mRNA and protein in group B (4.89 ± 0.51,9.30 ± 1.53;1.15 ±0.10,1.44 ± 0.14) were lower than those in group C (17.58 ± 2.50,20.13 ± 1.00;2.56 ± 0.10,2.82 ± 0.09) and group D (15.94-± 2.52,26.21 ± 3.00;2.34 ± 0.11,4.51 ± 0.36) in 3 d (all P ＜ 0.05),and compared with group A (6.30 ± 1.52,5.32 ± 1.06;1.32 ± 0.10,2.42 ± 0.14),there was significant difference (all P ＞ 0.05);TLR4 and NF-κB mRNA and protein expression levels in group B were lower than those in group C and group D in 7 d(all P ＜0.05),and compared with group A there was no significant difference (all P ＞ 0.05).The apoptotic cell number of brain tissues in 3 d:group B (13.67 ±2.52) were lower than those in group C (27.67 ±2.52) and group D (41.00 ±3.61) (all P ＜0.05),and compared with the group A (6.00 ±2.00),the difference was not statistically significant (P ＞ 0.05).Conclusions Omega-3 fish oil fat emulsion plays an important role in protecting neonatal rats with HIBD.The mechanisms were likely to reduce TLR4,NF-κB and cell apoptosis levels.
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Mitochondrial permeability transition pore plays a central role in alterations of mitochondrial structure and function,leading to neuronal injury,which is a nonspecific,voltage dependence of complex channel.Hypoxia-ischemia can affect the function of mitochondria,causing mPTP permeability change and leading to cell death.Hypoxia-ischemia brain injury(HIBI) which is caused by perinatal asphyxia threatens neonatal life and leads to neurological sequelae of severe diseases.And mitochondrial dysfunction plays an important role in HIBI.This paper mainly elaborates the relationship between the mPTP and HIBI.
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ObjectiveTo explore effective treatment for moderate and severe neonatal hypoxic-ischemic encephalopathy(HIE).Methods46 cases of moderate to severe HIE were randomly divided into two groups.Control group of 21 cases only accepted the HIE conventional treatment,treatment group,25 cases accepted the HIE conventional treatment and were also given brain protein hydrolyzate combined naloxone treatment,the efficacy of various clinical indicators of the two groups were compared.ResultsThe remarkable effective rate and the total effective rate of the treatment group were significantly higher ( all P ＜ 0.01 ).Consciousness recovery time,recovery time of the original ability,convulsions,muscle tension,recovery time,sucking ability,recovery time,hospital days of treatment group were significantly lower than the control group( P ＜ 0.05 or P ＜ 0.01 ).ConclusionThe effect of naloxone therapy for moderate to severe HIE is significant,and the therapy has high clinical value.
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Objective To investigate the clinical value of serum cardiac troponin Ⅰ(cTNⅠ) in diagnosis of cardiac injury in neonatal hypoxic ischemic encephalopathy(HIE).Methods 20 healthy newborns were selected as the control group.58 patients with HIE were divided into mild group(n=20),medium group(n=19) and the severe group(n=19),respectively.The level of cTNⅠ was detected by immunofluorescence.Results Serum levels of cTNⅠ in experimental group were obviously higher than that of the control group;There were significant difference between any two groups(P
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Objective To explore the role of caspase-3 activation and DNA fragmentation in later period of neonatal rat hypoxic-ischemic brain damage(HIBD). Methods DNA fragmentation,caspase-3 mRNA and caspase-3 protein were measured in 2 wks、3 wks and 4wks after setting HIBD animal model in newborn wistar rats by FCM, RT-PCR and Immunohistochemistry. Results (1) Apoptosis lasted 4ks after HIBD. This suggested a long lasting role of apoptosis in neonatal HIBD by TNNEL and EM.(2)Caspase-3 mRNA expression was estimated by semi-quantitative RT-PCR. It was higher in HIBD group(0.771?0.074) than in control group(0.620?0.038, P0.05. Average Avalue of Caspase-3 protein in HIBD group(0.374 ?0.038) at 3 wks was significantly higher than that in control group(0.356?0.020,P
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Objective To explore the expression and effect of interleukin(IL)-18 after hypoxic-ischemic brain damage(HIBD) in neonatal rats. Methods The HIBD model of seven-day-old Wistar rats was established. The mRNA and protein for IL-18 in cerebral cortex of control group, HIBD3 h, 8 h, 24 h, 3 d, 6 d and 14 d group were analyzed by RT-PCR and immunohistochemistry respectively, at the same time histological changes were observed. Results The expression of IL-18 mRNA and protein was low in control group[mRNA: 0.321 8?0.046 6; protein: (6.033? 1.019)cells/field]. After HIBD, the level of mRNA/protein for IL-18 in ischemic cortex increased progressively at 24 h to 6 d [mRNA: 24 h: 0.582 3?0.074 0, 3 d:0.697 6 ?0.107 3, 6 d: 0.911 0?0.064 7; protein: 24 h: (19.133?2.094)cells/field, 3 d: (28.900 ?1.589) cells/field, 6 d: (52.883?3.203)cells/field; P
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Objective To study expressions of heme oxygenase-1 mRNA and protein in rat hippocampus after hypoxic-ischemia brain damage(HIBD) as well as the relationship with apoptosis in brain.Methods Seven-day-old SD rats were randomly divided into hypoxic-ischemia brain damage group and sham control group.Expressions of HO-1 protein and mRNA as welll as the relationship with apoptosis after HIBD in neonatal rat were determined by immunohisochemistry and in situs hybridizaion as well as terminal deoxynucleotidy transferase mediated UTP-biotin nick end labeling(TUNEL).Results 1.In the right hippocampus,expression of HO-1 gene increased sharply at 4 h (P
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Objective To observe the alteration of astrocyte and apoptosis in neonatal hypoxic-ischemic encephalopathy(HIE).Me-thods The pathological brain specimens of 25 newborns who died of HIE were observed macroscopically and microscopically,included male 14 cases and female 11 cases.The immunochemistry staining with glial fibrillary acidic protein(GFAP)and in situ end terminal dexynucleotidy 1 transferase mediated deoxyuridine triphosphate-biotion nick and labeling(TUNEL)methods were used to observe the changes of astrocyte and the neurons apoptosis in HIE.The relationship between the change of astrocyte and the neurons apoptosis and the occurrence of HIE and course of disease were further synthetically analyzed.Results The brain specimens of 25 newborn HIE had apoptosis cells at the different level.The degree of apoptosis of cerebral neurons was severe in the cases of 24 h-6 d survival(P