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RESUMEN Introducción: Las porfirias hepáticas agudas son un trastorno genético causado por actividad irregular en la síntesis del grupo hemo. Aunque son de baja incidencia, su presencia puede aumentar el riesgo de muerte y afectar la calidad de vida de los pacientes. Se realizó una búsqueda bibliográfica con un intervalo desde el año 2015 al 2020, sobre porfirias hepáticas agudas. Objetivos: Actualizar sobre las alternativas diagnósticas y terapéuticas para las porfirias hepáticas agudas en adultos. Desarrollo: La exposición a ciertos factores precipitantes como fármacos, infecciones y estrés, conllevan a una crisis aguda de porfiria, que desencadenan síntomas neuroviscerales y requiere hospitalización. Existen teorías aisladas que explican el mecanismo de daño durante el ataque agudo, como la hiperactividad autónoma, inflamación, disfunción endotelial, mitocondrial, lesión renal y neurotoxicidad. Sin embargo, el reconocimiento clínico de estos mecanismos sin un diagnóstico conocido de porfiria es un reto para el personal médico, debido a la presencia de síntomas y signos inespecíficos, lo que retrasa el diagnóstico. Debido a la dependencia de la hemina de por vida, se han optado por nuevas alternativas terapéuticas como la supresión genética y el trasplante hepático. El pronóstico es favorable cuando se realiza el diagnóstico a tiempo. Conclusiones: Las alternativas diagnósticas y terapéuticas para las porfirias hepáticas agudas en adultos han evolucionado hacia el trasplante ortotópico hepático y la terapia génica, la cual se ha convertido en un enfoque terapéutico prometedor y validado para el tratamiento de los pacientes con porfirias hepáticas.
ABSTRACT Introduction: Acute hepatic porphyria is a genetic disorder caused by irregular activity in the synthesis of the heme group. Although they are of low incidence, their presence can increase the risk of death and affect the quality of life of patients. A bibliographic search was carried out with a time interval from 2015 to 2020 on acute hepatic porphyria. Objectives: To update on the diagnostic and therapeutic alternatives for acute hepatic porphyria in adults. Development: Exposure to certain precipitating factors such as drugs, infections, and stress leads to an acute porphyria crisis, which triggers neurovisceral symptoms and requires hospitalization. There are isolated theories that explain the mechanism of damage during the acute attack, such as autonomic hyperactivity, inflammation, endothelial and mitochondrial dysfunction, kidney damage, and neurotoxicity. However, clinical recognition of these mechanisms without a known diagnosis of porphyria is challenging for medical personnel, due to the presence of nonspecific symptoms and signs, delaying diagnosis. Due to the dependence on hemin for life, new therapeutic alternatives such as gene suppression and liver transplantation have been chosen. The prognosis is favorable when the diagnosis is made in time. Conclusion: Diagnostic and therapeutic alternatives for acute hepatic porphyria in adults have evolved towards orthopedic liver transplantation and gene therapy, which has become a promising and validated therapeutic approach for the treatment of patients with hepatic porphyria.
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Hemin can improve the stress resistance of plants through the heme oxygenase system. Additionally, substances contained in plants, such as secondary metabolites, can improve stress resistance. However, few studies have explored the effects of hemin on secondary metabolite content. Therefore, the effects of hemin on saponin synthesis and the mechanism of plant injury relief by hemin in
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Resumen Introducción. La porfiria es un conjunto de enfermedades metabólicas que tienen como base fisiopatológica la acumulación de precursores tóxicos. Su similitud clínica con enfermedades como el síndrome de Guillain-Barre puede retrasar el diagnostico, aumentando la posibilidad de complicaciones. Presentación del caso. Paciente femenino quien presentó síntomas inespecíficos de porfiria y síndrome de Guillain-Barre. La mujer fue evaluada de manera integral y recibió tratamiento para ambas patologías, respondiendo de manera inusual. Conclusión. La respuesta farmacológica atípica encontrada y la relación causa-efecto entre ambas entidades se justifica a la luz de sus procesos fisiopatológicos y la respuesta inmune desencadenada por los mismos.
Abstract Introduction: Porphyria is a group of metabolic diseases whose physiopathological basis is the accumulation of toxic precursors. Its clinical similarity to diseases such as Guillain-Barré Syndrome may delay diagnosis, increasing the possibility of complications. Case presentation: Female patient who presented nonspecific symptoms of porphyria and Guillain-Barré syndrome. The woman was comprehensively assessed and treated for both conditions, and had an unusual response. Conclusion: The atypical pharmacological response found and the cause-effect relationship between both entities is explained by their physiopathological processes and the immune response triggered by them.
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Objective To observe the influence of Hemin on both the expression of neuroglobin (Ngb) and Tau protein phosphorylation in rats with vascular dementia (VD),and explore the effect and mechanism of Ngb in VD. Methods VD model was established in rats with a permanent bilateral common carotid arteries occlusion(2-VO). Fifty four healthy male SD rats were randomly divided into 3 groups:sham operation group,VD group and Hemin group. According to ischemic time,the animals in each group were randomly allocated into 1 week subgroup,4 weeks subgroup and 8 weeks subgroup(n=6 in each subgroup). The learning and memory ability of rats were evaluated by Morris water maze test. The brain histopathological changes were observed by HE staining and the expression of Ngb and phosphorylated Tau ( p-Tau) was de-termined by Western blot. Results Compared with the sham operation group,after 2-VO the escape latency extended (all P<0. 05) and cross-platform performance reduced in rats in both VD group and Hemin group (all P<0. 05). The learning and memory ability of rats in Hemin group was better than that in VD group at the corresponding time point:the increase in the number of crossing platforms(1 week:Hemin group (7. 00± 0. 89) times vs VD group (5. 50±1. 22) times,t=2. 42,P<0. 05;4 weeks:Hemin group (5. 33±0. 52) times vs VD group (3. 50±1. 04) times,t=3. 84,P<0. 01;8 weeks:Hemin group (6. 50±0. 55) times vs VD group (4. 50±1. 05) times,t=4. 14,P<0. 01). The expression of Ngb and phosphorylated Tau (p-Tau) increased in VD group and Hemin group (P<0. 01). Compared with VD group,the expression of Ngb in Hemin group was increased(1 week:Hemin group (3. 45±0. 23) vs VD group (2. 56±0. 08),t=5. 67,P<0. 01;4 weeks:Hemin group (3. 08±0. 13) vs VD group (2. 28±0. 08),t=7. 96,P<0. 01;8 weeks:Hemin group (2. 82± 0. 12) vs VD group (2. 05±0. 10),t=7. 28,P<0. 01),while p-Tau was decreased (1 week:Hemin group (1. 57±0. 12) vs VD group (2. 40±0. 15),t=7. 62,P<0. 01;4 weeks:Hemin group ( 2. 14±0. 21) vs VD group (3. 18±0. 14),t=8. 23,P<0. 01;8 weeks:Hemin group (1. 83±0. 13) vs VD group (2. 79±0. 19), t=4. 91,P<0. 01). In VD group and Hemin group,the learning and memory ability exhibited a negative cor-relation with Ngb (r=-0. 892,P<0. 01),whereas a positive correlation with p-Tau (r=0. 932,P<0. 01). Conclusion Hemin induces high expression of Ngb and inhibits Tau phosphorylation in VD rats. Ngb may play a neuroprotective role in the development of VD by regulating Tau phosphorylation.
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Objective@#To observe the therapeutic effects and related mechanism of hemin on the progression of hepatic fibrosis in rats.@*Methods@#Sixty male Wistar rats were randomly divided into normal control group, 4-week model group, 6-week model group, hemin inhibitor zinc protoporphyrin-IX (ZnPP-IX) intervention group and hemin intervention group. Hemin intervention group in complex liver fibrosis model was intraperitonealy administered ZnPP-IX or hemin every other day for 2 weeks from the fourth week. The mRNA expression of HO-1, α-smooth muscle actin (α-SMA) and nuclear factor-κB (NF-κB) in the liver tissue was detected by real-time polymerase chain reaction. Immunohistochemistry was used to detect HO-1 and localization of α-SMA expression. Serum hyaluronic acid, propeptide of type III collagen and hepatic transforming growth factor beta (TGFβ), and interleukin 6 (IL-6) expressions were detected by enzyme-linked immunosorbent assay. The content of hydroxyproline in hepatic tissues was measured by alkaline hydrolysis method. One-way ANOVA was used to compare the mean of each group. The difference between the two groups was compared by independent samples t- test. P-values < 0.05 was considered statistically significant.@*Results@#Compared with model groups and ZnPP-IX intervention group, Hemin's intervention significantly increased the expression of HO-1 mRNA (P < 0.01) and protein distribution in liver tissues, while the expression of alpha-SMA mRNA was significantly decreased (P < 0.05) in portal space and areas around the fibrotic septum, and hepatic sinus. Hyp content and serum hyaluronic acid and propeptide of type III collagen decreased significantly (P < 0.05). Meanwhile, NF-κB p65 mRNA expression and the downstream production of TGFβ and IL-6 in Hemin intervention group were also inhibited (P < 0.05).@*Conclusion@#Hemin can significantly inhibit the progression of hepatic fibrosis in rats by up-regulating HO-1 expression, and the inhibiting activity of NF-κB p65 leads to downstream of the inflammatory factors.
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Objective To use hemin as a catalyst in the formation of disulfide bonds in the synthesis of linaclotide. Methods The linaclotide peptide was synthesized by the standard 9-fluorenylmethyl(Fmoc)solid-phase synthetic strategy. Wang resin and Trt-protected cysteine were used in the synthesis. Hemin was used in random oxidation of line linaclotide. The result was compared with those of air,dimethyl sulfoxide(DMSO),and I2 oxidation systems. Results and Conclusion Hemin is a highly effective catalyst for disulfide bond formation in linaclotide synthesis. It overcomes some disadvantages in oxidation reactions with conventional oxidative re-agents,and supplies a convenient way for the synthesis of peptide with concentrated disulfide bonds.
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A simple colorimetric method for detection of isocarbophos was developed based on the enhanced peroxidase-like activity of hemin. Hemin could catalyze the oxidation of peroxidase substrate 3,3′,5,5′-tetramethylbenzidine (TMB) by H2O2, which made TMB to lose one electron and caused reaction solution color changing from initial transparent to blue-green. Adding isocarbophos improved hemin affinity to substrates, which further enhanced peroxidase-like activity of hemin and made TMB to lose two electrons. The color of TMB solution was further changed from blue-green to yellow, and the degree of color change was proportional to the concentration of isocarbophos. Under the optimal conditions, the present analytical method for isocarbophos detection had a dynamic range from 2 μg/L to 100 μg/L with a detection limit of 1.2 μg/L (3σ). The selectivity assay demonstrated that other organophosphorus pesticides exhibited negligible interferences for isocarbophos detection. The application of the proposed method in the practical samples showed that the mean recovery of isocarbophos was in the range of 94.4％-113.0％, thus it could be widely applied to rapidly and sensitively detect isocarbophos in the agricultural products.
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Objective To investigate the effects of hemin on the quantity and apoptosis of human umbilical cord blood-derived late endothelial progenitor cells (EPCs) in vitro.Methods Mononuclear cells were isolated from human cord blood by density gradient centrifugation and were induced to differentiate to late EPCs in vitro.The second to third generation of attached late EPCs in good state were randomly plated for 24 h under different concentrations(0, 5, 10, 15 and 20 μmol/L)of hemin.Cell viability and proliferation were measured with typan blue staining and cell counting kit-8, respectively.Cell adhesion was analyzed by adhesive assay, and cell apoptosis was detected by flow cytometry.Results Compared to control group, hemin promoted viability of late EPCsat lower concentrations(5and 10μmol/L).Meanwhile, proliferation and adhesion were also improved and apoptosis was inhibited when the concentrations of hemin were 5,10, or 15 μ mol/L.All these effects were most prominent when hemin concentration was 10 μmoL/L, while the effects above were reversed when hemin concentration was moderated to 20 μmol/L.In addition, hemin showed a time-dependent manner in promoting cell proliferation and adhesion, and inhibiting apoptosis.That effects were most obvious at 24 h.Conclusions Lower concentration of herin augments the quantity and adhesion of late EPCs, inhibits cell apoptosis, while higher concentration present the reversed effects.
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Objective To investigate the effect of ischemic post-conditioning (IPO) on the level of Heme oxygenase-1 (HO-1) in acute ischemia - reperfusion (I/R) injury of lung in order to illuminate its protective mechanism.Methods Forty-eight adult SD rats were randomly divided (random number) into 6groups ( n =8 each):sham operation group ( S group) ; I/R group in which the hilum of left lung was clamped for 45 min followed by 105 min reperfusion; IPO group in which left lung hilum was clamped for 45min and post - conditioned by alternation of 30 s reperfusion with 30 s re-occlusion for three times before perfect perfusion for 102 min; Hemin (HM) + I/R group; ZnPPⅨ (zinc protoporphyrin Ⅸ) + IPO group and HM + S group.Arterial partial pressure of oxygen ( PaO2 ) and malondialdehyde (MDA) content in blood serum were assayed.The left lung was removed for determination of wet/dry (W/D) lung weight ratio and level of HO-1 protein was detected by immunohistochemical technique and pathohistological changes were observed under light microscopic examination. Comparisons among multiple groups were studied by using one-way analysis of variance (ANOVA). Statistical comparisons within groups were analyzed by using paired t -test.Results The level of HO-1 in lung tissue was significantly increased in the I/R group compared with the S group and the HM + S group (P ＜0.01,P ＜0.05).Compared to the I/R group,the IPO and the HM + I/R groups had significant higher level of HO-1 ( P ＜ 0.05,P ＜ 0.01 ).The PaO2 was significantly lower in all experimental groups than that in the S group (90 ± 11 ) mmHg.However,the values of PaO2 in the IPO and the HM + I/R groups were higher than that in the I/R group (P ＜ 0.01 ).In addition to severe lung tissue damage evidenced by pathohistological changes,the lung wet/dry (W/D) weight ratio and MDA level in blood serum were significantly higher in the I/R group than those in the S group (P ＜0.01 ),whereas the lung damage was attenuated either by IPO or by HM pretreatment (P ＜ 0.05,IPO or HM + I/R vs.I/R).Conclusions IPO can attenuate the lung ischemia - reperfusion injury through upregulating the level of HO-1 protein and inhibiting lipid peroxidation injury.
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Objective: To study the expression of neuroglobin (Ngb) in rat cerebral ischemia model and the neuroprotective effect of Ngb after ischemia and hypoxia. Methods: Totally 113 Sprague-Dawley rats were randomly divided into sham-operated group, middle cerebral artery occlusion (MCAO) group, hemorrhagic infarction (HI) group and hemin treatment group. The brain water content, infarcted tissue volume, neuropathologic changes (H-E staining) and expression of Ngb (immunocytochemical staining) were examined 3, 6, 12, and 24 h after model establishment. Results: The brain water contents and the infarcted tissue volumes in the hemin treatment group were significantly different from those of the MCAO group and HI group (P<0.01). The brain edema was obviously increased in HI group at 12 h. Neuropathologic examination showed that there were fewer necrotic neurons, milder edema and stronger Ngb expression in the Hemin treatment group than in the MCAO group and HI group. Immunocytochemical staining showed that the Ngb positive neurons in Hemin treatment group were more than those in the MCAO and HI groups. Conclusion: Earlier peak of brain edema may lead to aggravation of disease. Hemin-induced Ngb expression may relieve brain damage during focal cerebral ischemia.
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The results of this study confirm that the availability of hemin influences the expression of selected membrane proteins of Porphyromonas gingivalis, Prevotella intermedia, and Prevotella nigrescens. A 30 kDa (heated 24 kDa) hemin-binding protein whose expression is hemin regulated was identified and purified in P. gingivalis. A strong hemin-binding function was found by LDS-PAGE and TMBZ staining when P. gingivalis cells were grown under hemin-limited conditions. A 50 kDa cell envelope associated protein, whose expression is hemin regulated, is considered to be a putative hemin binding protein from P. intermedia and P. nigrescens, respectively. N-terminal amino acid sequence analysis of CNBr-digested 24 kDa hemin binding protein from P. gingivalis revealed that this protein belongs to a new, so far undescribed hemin-binding class of proteins. N-terminal amino acid sequence of a 50 kDa putative hemin binding protein from P. intermedia was identical with Enolase from Streptococcus intermedia. Work is in progress to further characterize the molecular structure of these proteins.
Subject(s)
Amino Acid Sequence , Carrier Proteins , Hemin , Membrane Proteins , Molecular Structure , Phosphopyruvate Hydratase , Porphyromonas gingivalis , Porphyromonas , Prevotella intermedia , Prevotella nigrescens , Prevotella , Sequence Analysis, Protein , StreptococcusABSTRACT
The whole cell extract of Helicobacter pylori strain 26695 was treated with the hemin-agarose resin and the bound fraction was analyzed by 2-Dimensional electrophoresis. The 2-D-PAGE-displayed spots were eluted and analyzed by matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS). Among the 120 spots processed, 94 protein spots were identified to represent 58 genes. Forty-five protein spots that represented thirty-four genes were newly identified in this study, including iron-containing proteins and hemin-containg proteins such as fumarate reductase, iron-sufur subunit(FrdB), ribonucleoside diphosphate reductase, beta subunit (NrdB), glutamyl-tRNA reductase (HemA), nikel-cobalt-cadnium resistance protein (NccB), and porphobilinogen deaminase (HemC).
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Chromatography, Affinity , Electrophoresis , Helicobacter pylori , Helicobacter , Hydroxymethylbilane Synthase , Mass Spectrometry , Oxidoreductases , Proteome , Ribonucleoside Diphosphate Reductase , Succinate DehydrogenaseABSTRACT
Objective To investigate the neuroprotective effect of heme oxygenase-1 induced by hemin on the rat brain after ischemia-reperfusion. Methods The global cerebral ischemia-reperfusion model in 48 Wistar rats was surgically prepared by four-vessel occlusion method (4-VO) and another 8 rats underwent sham-operation as normal control. Hemin was injected over 5 min at the lateral ventricle at 15 min, 24 h and 48 h after reperfusion in 24 ischemia-reperfusion rat models and normal saline was applied to another 24 rat models at the same time points as negative control. The effect of hemin was evaluated on the pathologic outcome and on the immuohistochemical reaction for HO-1 after 10-minute global cerebral ischemia followed by 24 h, 48 h and 72 h reperfusion. Results The peak level of HO-1-like immunoreactivity was found at 48 h after the reperfusion as compared with the matched rats in normal saline group (P
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Objective To study the effect of artemether (Art) on total antioxidant capacity (T-AOC) in adult Schistosoma japonicum. Methods In vitro, the T-AOC was determined in five-week old worms incubated without or with Art and/or hemin for 24 h, and the worms were continuously incubated for 96 h, then worm survival was assessed. In vivo, T-AOC was determined in worms freshly recovered from mice 6 - 24 h after treatment with Art 300 mg/kg. Results Throughout 96 h incubation no worms were killed by 50 μmol/L Art or 50 μmol/L hemin alone, but approximatdy 80% of them were killed by Art plus hemin. Addition of reduced glutathione and vitamin E could significantly block the cidal action of the combined treatment. No effect on T-AOC was seen in the worms exposed to Art or heroin alone for 24 h, but the combined treatment led to a pronounced T-AOC reduction in female worms in vitro. Such a drug effect on female worms was demonstrated in vivo. After female worms were exposed to Art for 6 - 24 h in vivo, their T-AOC was significantly reduced by 40% - 64%. However, no drug effect on male worms' T-AOC was observed in vivo and in vitro exposed to Art plus hemin. Conclusion Art-induced T-AOC reduction in female worms may sensitize them to lethal damages of endogenous and exogenous oxygen radicals.
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In the study presented here, identification, purification, and partial characterization of a hemin-regulated protein in Prevotella nigrescens were carried out. The results of this study confirm that the availability of hemin influences the expression of a selected membrane protein as well as the growth rate of P. nigrescens ATCC 33563. The 50 kDa cell envelope associated protein, whose expression is hemin regulated, is considered to be a putative hemin-binding protein from P. nigrescens. Disulfide bonds were not present in this protein, and N'-terminal amino acid sequence analysis revealed that this protein belongs to a new, so far undescribed protein. The 50 kDa protein was found to be rich in hydrophilic amino acids, with glycine comprising approximately 60% of the total amino acids. The study described here is the first to identify, purify, and biochemically characterize a putative hemin-binding protein from P. nigrescens. Work is in progress to further characterize the molecular structure of this protein.
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Amino Acids , Glycine , Hemin , Membrane Proteins , Molecular Structure , Prevotella nigrescens , Prevotella , Sequence Analysis, ProteinABSTRACT
Objective To observe the effects of hemin on the expression of hemeoxygenase(HO) on the human umbilical vein endothelial cells.Methods The hemin and zinc protoporphyrin-Ⅸ were added in the cultured endothelial cells to induce and inhibit the expression of HO-1,respectively.The expressions of HO-1 and HO-2 mRNA were detected using reverse transcription polymerase chain(RT-PCR) and the relative amount of CO released into the media was quantitated as carboxyhemoglobin(COHb) by enzyme linked immunosorbent assay(ELISA).The proliferation of endothelial cells was detected by methyl thiazolyl tetrazolium test(MTT).Results The expression of HO protein was mainly detected in the cytoplasm of endothelial cell.The expression of HO-1 mRNA in endothelial cell and the amount of COHb in the media increased significantly with the treatment of hemin.Conclusion The expression of HO-1 and the increase of endogenous CO are the molecular bases of the proliferation of endothelial cells,and the HO/CO system may play an important role in the development of cardiovascular diseases.
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Methicillin-resistant Staphylococcus aureus colony variants (SCVs) are frequently auxotrophic for hemin, menadione, thiamine, and CO2 involved in biosynthesis of the electron transport chain element. This phenotype grows slowly, and forms very small, nonhemolytic colonies in routine culture, so it may be led to the misidentification of this organism. We isolated an organism with catalase-positive, gram-positive cocci in cluster from the urine of a 55-years-old woman with persistent and relapsing bladder stone, who had undergone the antibiotic treatment with cefotaxime, ceftizoxime, amikacin, and/or micronomicin, intermittently for three years. The possibility of SCVs should have been ruled out because this organism didn't grow on Mueller-Hinton agar (MHA) for the susceptibility test. It formed small colonies on blood agar plate overnight, and grew only on MHA with supplement of hemin, or with 5% CO2. This organism was coagulase-positive, DNase-positive, manitol-salt positive, and identified as S. aureus with VITEK GPI card. The susceptibility test could be performed after adding hemin(1mg/mL) into bacterial suspension and showed susceptibility against vancomycin, teicoplanin, and rifampin. Because these phenotypes can be misidentifide as other non-pathogenic organisms due to their atypical characteristics, we should consider SCVs in case of small, nonhemolytic colonies with catalase-positive, gram-positive cocci in cluster, showing no growth on MHA. In addition, infections caused by SCVs are recently recognized in relation to persistent and relapsing infection, so they could be isolated from the patients with long-term antibiotic therapy.
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Female , Humans , Agar , Amikacin , Cefotaxime , Ceftizoxime , Electron Transport , Gram-Positive Cocci , Hemin , Methicillin Resistance , Methicillin-Resistant Staphylococcus aureus , Phenotype , Rifampin , Teicoplanin , Thiamine , Urinary Bladder Calculi , Urinary Bladder , Vancomycin , Vitamin K 3ABSTRACT
AIM: To explore the effect of exogenous carbon monoxide (CO) on the hypoxic pulmonary arterial hypertension in the rat. METHODS: 60 rats were randomly divided into 5 groups: Normal group\, hypoxic group\, Hermin group\, Znpp group and CO group. HO-1 activity was examined by spectrophotometer and lung tissues was stained by immunohistochemical method. HO-1 mRNA level was tested by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: (1) The pulmonary arterial pressure (18.52?3.24 mmHg) in CO group was higher than anoxic group and lower than hypoxic group (P
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AIM: To observe the effect of hemin on the expression of heme oxygenase-1(HO-1) in rat vascular smooth muscle cells(VSMCs). METHODS: Wistar rat aortic VSMCs were cultured in vitro and induced to proliferate by angiotensinⅡ(AngⅡ),hemin(a substrate and inducer of HO-1) and zinc protoporphyrin-Ⅸ(ZnPP,an inhibitor of HO-1)were added to induce and inhibit the expression of HO-1,respectively.The expression of HO-1 mRNA and protein were detected using reverse transcription polymerase chain reaction (RT-PCR)and Western blot,respectively. The relative amount of CO released into the media was quantitated as carbon monoxide hemoglobin(COHb)by enzyme-linked immunosorbent assay(ELISA),the proliferation of VSMCs was detected by MTT. RESULTS: The expression of HO-1 mRNA and protein in VSMCs and the amount of COHb in the media were increased significantly by hemin.Meanwhile the proliferation of VSMCs was suppressed markedly. CONCLUSION: The change of HO-1 mRNA and protein expression is the molecular base of the antiproliferation of endogenous CO .The HO-CO system might play a significant role in the development of cardiovascular diseases characterized by proliferation of VSMCs.
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Objective:To study the expression of neuroglobin (Ngb) in rat cerebral ischemia model and the neuroprotective effect of Ngb after ischemia and hypoxia. Methods: Totally 113 Sprague-Dawley rats were randomly divided into sham-operated group, middle cerebral artery occlusion (MCAO) group, hemorrhagic infarction (HI) group and hemin treatment group. The brain water content, infarcted tissue volume, neuropathologic changes (H-E staining) and expression of Ngb (immunocytochemical staining) were examined 3, 6, 12, and 24 h after model establishment. Results: The brain water contents and the infarcted tissue volumes in the hemin treatment group were significantly different from those of the MCAO group and HI group (P