Hypertonic saline decreases monocyte chemotactic protein 1 expression in microglia may be through inhibition of p38 MAPK signaling pathway
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Objective To explore whether hypertonic saline (HS) could affect the microglial activation and release of monocyte chemotactic protein 1 (MCP-1) in vitro experiments,and to study the mechanism.Methods Microglia isolated from primary mixed glia cells by shaking method were divided into four groups:control group,hypoxia + glucose free medium group (hypoxia group),100 mmol/L HS + hypoxia + glucose free medium group (HS group) and SB203580 (a specific inhibitor of p38 MAPK) group.Oxygen-glucose deprivation (OGD) was performed in all experiment groups but control group.Double immunofluorescence and ELISA were used to determine whether HS could decrease the production of MCP-1 after OGD,and western blot was employed to determine the effect of HS on the level of phosphorylated p38 MAPK.Results Double immunofluorescence showed that 100 mmol/L HS attenuated MCP-1 level in HS group after treatment with 100 mmol/L HS compared with hypoxia group,and the level of MCP-1 in cultured medium released by microglia was significantly decreased after 100 mmol/L HS or SB203580 treatment for 4 h.There was no significant difference in MCP-1 between HS group and SB203580 group (P ＞ 0.05),but compared with control group (107.956 ± 8.921),there were higher levels of MCP-1 in hypoxia group (173.467 ±9.027),HS group:(145.957 ± 10.952),and SB203580 group (136.279 ± 15.63),P ＜0.05.At 30 min,1 h,2 h and 4 h after hypoxia,western blot showed that the levels of phosphorylated p38 MAPK markedly decreased in HS group as compared to the hypoxia group at corresponding intervals (control group:0.590±0.105.Hypoxia group:30 min,1.553 ±0.215; 1 h,1.212±0.161; 2 h,1.179 ± 0.105; 4 h,1.178 ±0.122.HS group:30 min,1.028 ±0.168; 1 h,0.852 ±0.112; 2 h,0.927 ±0.121; 4 h,0.815 ± 0.107; P ＜ 0.05).Conclusions HS decreasing MCP-1 level in microglia after hypoxia may be attributed to the inhibition of p38 MAPK signaling pathway.
Key words:
Hypertonic saline; Cerebral edema; Hypoxia; Microglia; monocyte chemotactic protein-1; p38; SB203580; Inflammatory responseKeywords:
Hypoxia
Hypertonic saline
Monocyte
Objective To investigate the expression of hypoxia inducible factor 1α(HIF-1α) protein and the activation of phosphoinositid 3-kinase/Akt(PI3K/Akt) signaling pathway in neurons under hypoxia ischemia condition,and to elucidate the role of PI3K/Akt on HIF-1α regulation in the developing neurons after hypoxia ischemia brain damage(HIBD).Methods Fifty-six SD rats aged 10 days were randomly divided into normal control group(n=12),sham operation group(n=12),experimental group(n=24),wortmannin treated group(n=4) and DMSO/PBS treated group(n=4).In the experimental group,the rats were anesthetized with ethylether.The right common carotid artery was exposed and ligated.Then,they were exposed to hypoxia in a normobaric chamber lled with 8% oxygen and 92% nitrogen for 2.5 hours.In the sham control group,the right common carotid artery was exposed but was not ligated or exposed hypoxia.In the normal control group,the rats recevied no further processing.For wortmannin treated group and DMSO/PBS treated group,the rats received intraventricular injection of wortmannin or DMSO/PBS 30 minutes before hypoxia ischemia.The brain tissues were harvested from the rats in the normal control,sham operation and experimental groups at 4,8 and 24 hours after hypoxia ischemia,but in the wortmannin and DMSO/PBS treated groups only at 4 hours.The HIF-1α protein expression and Akt protein expression were detected with immunohistochemistry method.HIF-1α,Akt and p-Akt protein expression were measured by Western blot analysis.Results In the experimental group,the HIF-1α expression was signi cantly increased at 4 hours after operation,reached the peak level at 8 hours,and began to decrease at 24 hours.The p-Akt protein was signi cantly increased at 4 hours,and began to decrease at 8 hours.However,the expression levels of HIF-1α and p-Akt protein in the normal control group wereextremely low at each time point.So,the expression levels of HIF-1α in the experimental group was signi cantly higher than that in the normal control groups(P 0.01),the expression of p-Akt protein in the experimental group at 4 and 8 hours was signi cant higher than that in the normal control group(P 0.05).The change of Akt protein in the experimental group was not time-dependent,and no signi cant di erence was evident when compared with that of the normal control group(P 0.05).Using wortmannin,the PI3K/Akt speci c inhibitor,HIF-1α protein expression was signi cantly decreased when compared with the DMSO/PBS treated group and experimental group(P 0.01).Conclusion These results suggested that the HIBD of neonatal rats may activate PI3K/Akt signaling pathway and further induce the expression of HIF-1α,indicating PI3K/Akt signaling pathway and HIF-1α could be a potential target for treatment of neonatal HIBD.
Wortmannin
Hypoxia
Phosphoinositide 3-kinase
Hypoxia-Inducible Factors
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Objective To investigate the effect of hypoxic preconditioning on anti-inflammatory responses of bone marrow mesenchymal stem cells (BMSCs) in rats through in vitro and in vivo experiments.Methods In vitro experiment The isolated rat BMSCs were cultured by whole bone marrow adherence method.The cells at passage 3 were seeded in 24-well plates at a density of 1 × 106 cells/ml and randomly divided into 5 groups (n =8 wells each) using a random number table:control group (group C),normoxia-incubated group (group N),hypoxic preconditioning group (group H),hypoxia preconditioning + STAT3 inhibitor Stattic group (group HS) and hypoxia preconditioning + anti-IL-10 monoclonal antibody group (group HA).In group C,BMSCs were incubated in DMEM culture medium.In group N,BMSCs were exposed to21％ O2-74％ N2-5.0％ CO2 for48 h.In group H,BMSCs were exposed to 0.5％ O2-94.5％ N2-5.0％ CO2 for 24 h followed by 24 h exposure to normoxia.In HS and HA groups,500 μg/ml Stattic and 100 μg/rnl anti-IL-10 monoclonal antibody were added to the culture medium before hypoxia preconditioning,respectively.The expression of phosphorylated STAT3 (p-STAT3) and IL-10 was determined by Western blot.In vivo experiment Healthy male Sprague-Dawley rats,weighing 300-350 g,in which intrathecal catheters were successfully implanted without complications,underwent spinal cord ischemia by occlusion of the thoracic aorta combined with controlled hypotension.Three hundred rats with spinal cord I/R injury were randomly divided into C,N,H,HS and HA groups (n =60 each) using a random number table.Immediately after onset of reperfusion,DMEM medium 300 μl was injected intrathecally in group C,and BMSC suspension 300 μl (1 × 106 cells/ml) was injected intrathecally in N,H,HS and HA groups.Neurological function was scored before ischemia and at 4,12,24 and 48 h of reperfusion (T0-,).The animals were then sacrificed and the lumbar segment of spinal cord was removed for detection of the content of IL-10,TNF-α,IL-1β,IL-6,monocyte chemotactic protein-1 (MCP-1),and macrophage inflammatory protein-1 α (MIP-1 α) (by ELISA) and the number of activated microglia (by immuno-histochemistry).Results Compared with C and N groups,the expression of pSTATβ and IL-10 was significantly up-regulated,the neurological function score and IL-10 content were increased,the content of TNF-α,IL-1β,IL-6,MCP-1 and MIP-1α and the number of activated microglia were decreased in group H (P ＜ 0.05).Compared with group H,the expression of p-STAT3 and IL-10 in group HS and expression of IL-10 in group HA was significantly down-regulated,and the neurological function score and IL-10 content were decreased,and the content of TNF-α,IL-13,IL-6,MCP-1 and MIP-1α and the number of activated microglia were increased in HS and HA groups (P ＜ 0.05).Conclusion Hypoxic preconditioning can enhance anti-inflammatory effects of BMSCs,thus increasing BMSCs-induced reduction of spinal cord ischemia-reperfusion injury in rats.
Key words:
Cell hypoxia; Ischemica preconditioning; Mesenchymal stem cells transplantation ; Spinal cord ; Inflammation
Hypoxia
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Objective
To evaluate the effect of Tanshinonne ⅡA preconditioning on nuclear factor kappa B (NF-κB) signaling pathway in N9 cells subjected to oxygen-glucose deprivation and restoration (OGD/R).
Methods
N9 cells cultured in vitro were divided into 4 groups (n=16 each) by using a random number table method: control group (C group), OGD/R group, vehicle group (V group) and Tanshinone IIA preconditioning group (TP group). N9 cells were subjected to O2-glucose deprivation for 4 h followed by restoration of O2-glucose supply for 24 h to establish the OGD/R model.Group C receive no treatment.In group TP, N9 cells were cultured in medium containing Tanshinone ⅡA (final concentration 5 mg/L) for 24 h before the model was established.Dimethyl sulfoxide was added to the culture medium in group V. At the 24 h of reoxygenation, the level of lactate dehydrogenase (LDH) and nitric oxide(NO)in culture medium was detected by spectrophotometry, cell apoptosis was assessed by using TUNEL, and the expression of NF-κB in nucleus was detected by Western blot.The apoptosis rate was calculated.
Results
Compared with group C, the levels of LDH, IL-β, TNF-α and NO in culture medium and apoptosis rate were significantly increased, and the expression of NF-κB in nucleus was up-regulated in OGD/R, V and TP groups (P 0.05).
Conclusion
The mechanism by which Tanshinonne ⅡA preconditioning reduces OGD/R injury to N9 cells is related to inhibiting NF-κB signaling pathway.
Key words:
TANSHINONE; Hypoxia-ischemia, brain; NF-kappa B
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Objective To investigate the effects of hydrogen gas on the myocardial injury in rats with endotoxemia.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 4 groups (n =12 each ):control group (group C ),hydrogen gas control group (group HC ),endotoxemia group (group E) and hydrogen gas + endotoxemia group (group LH).Endotoxemia was induced by intraperitoneal lipopolysaccharide (LPS) 20 mg/kg in groups E and LH,while the equal volume of normal saline was given in groups C and HC.After LPS administration,the rats were exposed to the air containing 2％ hydrogen gas for 6 h in groups HC and LH,and the rats were exposed to the air for 6 h in groups C and E.Blood samples were taken from the abdominal aorta after 6 h inhalation of hydrogen gas to determine the serum level of cTnI.The hearts were then removed to determine the content of TNF-α and IL-6 and expression of phosphorylated nuclear factor κB ( NF-κB) inhibitory protein (p-IκB-α) and p38 mitogen-activated protein kinase (p-p38MAPK) in the myocardial tissues.Results Compared with group C,no significant change was found in the levels of cTnI,TNF-α and IL-6 and expression of p-IκB-α and p-p38MAPK in group HC ( P ＞ 0.05),and the levels of cTnI,TNF-α and IL-6 were significantly increased and the expression of p-IκB-α and p-p38MAPK was up-regulated in groups E and LH ( P ＜ 0.05).Compared with group E,the levels of cTnI,TNF-α and IL-6 were significantly decreased and the expression of p-IκB-α and p-p38MAPK was down-regulated in group LH ( P ＜ 0.05).Conclusion Hydrogen gas can reduce the myocardial injury in rats with endotoxemia,and inhibition of the p38MAPK and NF-κB pro-inflammatory pathway and reduction of the inflammatory response of myocardial tissues are involved in the mechanism.
Key words:
Hydrogen; Toxemia; Myocardium
Intraperitoneal injection
Group A
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Objective
To explore the anti-inflammatory effect of dexmedetomidine(Dex) in attenuating hypoxia/reoxgenation(H/R) injury of H9C2 cells.
Methods
Rat cardiomyocyte cell line H9C2 cells were cultured in vitro, and Na2S2O4 was used to establish the hypoxia and reoxygenation injury model on H9C2 cells. Cultured H9C2 cells were divided into three groups: normal control group (group C), the cells were cultured as usual, group H/R, the cells were subjected to 1 h hypoxia induced by 4 mmol/L Na2S2O4, then followed by 12 h reoxygenation by replaced the normal media, Dex preconditioning group (group D), Dex at various concentrations(0.1, 1.0, 10.0 μmol/L) was performed prior to Na2S2O4-induced H/R injury, the rest of the steps are essentially the same as the group H/R. The cell survival rate 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyltetrazolium bromide(MTT) and lactate dehydrogenase(LDH) activity were detected after treatment, the cellular morphology was observed by inverted miscroscope, the TNF-α, IL-6, IL-1β mRNA expression were detected by reverse transcription-polymerase chain reaction(RT-PCR).
Results
Compared with the group C, the cell survival of group H/R decreased to(44±12)%(P<0.01), LDH activity increased significantly(P<0.01), compared with the group H/R, the cell survival rate and LDH activity of the group D were improved, Dex at 1 μmol/L concentration preconditioning significantly restored cell viability to(75±7)%(P<0.05) and reduced the activity of LDH significantly(P<0.05). The condition of cell necrosis, irregular cell arrangement, and the decline of cell membrane refractive index caused by H/R injury were partly reversed by Dex. Compared with the group C, the TNF-α, IL-6, IL-1β mRNA expression level of the group D and the group H/R increased significantly. Compared with group H/R, the TNF-α, IL-6, IL-1β mRNA expression levels of group D decreased significantly(P<0.05).
Conclusions
Dex preconditioning attenuates hypoxia and reoxygenation injury of H9C2 cells. The mechanism may be related to inhibiting inflammatory reaction.
Key words:
Dexmedetomidine; Proconditioning; Hypoxia/reoxygenation injury; Inflammatory response
Hypoxia
Viability assay
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Objective To study the protective effect of polydatin (PD) on hypoxia/re-oxygenation induced HK2 cell injury in vitro. Methods Human kidney proximal tubular epithelial cell line HK2 cell was used as target cell. The cells were divided into 4 groups: control group, model group, pyrrolidine dithiocarbamate (PDTC) group and PD group. Except the control group, the cells in the other three groups were exposed to hypoxia for 24 h, 30 min before which PD and PDTC were respectively added to the culture media of PDTC group and PD group, then to normoxia for 6 h. Cell survival was assessed by MTT, the protein expression of nuclear factor-κB (NF-κB) p65 was measured by immunohistochemistry, the mRNA and protein expressions of ICAM-1 were measured by RT-PCR and ELISA respectively. Results The HK2 survival cells were significantly more in PD treatment group than those in model group (P0.05). The NF-κB p65 expressions, ICAM-1 mRNA transcriptions and protein expressions of HK2 cells, were significantly decreased in PD treatment group compared with those in control group (P0.05). There were no significant differences of the parameters mentioned above were found between the PDTC group and the PD group (P0.05). Conclusion Polydatin has a protective effect on hypoxia/re-oxygenation induced HK2 cell injury, presumably via inhibiting the activation of NF-κB, downregulating the ICAM-1 mRNA transcription and protein expression on the surface of HK2 and finally reducing the adhesion of polymorphonuclear neutrophils.
Pyrrolidine dithiocarbamate
Hypoxia
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To investigate the expression of p38 mitogen-activated protein kinase (MAPK) in hyperoxic lung injury (HLI), and explore the protective effect of N-acetylcysteine (NAC) on HLI and its mechanism.Thirty Wistar rats aged 3 weeks old were divided into five groups with 6 rats in each group according to random digits table: room-air group (A), hyperoxia injury group (B), hyperoxia+NAC group (C), hyperoxia+p38 MAPK inhibitor (SB203580) group (D), hyperoxia+NAC+SB203580 group (E). Rats in NAC groups were injected with NAC (200 mg/kg) intraperitoneally, and they received an intravenous injection of SB203580 (0.5 mg/kg) in SB203580 groups. The animals were sacrificed after 7 days of experiment. Lung pathology and grade of lung tissue injury were examined with light microscopy, lung wet/dry (W/D) ratio, total protein (TP) level in bronchoalveolar lavage fluid (BALF) and permeability coefficient were evaluated. The location and quantity of phosphorylation p38 MAPK (p-p38 MAPK) protein were detected by immunohistochemistry and Western blotting analysis respectively.The pathological changes in the lung in B group included severe alveolar oedema with inflammatory cells aggregation and red blood cell leakage, while the lung pathological pictures in C, D, E groups were improved significantly compared with B group. p-p38 MAPK positive cells increased in B group compared with those in A group, involving many types of pulmonary cells, especially in infiltrating inflammatory cells. In C, D, E groups, the positive cells remarkably decreased compared with B group. p-p38 MAPK content was higher in B group than that in A group (0.20+/-0.03 vs. 0.11+/-0.01, P<0.05), and p-p38 MAPK expressions in C, D, E groups decreased significantly compared with B group (0.16+/-0.02, 0.15+/-0.01, 0.14+/-0.02 vs. 0.20+/-0.03, all P<0.05), but were higher than those in A group (all P<0.05). There was no significant difference in p-p38 MAPK quantity among three groups. Changes in W/D ratio, TP and permeability coefficient among groups were comparable with those of p-p38 MAPK protein quantity.Reactive oxygen species (ROS) activated p38 MAPK signaling pathway. NAC may exert a protective effect on HLI through attenuation of hyperoxia-induced p38 MAPK activation.
Hyperoxia
Group B
Group A
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Objective To investigate the effects of diazoxide pretreatment on the expression of hypoxia-inducible factor-1α (HIF-1α) mRNA and p53 mRNA in rat myocardial microvascular endothelial cells exposed to hypoxia-reoxygenation (H/R).Methods The SD rat myocardial microvascular endothelial cells were cultured. The cells were seeded in 96-well plates ( 100 μl/hole) or in 6 cm diameter dishes (2 ml/dish) with the density of 1 ×106/ml and randomly divided into 4 groups ( n = 24 each): normal control group (group C), H/R group, H/R +diazoxide pretreatment group (group DZ) and H/R + diazoxide pretreatment + mitochondrial ATP-sensitive potassium channel blocker 5-hydroxydecanoate (5-HD) group (group DZ + 5-HD). The cells were exposed to 2 h hypoxia followed by 2 h reoxygenation. Diazoxide 100 μmol/L and diazoxide 100 μmol/L + 5-HD 100 μmol/L were added to the culture medium 2 h before hypoxia in DZ and DZ + 5-HD groups respectively. The cell vitality, apoptotic rate and expression of HIF-1α mRNA and p53 mRNA were detected at the end of reoxygenation. Results Compared with group C, the cell vitality was significantly decreased, apoptotic rate increased and the expression of HIF- 1α mRNA and p53 mRNA up-regulated in H/R group ( P ＜ 0.01). Compared with group H/R, the cell vitality was significantly increased, apoptotic rate decreased, the expression of HIF-1α mRNA up-regulated and the expression of p53 mRNA down-regulated in group DZ ( P ＜ 0.05 or 0.01 ). 5-HD could inhibit diazoxide pretreatment-induced changes mentioned above (P ＜ 0.05 ). Conclusion Diazoxide pretreatment can reduce H/R injury in rat myocardial microvascular endothelial cells through up-regulating the expression of HIF-1α and down-regulating the expression of p53, and the mechanism is related to activation of mitochondrial ATP-sensitive potassium channels.
Key words:
Dazoxide; Heart; Endothelium, vascular; Oxygen; Cell hpoxia; Hypoxia-inducible factor 1, alpha subunit; Tumor suppressor protein p53
Diazoxide
Hypoxia
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To investigate the expression of hypoxia inducible factor 1alpha (HIF-1alpha) protein and the activation of phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathway in neurons under hypoxia ischemia condition, and to elucidate the role of PI3K/Akt on HIF-1alpha regulation in the developing neurons after hypoxia ischemia brain damage (HIBD).Fifty-six SD rats aged 10 days were randomly divided into normal control group (n=12), sham operation group (n=12), experimental group (n=24), wortmannin treated group (n=4) and DMSO/PBS treated group (n=4). In the experimental group, the rats were anesthetized with ethyl ether. The right common carotid artery was exposed and ligated. Then, they were exposed to hypoxia in a normobaric chamber filled with 8% oxygen and 92% nitrogen for 2.5 hours. In the sham control group, the right common carotid artery was exposed but was not ligated or exposed hypoxia. In the normal control group, the rats received no further processing. For wortmannin treated group and DMSO/PBS treated group, the rats received intraventricular injection of wortmannin or DMSO/PBS 30 minutes before hypoxia ischemia. The brain tissues were harvested from the rats in the normal control, sham operation and experimental groups at 4, 8 and 24 hours after hypoxia ischemia, but in the wortmannin and DMSO/PBS treated groups only at 4 hours. The HIF-1alpha protein expression and Akt protein expression were detected with immunohistochemistry method. HIF-1alpha, Akt and p-Akt protein expression were measured by Western blot analysis.In the experimental group, the HIF-1alpha expression was significantly increased at 4 hours after operation, reached the peak level at 8 hours, and began to decrease at 24 hours. The p-Akt protein was significantly increased at 4 hours, and began to decrease at 8 hours. However, the expression levels of HIF-1alpha and p-Akt protein in the normal control group were extremely low at each time point. So, the expression levels of HIF-1alpha in the experimental group was significantly higher than that in the normal control groups (P < 0.01), the expression of p-Akt protein in the experimental group at 4 and 8 hours was significant higher than that in the normal control group (P < 0.05). The change of Akt protein in the experimental group was not time-dependent, and no significant difference was evident when compared with that of the normal control group (P > 0.05). Using wortmannin, the PI3K/Akt specific inhibitor, HIF-1alpha protein expression was significantly decreased when compared with the DMSO/PBS treated group and experimental group (P < 0.01).These results suggested that the HIBD of neonatal rats may activate PI3K/Akt signaling pathway and further induce the expression of HIF-1alpha, indicating PI3K/Akt signaling pathway and HIF-1alpha could be a potential target for treatment of neonatal HIBD.
Wortmannin
Hypoxia
Phosphoinositide 3-kinase
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Objective To investigate the effects of extracellular signal-regulated kinases (ERK1/2) signaling pathway on the expression of heme oxygenase-1 (HO-1) in acute lung injury of endotoxic shock induced by lipopolysaccharide (LPS) in rats.Methods Forty-eight pathogen-free male SD rats weighing 180 g-200 g were randomly divided into 4 groups (n=12 each):sham operation group (group S),endotoxic shock group (group SS),endotoxic shock and PD98059 group (group SE) and PD98059 group (group E).Rats in group S and group SS were administrated with DMSO 0.1 ml intravenously.Rats in Group SE and group E were injected with the inhibitor of ERK1/2 (PD98059) in 0.1 ml DMSO intravenously.30 min later,rats in Group S and group E received 0.5 ml normal saline intravenously while rats in group SS and group SE received LPS 10 mg/kg in 0.5 ml normal saline intravenously.The invasive arterial pressure was monitored,if there was an initial 25％ decrease in mean arterial pressure,then the model can be put to use.The lung injury degree was judged by microscopic examination,moisture content,malondialdehyde (MDA) content and superoxide dismutase (SOD) activity.The ERK1/2 protein,p-ERK1/2 protein and HO-1 protein were measured by Western blot.HO-1 mRNA level were measured by RT-PCR.Results The grade of the pathology (4.5 ±2.1),MDA content (3.12±1.30) nmol/mg,moisture content(81±6)％ in group SS were significantly higher than that in group S (2.0±1.0),(78±5)％,(1.79±0.12) nmol/mgand group E (2.1±1.1),(77±4)％,(1.83±-0.20) nmol/mg,(P＜0.05).But significantly lower than that in group SE(6.4±1.3),(87±5)％,(4.62±0.92) nmol/mg (P＜0.05).The SOD activity in group SS (20.2±2.4) NU/mg were significantly lower than that in group S (30.9± 2.9) NU/mgand group E (32.2±1.2) NU/mg(P＜0.05),but significantly higher than that in group SE(14.9±3.2) NU/mg(P＜0.05).ERK1/2 protein (0.43±0.09) and p-ERK1/2 protein (1.46 ±0.22),HO-1mRNA (1.834± 0.023) and HO-1 protein (1.17± 0.25) in group SS were significantly higher than that in group S,group SE and group E (P＜0.05).And there were no significant difference in group S and group P among all the indexes (P＞0.05).Conclusions Using the inhibitor of ERK1/2 signaling pathway in endotoxic shock rats worsened lung injury,and its mechanism may be related to decreased HO-1 expression by inhibition of ERK1/2 signaling pathway.
Key words:
Extracellular signal-regulated kinases; Endotoxic shock; Lung; Heme oxygenase-1
Malondialdehyde
Group A
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