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Limb remote ischemic postconditioning protects cerebral ischemia from injury associated with expression of HIF-1α in rats.

Zong Y, Jiang L, Zhang M, Zhou F, Qi W, Li S, Yang H, Zou Y, Xia Q, Zhou X, Hu X, Wang T - BMC Neurosci (2015)

Bottom Line: However, whether the neuroprotective effect of LRIP could be associated with HIF-1α is somewhat unclear.Here we tested the hypothesis that Limb remote ischemic postconditioning (LRIP) protecting brain from injury in middle cerebral artery occlusion (MCAO) rat model was associated with HIF-1α expression.Meanwhile, the result of Q-PCR and western blot revealed that the overexpression of HIF-1α induced by IRI could be notably suppressed by LRIP treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Morphology Lab and Department of Graduate, Chengdu Medical College, Sichuan, 610500, China. 18203228814@163.com.

ABSTRACT

Background: Limb remote ischemic postconditioning (LRIP) can ameliorate cerebral ischemia-reperfusion injury (IRI), while the underlying mechanism remains elusive. Hypoxia-inducible factor 1α (HIF-1α) is an important transcription factor during cerebral ischemia damage. However, whether the neuroprotective effect of LRIP could be associated with HIF-1α is somewhat unclear. Here we tested the hypothesis that Limb remote ischemic postconditioning (LRIP) protecting brain from injury in middle cerebral artery occlusion (MCAO) rat model was associated with HIF-1α expression.

Results: LRIP was conducted with 3 cycles of 10 min occlusion/10 min reperfusion at the beginning of reperfusion. The analysis of neurobehavioral function and triphenyltetrazolium chloride (TTC) staining showed the neurological deficit, brain infarct and cerebral edema, caused by ischemia-reperfusion injury (IRI), were dramatically ameliorated in LRIP administrated animals. Meanwhile, the result of Q-PCR and western blot revealed that the overexpression of HIF-1α induced by IRI could be notably suppressed by LRIP treatment.

Conclusions: LRIP exhibits a protective effect against cerebral ischemia/reperfusion and the possible mechanism is associated with the suppression of HIF-1α in stroke rats.

No MeSH data available.


Related in: MedlinePlus

Immunohistochemical staining for HIF-1α in ischemic cerebral cortex at 3d reperfusion after MCAO injury. a Immunofluorescence double staining for HIF-1α/NeuN in neurons treated by LRIP. b Immunofluorescence double staining for HIF-1α/GFAP in astrocytes treated by LRIP. The immunofluorescence showed nucleus were stained by DAPI with blue color and HIF-1α were stained with green color, neurons were stained by NeuN and astrocytes were stained by GFAP with red color, and the co-expression of NeuN with HIF-1α within the same cell showed blue color (merged), the co-expression of GFAP with HFI-1α within the same cell showed white color (merged). The arrow showed double staining for HIF-1α/NeuN or HIF-1α/GFAP (scale bar = 20 μm). c HIF-1α immunoreactivity was marked with brown color in cytoplasm (scale bar = 20 μm)
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Fig3: Immunohistochemical staining for HIF-1α in ischemic cerebral cortex at 3d reperfusion after MCAO injury. a Immunofluorescence double staining for HIF-1α/NeuN in neurons treated by LRIP. b Immunofluorescence double staining for HIF-1α/GFAP in astrocytes treated by LRIP. The immunofluorescence showed nucleus were stained by DAPI with blue color and HIF-1α were stained with green color, neurons were stained by NeuN and astrocytes were stained by GFAP with red color, and the co-expression of NeuN with HIF-1α within the same cell showed blue color (merged), the co-expression of GFAP with HFI-1α within the same cell showed white color (merged). The arrow showed double staining for HIF-1α/NeuN or HIF-1α/GFAP (scale bar = 20 μm). c HIF-1α immunoreactivity was marked with brown color in cytoplasm (scale bar = 20 μm)

Mentions: In this study, we tested the activation and distribution of HIF-1α in cerebral cortex by using immunohistochemistry. As shown in Fig. 3, immunofluorescence confirmed that HIF-1α was mainly located in cytoplasm of neurons, but few in astrocytes, while ischemia injury could induce HIF-1α increase. In sham group, we showed that HIF-1α exhibited a basic expression in cortex of brain. After ischemia–reperfusion, the number of HIF-1α positive neurons was significantly increased at each time point (p < 0.05; Fig. 4). Moreover, LRIP treatment decreased effectively the number of HIF-1α positive neurons and exhibited statistic significance at 1 and 3 days (p < 0.01; Fig. 4). These showed that ischemic postconditioning could suppress the expression of HIF-1α in neurons under ischemia condition.Fig. 3


Limb remote ischemic postconditioning protects cerebral ischemia from injury associated with expression of HIF-1α in rats.

Zong Y, Jiang L, Zhang M, Zhou F, Qi W, Li S, Yang H, Zou Y, Xia Q, Zhou X, Hu X, Wang T - BMC Neurosci (2015)

Immunohistochemical staining for HIF-1α in ischemic cerebral cortex at 3d reperfusion after MCAO injury. a Immunofluorescence double staining for HIF-1α/NeuN in neurons treated by LRIP. b Immunofluorescence double staining for HIF-1α/GFAP in astrocytes treated by LRIP. The immunofluorescence showed nucleus were stained by DAPI with blue color and HIF-1α were stained with green color, neurons were stained by NeuN and astrocytes were stained by GFAP with red color, and the co-expression of NeuN with HIF-1α within the same cell showed blue color (merged), the co-expression of GFAP with HFI-1α within the same cell showed white color (merged). The arrow showed double staining for HIF-1α/NeuN or HIF-1α/GFAP (scale bar = 20 μm). c HIF-1α immunoreactivity was marked with brown color in cytoplasm (scale bar = 20 μm)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4696280&req=5

Fig3: Immunohistochemical staining for HIF-1α in ischemic cerebral cortex at 3d reperfusion after MCAO injury. a Immunofluorescence double staining for HIF-1α/NeuN in neurons treated by LRIP. b Immunofluorescence double staining for HIF-1α/GFAP in astrocytes treated by LRIP. The immunofluorescence showed nucleus were stained by DAPI with blue color and HIF-1α were stained with green color, neurons were stained by NeuN and astrocytes were stained by GFAP with red color, and the co-expression of NeuN with HIF-1α within the same cell showed blue color (merged), the co-expression of GFAP with HFI-1α within the same cell showed white color (merged). The arrow showed double staining for HIF-1α/NeuN or HIF-1α/GFAP (scale bar = 20 μm). c HIF-1α immunoreactivity was marked with brown color in cytoplasm (scale bar = 20 μm)
Mentions: In this study, we tested the activation and distribution of HIF-1α in cerebral cortex by using immunohistochemistry. As shown in Fig. 3, immunofluorescence confirmed that HIF-1α was mainly located in cytoplasm of neurons, but few in astrocytes, while ischemia injury could induce HIF-1α increase. In sham group, we showed that HIF-1α exhibited a basic expression in cortex of brain. After ischemia–reperfusion, the number of HIF-1α positive neurons was significantly increased at each time point (p < 0.05; Fig. 4). Moreover, LRIP treatment decreased effectively the number of HIF-1α positive neurons and exhibited statistic significance at 1 and 3 days (p < 0.01; Fig. 4). These showed that ischemic postconditioning could suppress the expression of HIF-1α in neurons under ischemia condition.Fig. 3

Bottom Line: However, whether the neuroprotective effect of LRIP could be associated with HIF-1α is somewhat unclear.Here we tested the hypothesis that Limb remote ischemic postconditioning (LRIP) protecting brain from injury in middle cerebral artery occlusion (MCAO) rat model was associated with HIF-1α expression.Meanwhile, the result of Q-PCR and western blot revealed that the overexpression of HIF-1α induced by IRI could be notably suppressed by LRIP treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Morphology Lab and Department of Graduate, Chengdu Medical College, Sichuan, 610500, China. 18203228814@163.com.

ABSTRACT

Background: Limb remote ischemic postconditioning (LRIP) can ameliorate cerebral ischemia-reperfusion injury (IRI), while the underlying mechanism remains elusive. Hypoxia-inducible factor 1α (HIF-1α) is an important transcription factor during cerebral ischemia damage. However, whether the neuroprotective effect of LRIP could be associated with HIF-1α is somewhat unclear. Here we tested the hypothesis that Limb remote ischemic postconditioning (LRIP) protecting brain from injury in middle cerebral artery occlusion (MCAO) rat model was associated with HIF-1α expression.

Results: LRIP was conducted with 3 cycles of 10 min occlusion/10 min reperfusion at the beginning of reperfusion. The analysis of neurobehavioral function and triphenyltetrazolium chloride (TTC) staining showed the neurological deficit, brain infarct and cerebral edema, caused by ischemia-reperfusion injury (IRI), were dramatically ameliorated in LRIP administrated animals. Meanwhile, the result of Q-PCR and western blot revealed that the overexpression of HIF-1α induced by IRI could be notably suppressed by LRIP treatment.

Conclusions: LRIP exhibits a protective effect against cerebral ischemia/reperfusion and the possible mechanism is associated with the suppression of HIF-1α in stroke rats.

No MeSH data available.


Related in: MedlinePlus