Hypoxic preconditioning relieved ischemic cerebral injury by promoting immunomodulation and microglia polarization after middle cerebral artery occlusion in rats

Wu, Shizheng; Li, Hao; Dang, Zhancui; Wu, Yue

doi:10.1016/j.brainres.2019.146388

Cited by 20 publications

(15 citation statements)

References 45 publications

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“…Microglia commonly exhibit a neural-specific phenotype and retain a relatively quiescent surveillance phenotype to constantly monitor the brain parenchyma [24][25][26] . During the process of neurological inflammation, microglial cells perform different functions through polarization towards different phenotypes 27 . In our study, the lncRNA NEAT1 may have inhibited microglial polarization towards the pro-inflammatory (M1) phenotype; however, the detailed mechanism by which the lncRNA NEAT1 controls microglia M1 is not clear and requires further study.…”

Section: Discussionmentioning

confidence: 99%

Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion

Xia

et al. 2020

Sci Rep

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Acute cerebral ischaemia may lead to serious consequences, including brain injury caused by uncontrolled reperfusion, which occurs when circulation is re-established. The long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) plays an important role in the immune system. However, the potential roles and underlying molecular mechanisms of NEAT1 in cerebral ischaemia/reperfusion (I/R) injury remain unclear. The aim of the present study was to investigate the function of the lncRNA NEAT1 in cerebral I/R injury and its potential beneficial effects on neurons. In our study, oxygen–glucose deprivation (OGD)/reoxygenation (OGD/R) was induced in vitro to mimic cerebral I/R injury. Cholecystokinin-octopeptide (CCK-8) was used to measure cell viability, and flow cytometry was used to measure cell apoptosis. Real-time quantitative PCR (qRT-PCR) was used to measure the expression of phenotypic markers of classically activated (M1) and alternatively activated (M2) microglia, and western blotting was performed to detect the levels of proteins related to the AKT/STAT3 pathway. The expression of the lncRNA NEAT1 was significantly upregulated in patients with ischaemic stroke, and knockdown of the lncRNA NEAT1 alleviated OGD/R-induced apoptosis and increased neuronal viability. Furthermore, the lncRNA NEAT1 may inhibit microglial polarization towards the M1 phenotype to reduce the damage caused by OGD/R and reduce the activity of the AKT/STAT3 pathway. In conclusion, the lncRNA NEAT1 may be a potential target for new therapeutic interventions for cerebral I/R.

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Section: Discussionmentioning

confidence: 99%

Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion

Xia

et al. 2020

Sci Rep

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“…Rats were housed in a controlled environment with a 12 hr light–dark cycle and were randomly divided into four groups, including sham, HPC, HPC + MCAO, and MCAO groups ( n = 8). The procedures for HPC and MCAO induction wereas previously described (Huang, Wu, Li, Dang, & Wu, 2019). Simply, Oxygen pressure and barometric pressure were, respectively, adjusted as 42 mmHg and 0.53 × 10 5 Pa in a specific controlled environment, forming hypoxic environment.…”

Section: Methodsmentioning

confidence: 99%

Hypoxic preconditioning ameliorated neuronal injury after middle cerebral artery occlusion by promoting neurogenesis

et al. 2020

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Neuronal death and neurologic deficits are the major causes of disability in patients following cerebral infarction. Acute/programmed necrosis, autophagy, and apoptosis of brain neurons result from complex biochemical events triggered by stroke. Current treatments for cerebral infarction are limited; therefore, the development of effective treatment strategies would be of great value. At present, delivering

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“…Hypoxic preconditioning refers to a certain intensity and time of hypoxic exposure before hypoxic stress, which makes the body produce endogenous protection to enhance the body's tolerance to subsequent more severe hypoxia (7). Studies in animal models have shown that hypoxic preconditioning can reduce hypoxic damage and play a neuroprotective role in neonatal rats (8), and can significantly increase the exercise capacity of the rats in a hypoxic environment after hypoxic preconditioning (9).…”

Section: Introductionmentioning

confidence: 99%

Effects of hypoxic preconditioning combined with altitude training on CD55, CD59 and the immune function of swimmers

2021

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Background: Hypoxic preconditioning refers to a certain intensity and time of hypoxic exposure before hypoxic stress, which makes the body produce endogenous protection to enhance the body's tolerance to subsequent more severe hypoxia. However, there are few studies on the effects of hypoxic preconditioning combined with altitude training on the immune system of athletes. Methods: Nine swimmers from Shanghai underwent 3-week hypoxic preconditioning [living high-training low (HiLo)] combined with 3-week altitude training. CD55 and CD59 expression in red blood cells (RBCs), CD55 and CD59 expression in white blood cells (WBCs), RBC count, WBC count, T lymphocyte CD3, CD4, CD8 expression, and immunoglobulins IgG, IgM, and IgA were measured 4 times: before the start of hypoxic preconditioning, in the first week of hypoxic preconditioning, at the end of hypoxic preconditioning (i.e., before the start of altitude training), and at the end of altitude training. Results: CD55 and CD59 expression in RBCs significantly increased in the first week of hypoxic preconditioning (P<0.05), returned to baseline levels at the end of preconditioning, and significantly increased again during altitude training (P<0.05). CD55 and CD59 expression in WBCs decreased significantly during hypoxic preconditioning (P<0.05) and increased significantly during altitude training (P<0.05). CD3 expression first decreased and then increased in the hypoxic preconditioning phase, then decreased again in the altitude training phase. However, there was no significant difference in each phase. CD4/CD8 expression after altitude training was significantly lower than that before altitude training (P<0.05), but was not significantly different from that before the start of hypoxic preconditioning. IgG, IgM, and IgA did not fluctuate significantly throughout the experimental phase. Conclusions: After hypoxic preconditioning combined with altitude training, the expression of CD55 and CD59 on the surface of RBCs and WBCs increased significantly, and T lymphocyte CD4/CD8 expression also increased. These results suggest an improvement in the complement regulation system and RBC immune function. Hypoxic preconditioning can therefore improve immunity and enhance the physical function of athletes during altitude training.

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Hypoxic preconditioning relieved ischemic cerebral injury by promoting immunomodulation and microglia polarization after middle cerebral artery occlusion in rats

Cited by 20 publications

References 45 publications

Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion

Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion

Hypoxic preconditioning ameliorated neuronal injury after middle cerebral artery occlusion by promoting neurogenesis

Effects of hypoxic preconditioning combined with altitude training on CD55, CD59 and the immune function of swimmers

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