Establishment of an experimental rat model of high altitude cerebral edema by hypobaric hypoxia combined with temperature fluctuation

Jing, Lin-Lin; Wu, Ningzi; He, Lei; Shao, Jin; Ma, Hui‐Ping

doi:10.1016/j.brainresbull.2020.10.017

Cited by 13 publications

(6 citation statements)

References 47 publications

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“…Another study discovered that increased MDA content and decreased SOD activity in rat brain tissue significantly induced BBB hyperpermeability in the rat ischemia-reperfusion injury model [ 45 ]. The increase in the H 2 O 2 level induced BBB hyperpermeability in the rat model of high-altitude cerebral edema [ 46 ]. Collectively, the increased oxidative stress levels and proinflammatory cytokine levels might degrade ECM and TJs proteins and then induce BBB damage.…”

Section: Discussionmentioning

confidence: 99%

Rac1/Wave2/Arp3 Pathway Mediates Rat Blood-Brain Barrier Dysfunction under Simulated Microgravity Based on Proteomics Strategy

Yan¹,

Liu²,

Lv³

et al. 2021

IJMS

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The blood-brain barrier (BBB) is critical to maintaining central nervous system (CNS) homeostasis. However, the effects of microgravity (MG) on the BBB remain unclear. This study aimed to investigate the influence of simulated MG (SMG) on the BBB and explore its potential mechanism using a proteomic approach. Rats were tail-suspended to simulate MG for 21 days. SMG could disrupt the BBB, including increased oxidative stress levels, proinflammatory cytokine levels, and permeability, damaged BBB ultrastructure, and downregulated tight junctions (TJs) and adherens junctions (AJs) protein expression in the rat brain. A total of 554 differentially expressed proteins (DEPs) induced by SMG were determined based on the label-free quantitative proteomic strategy. The bioinformatics analysis suggested that DEPs were mainly enriched in regulating the cell–cell junction and cell–extracellular matrix biological pathways. The inhibited Ras-related C3 botulinum toxin substrate 1 (Rac1)/Wiskott–Aldrich syndrome protein family verprolin-homologous protein 2 (Wave2)/actin-related protein 3 (Arp3) pathway and the decreased ratio of filamentous actin (F-actin) to globular actin contributed to BBB dysfunction induced by SMG. In the human brain microvascular endothelial cell (HBMECs), SMG increased the oxidative stress levels and proinflammatory cytokine levels, promoted apoptosis, and arrested the cell cycle phase. Expression of TJs and AJs proteins were downregulated and the distribution of F-actin was altered in SMG-treated HBMECs. The key role of the Rac1/Wave2/Arp3 pathway in BBB dysfunction was confirmed in HBMECs with a specific Rac1 agonist. This study demonstrated that SMG induced BBB dysfunction and revealed that Rac1/Wave2/Arp3 could be a potential signaling pathway responsible for BBB disruption under SMG. These results might shed a novel light on maintaining astronaut CNS homeostasis during space travel.

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Section: Discussionmentioning

confidence: 99%

Rac1/Wave2/Arp3 Pathway Mediates Rat Blood-Brain Barrier Dysfunction under Simulated Microgravity Based on Proteomics Strategy

Yan¹,

Liu²,

Lv³

et al. 2021

IJMS

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“…Herein, this stress leads to the production of ROS and providently weakens the antioxidant defense system. Hence, evidence reported that HACE under oxidative insult causes destruction of BBB structural formation and finally leads to cellular swelling [11]. HIF-1α is abundantly known as the master regulator in response to any hypoxic changes that stimulate cellular adaptation in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, we examined the VEGF and HIF-1α expression by qRT-PCR that induced by AHH in the brain, showed that the cerebral tissue opposed the AHH brain injury by up-regulating the hypoxia-inducible factor and angiogenesis by increasing the consumption of oxygen and certain nutrients in response to compensate the hypoxia mechanism. Herein, VEGF is a well-known mediator engaged in BBB permeability, vascular leakage, and angiogenesis induced by AHH [5,11].…”

Section: Discussionmentioning

confidence: 99%

Experimental Brain Injury Induced by Acute Hypobaric Hypoxia Stimulates Changes in mRNA Expression and Stress Marker Status

Tahir

Almezgagi

2021

Int J Res Rev

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The present study was proposed to investigate the brain injury under acute hypobaric hypoxia following alteration in mRNA expression and stress markers in a time-dependent manner. SD clean graded male rats were randomly divided into four groups for this experimental brain injury, the control group at Xining (altitude, 2270m) and hypoxia treatment groups with different time exposure day1, day2, and day3 at (altitude, 7000m) in a hypobaric chamber. After day3 exposure, the brain tissues were collected. The level of mRNA expression of VEGF and HIF1-α was assessed using qRT-PCR. The oxidative stress level of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined with commercial kits. AHH with time duration significantly increased the MDA level and decreased in the activity of SOD was seen in all hypoxia treated groups as compared to the control (P< 0.001). The mRNA expression level of HIF1-α and VEGF in day1, day2, and day3 AHH groups was markedly raised when it is compared to control (P< 0.05). Ultimately, in conclusion, such results indicate that AHH stimulates oxidative stress induces brain damage in rats. Keywords: Acute hypobaric hypoxia, Brain injury, HIF-1α, Oxidative stress.

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“…MDA is an end product of oxygen free radicals reacting with unsaturated fatty acids in the cell membrane, and it is commonly employed as a marker of lipid peroxidation [26]. Its content can reflect the severity of cell damage; as the cells are damaged by ROS, the content of MDA increased [27]. Similarly, protein carbonylation content is regarded as a biomarker of oxidative stress [28].…”

Section: Psgrx Positively Regulates the Response To Low Temperaturementioning

confidence: 99%

“…Taken together, these results indicated that psgrx was considered to be involved in low-temperature regulation and acted as a positive regulator of low-temperature tolerance to ANT206. MDA is an end product of oxygen free radicals reacting with unsaturated fatty acid in the cell membrane, and it is commonly employed as a marker of lipid peroxidation [26] Its content can reflect the severity of cell damage; as the cells are damaged by ROS, th content of MDA increased [27]. Similarly, protein carbonylation content is regarded as a biomarker of oxidative stress [28].…”

Section: Psgrx Positively Regulates the Response To Low Temperaturementioning

confidence: 99%

Glutaredoxin Interacts with GR and AhpC to Enhance Low-Temperature Tolerance of Antarctic Psychrophile Psychrobacter sp. ANT206

Wang

Hou

et al. 2022

IJMS

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Glutaredoxin (Grx) is an important oxidoreductase to maintain the redox homoeostasis of cells. In our previous study, cold-adapted Grx from Psychrobacter sp. ANT206 (PsGrx) has been characterized. Here, we constructed an in-frame deletion mutant of psgrx (Δpsgrx). Mutant Δpsgrx was more sensitive to low temperature, demonstrating that psgrx was conducive to the growth of ANT206. Mutant Δpsgrx also had more malondialdehyde (MDA) and protein carbonylation content, suggesting that PsGrx could play a part in the regulation of tolerance against low temperature. A yeast two-hybrid system was adopted to screen interacting proteins of 26 components. Furthermore, two target proteins, glutathione reductase (GR) and alkyl hydroperoxide reductase subunit C (AhpC), were regulated by PsGrx under low temperature, and the interactions were confirmed via bimolecular fluorescence complementation (BiFC) and co-immunoprecipitation (Co-IP). Moreover, PsGrx could enhance GR activity. trxR expression in Δpsgrx, Δahpc, and ANT206 were illustrated 3.7, 2.4, and 10-fold more than mutant Δpsgrx Δahpc, indicating that PsGrx might increase the expression of trxR by interacting with AhpC. In conclusion, PsGrx may participate in glutathione metabolism and ROS-scavenging by regulating GR and AhpC to protect the growth of ANT206. These findings preliminarily suggest the role of PsGrx in the regulation of oxidative stress, which could improve the low-temperature tolerance of ANT206.

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Establishment of an experimental rat model of high altitude cerebral edema by hypobaric hypoxia combined with temperature fluctuation

Cited by 13 publications

References 47 publications

Rac1/Wave2/Arp3 Pathway Mediates Rat Blood-Brain Barrier Dysfunction under Simulated Microgravity Based on Proteomics Strategy

Rac1/Wave2/Arp3 Pathway Mediates Rat Blood-Brain Barrier Dysfunction under Simulated Microgravity Based on Proteomics Strategy

Experimental Brain Injury Induced by Acute Hypobaric Hypoxia Stimulates Changes in mRNA Expression and Stress Marker Status

Glutaredoxin Interacts with GR and AhpC to Enhance Low-Temperature Tolerance of Antarctic Psychrophile Psychrobacter sp. ANT206

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