Progesterone attenuates cerebral edema in neonatal rats with hypoxic-ischemic brain damage by inhibiting the expression of matrix metalloproteinase-9 and aquaporin-4

Wang, Xiaoyin; Zhang, Junhe; Yang, Yizhuo; Dong, Weihua; Wang, Fang; Wang, Li; Li, Xiaojuan

doi:10.3892/etm.2013.1116

Cited by 44 publications

(40 citation statements)

References 26 publications

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“…HIBD, caused either in part or by total cerebral hypoxia, cerebral blood flow reduction and suspensions, is widely regarded as a key factor in central nervous system diseases 5. A progressive increase in the incidence and mortality rate of HIBD has seen the rate increasing from 1 to 8 incidences per 1000 live births 1, 6. At present, treatment options are confined to supportive care due to the complex mechanism and severity of the condition 7.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Han

Wen

Wang

et al. 2018

J Cellular Molecular Medi

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Hypoxia–ischaemia (HI) remains a major cause of foetal brain damage presented a scarcity of effective therapeutic approaches. Dexmedetomidine (DEX) and microRNA‐140‐5p (miR‐140‐5p) have been highlighted due to its potentially significant role in the treatment of cerebral ischaemia. This study was to investigate the role by which miR‐140‐5p provides cerebral protection using DEX to treat hypoxic–ischaemic brain damage (HIBD) in neonatal rats via the Wnt/β‐catenin signalling pathway. The HIBD rat models were established and allocated into various groups with different treatment plans, and eight SD rats into sham group. The learning and memory ability of the rats was assessed. Apoptosis and pathological changes in the hippocampus CA1 region and expressions of the related genes of the Wnt/β‐catenin signalling pathway as well as the genes responsible of apoptosis were detected. Compared with the sham group, the parameters of weight, length growth, weight ratio between hemispheres, the rate of reaching standard, as well as Bcl‐2 expressions, were all increased. Furthermore, observations of increased levels of cerebral infarction volume, total mortality rate, response times, total response duration, expressions of Wnt1, β‐catenin, TCF‐4, E‐cadherin, apoptosis rate of neurons, and Bax expression were elevated. Following DEX treatment, the symptoms exhibited by HIBD rats were ameliorated. miR‐140‐5p and si‐Wnt1 were noted to attenuate the progression of HIBD. Our study demonstrates that miR‐140‐5p promotes the cerebral protective effects of DEX against HIBD in neonatal rats by targeting the Wnt1 gene through via the negative regulation of the Wnt/β‐catenin signalling pathway.

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Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Han

Wen

Wang

et al. 2018

J Cellular Molecular Medi

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“…Physiologically, AQP-4 is the main channel providing water transport into the nervous system water compartments and across the BBB, while in many pathological experiments, it participates in the formation of secondary brain edema in animal models, such as brain trauma after cerebral ischemia/hemorrhage, inflammation, epilepsy, metabolic encephalopathy, and brain tumors (Papadopoulos et al, 2004; Wang et al, 2013). Nevertheless, it also caused lots of controversy about the experimental results and mechanisms.…”

Section: Discussionmentioning

confidence: 99%

N-Butylphthalide Alleviates Blood–Brain Barrier Impairment in Rats Exposed to Carbon Monoxide

Zhang

Guo

et al. 2016

Front. Pharmacol.

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Carbon monoxide (CO) poisoning is one of the most important health concerns and may result in neuropathologic changes and neurologic sequelae. However, few studies have addressed the correlation between CO poisoning and blood–brain barrier (BBB) impairment. In this study, we investigated the effects of N-butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model. The results indicated that the brain water content was obviously increased, and the tight junctions between endothelial cells were disrupted, resulting in significant cerebral edema and BBB dysfunction in a rat model of CO poisoning. Meanwhile, the ultrastructure of endothelial cells and pericytes was seriously damaged, and the expressions of ZO-1 and claudin-5 were decreased at an early stage (<7 days). NBP treatment could efficiently maintain the ultrastructural and functional integrity of BBB, alleviate cerebral edema. Besides, NBP could also markedly increase the levels of both ZO-1 and claudin-5 proteins compared with those in rats exposed to CO (P < 0.05), whereas NBP had no apparent regulatory effect on AQP-4 expression. Taken together, this study highlights the importance of ZO-1 and claudin-5 proteins in maintaining BBB ultrastructure and function after CO poisoning. NBP, as a novel treatment approach, may effectively inhibit the down-regulation of ZO-1 and claudin-5 proteins (but not AQP-4), thereby preserving the barrier function and reducing cerebral edema after CO poisoning.

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“…Cerebral edema is a major complication related to hypoxic-ischemia, as edema might elevate intracranial pressure with enlargement of brain tissue, which finally leads to cell death (Panickar & Anderson, 2011). It has been hypothesized that during HI condition, the blood flow was interrupted and contribute to an electrolytic imbalance that leads to increased movement of water (increases Aquaporin 4 expression) by altering BBB integrity and thus leads to edema (Wang et al, 2013). To validate the above statement, we found a marked increase in edema level (water content) in HI insult group on equivalence with the sham control group.…”

Section: Discussionmentioning

confidence: 99%

Neurotherapeutic effect of mangiferin against hypoxic–ischemic encephalopathy in neonatal rats

Lv¹,

Wang²,

Hu³

et al. 2016

Afr. J. Trad. Compl. Alt. Med.

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Background: Hypoxic-ischemic encephalopathy (HIE) in perinatal condition is highly associated with mortality and several neurological disabilities. The present experiment was blueprinted to ascertain the protective efficacy of mangiferin (MF) against hypoxic-ischemic brain injury in neonatal rats. Materials and Methods: Fourth six neonatal rats (pups) were randomly separated into four groups as a sham group that received only water (control; n=12), pups exposed to Hypoxic-ischemic (HI) insult (HI group-II; n=11), pups receiving 20 (MF 20+HI-III; n=11) or 40 (MF 40+HI-IV; n=12) mg/kg b. wt of MF dissolved in water via i.p. for 7 consecutive days as pretreatment regimen before HI insult as well as one-time post treatment after HI insult. Results: MF pretreatment for seven days considerably attenuated the cerebral infarct size, edema level, lipid peroxidation (MDA), inflammatory markers (TNF-α, IL-1β, IL-6, and NF-p65 subunit) as well as greatly ameliorated the antioxidant activities of catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GSH) and thereby maintaining the redox balance. The number of viable neuronal count (nissl bodies) was exponentially increased on administration with both the dosages of MF. Both the dosages showed substantial protection against HIE, however, 40 mg of MF exhibit superior neuroprotection in equivalence with 20 mg of MF. Conclusion:The results of the present study distinctly proving the beneficial effect of MF against HIE by concomitantly improving neuronal count and antioxidant status. Hence, we recommend MF might be used for treating neonatal HIE with some standard drugs.

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Progesterone attenuates cerebral edema in neonatal rats with hypoxic-ischemic brain damage by inhibiting the expression of matrix metalloproteinase-9 and aquaporin-4

Cited by 44 publications

References 26 publications

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

N-Butylphthalide Alleviates Blood–Brain Barrier Impairment in Rats Exposed to Carbon Monoxide

Neurotherapeutic effect of mangiferin against hypoxic–ischemic encephalopathy in neonatal rats

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