Influence of hepatic ischemia-reperfusion on postoperative spatial cognitive function in mice

Wang, Y.Q.; Wu, Weiping; Wang, L.K.; Chen, K.; Li, Y.H.

doi:10.4238/2014.july.29.4

Cited by 9 publications

(6 citation statements)

References 17 publications

(17 reference statements)

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“…Subsequently, the blockage of blood vessels following stroke leads to diverse pathophysiologies including brain edema, neuronal loss, and cognitive dysfunction [37,38,39,40]. Cerebral cortex, hippocampus, and corpus striatum in the brain are the most vulnerable regions against oxidative stress and hypoxic injury induced by cerebral ischemia [41].…”

Section: Discussionmentioning

confidence: 99%

Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

et al. 2015

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Ischemic stroke results in the diverse phathophysiologies including blood brain barrier (BBB) disruption, brain edema, neuronal cell death, and synaptic loss in brain. Vitamin C has known as the potent anti-oxidant having multiple functions in various organs, as well as in brain. Dehydroascorbic acid (DHA) as the oxidized form of ascorbic acid (AA) acts as a cellular protector against oxidative stress and easily enters into the brain compared to AA. To determine the role of DHA on edema formation, neuronal cell death, and synaptic dysfunction following cerebral ischemia, we investigated the infarct size of ischemic brain tissue and measured the expression of aquaporin 1 (AQP-1) as the water channel protein. We also examined the expression of claudin 5 for confirming the BBB breakdown, and the expression of bcl 2 associated X protein (Bax), caspase-3, inducible nitric oxide synthase (iNOS) for checking the effect of DHA on the neurotoxicity. Finally, we examined postsynaptic density protein-95 (PSD-95) expression to confirm the effect of DHA on synaptic dysfunction following ischemic stroke. Based on our findings, we propose that DHA might alleviate the pathogenesis of ischemic brain injury by attenuating edema, neuronal loss, and by improving synaptic connection.

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Section: Discussionmentioning

confidence: 99%

Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

et al. 2015

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“…In a hepatic IRI rat model, long-term cognitive function was impaired [ 145 ]. In mice, liver IRI led to short-term dimensional cognitive deficits, which was time-dependent: the longer the time elapsed after the onset of ischaemia, the poorer was the cognitive function, which may be associated with the large amount of harmful substances produced at the time of IRI initiation, including ROS and inflammatory factors [ 146 ]. NF-κB can exacerbate liver ischaemia and reperfusion damage with remote effects of disrupting neurological development and brain damage repair processes, thereby impairing cognitive functions.…”

Section: Liver As the Primarily Damaged Organmentioning

confidence: 99%

Inflammatory response to the ischaemia–reperfusion insult in the liver after major tissue trauma

Palmer

Lupu

et al. 2022

Eur J Trauma Emerg Surg

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Background Polytrauma is often accompanied by ischaemia–reperfusion injury to tissues and organs, and the resulting series of immune inflammatory reactions are a major cause of death in patients. The liver is one of the largest organs in the body, a characteristic that makes it the most vulnerable organ after multiple injuries. In addition, the liver is an important digestive organ that secretes a variety of inflammatory mediators involved in local as well as systemic immune inflammatory responses. Therefore, this review considers the main features of post-traumatic liver injury, focusing on the immuno-pathophysiological changes, the interactions between liver organs, and the principles of treatment deduced. Methods We focus on the local as well as systemic immune response involving the liver after multiple injuries, with emphasis on the pathophysiological mechanisms. Results An overview of the mechanisms underlying the pathophysiology of local as well as systemic immune responses involving the liver after multiple injuries, the latest research findings, and the current mainstream therapeutic approaches. Conclusion Cross-reactivity between various organs and cascade amplification effects are among the main causes of systemic immune inflammatory responses after multiple injuries. For the time being, the pathophysiological mechanisms underlying this interaction remain unclear. Future work will continue to focus on identifying potential signalling pathways as well as target genes and intervening at the right time points to prevent more severe immune inflammatory responses and promote better and faster recovery of the patient.

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“…During pathological processes such as Alzheimer's disease, the hippocampal volume decreases more rapidly [11,12]. Our previous study proved that I/R had a close relationship with the incidence of POCD [13]. The primary aim in this study is to investigate the effect of I/R on hippocampus in rats with POCD.…”

Section: Introductionmentioning

confidence: 99%

“…During pathological processes such as Alzheimer’s disease, the hippocampal volume decreases more rapidly [ 11 , 12 ]. Our previous study proved that I/R had a close relationship with the incidence of POCD [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

The effects of hepatic ischemia/reperfusion injury on postoperative cognitive function in aged rats

Wang

Qiu

2019

Arch Med Sci

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Introduction: Hepatic ischemia/reperfusion injury (I/R) is a significant source of morbidity and mortality after liver surgery. The aim of this study was to investigate the effect of hepatic I/R injury on the hippocampus in rats with postoperative cognitive dysfunction (POCD). Material and methods: Adult male Sprague-Dawley rats (n = 160, age: 20-25 months, weight: 300-350 g) received I/R surgery with ischemia for 20 minutes, 30 minutes, and 40 minutes in different groups. Behavior tests of the Morris water maze (MWM) test and the passive avoidance test were applied. Population spike (PS) of pyramidal cells, nuclear factor kappa-B (NF-κB) and protein kinase γ (PKCγ) in the hippocampus were observed. Results: Within 10 days after surgery, in aged rats with varying impaired cognitive function, spike size and spike latency period were reduced, level of PKCγ was decreased and an increased level of NF-κB was observed in the I/R group, especially in the I/R group with ischemia for 40 minutes. The parameters showed no significant difference in rats in the I/R group compared with the sham group at the 18th day after surgery. Conclusions: Hepatic I/R injury has a negative impact on the postoperative cognitive function in aged rats, leading to hippocampus changes with PS abnormity and level changes of NF-κB, PKCγ. However, this cognitive deficit improved over time.

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Influence of hepatic ischemia-reperfusion on postoperative spatial cognitive function in mice

Cited by 9 publications

References 17 publications

Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

Inflammatory response to the ischaemia–reperfusion insult in the liver after major tissue trauma

The effects of hepatic ischemia/reperfusion injury on postoperative cognitive function in aged rats

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