Protective effects of tetramethylpyrazine analogue Z-11 on cerebral ischemia reperfusion injury

Zhai, Li; Jia, Yulei; Yaqing, Ji; Jinmin, Zou; Liu, Xinyong; Gao, Jing; Liu, Min

doi:10.1016/j.ejphar.2018.11.031

Cited by 28 publications

(14 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was reported that BRCA1 protects neurons from cerebral I/R injury through activating the Nrf2-associated antioxidant pathways (34). It has been reported that EDA enhances the oxidant defense capacity in brain tissue through promoting Nrf2/HO-1 signaling (35). MH was also reported to protect cerebral cortex and hippocampus neurons from cerebral I/R injury through the Nrf2/ARE pathway (36).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of combined treatment with mild hypothermia and edaravone against cerebral ischemia/reperfusion injury via oxidative stress and Nrf2 pathway regulation

Wang

et al. 2020

Int J Oncol

View full text Add to dashboard Cite

Mild hypothermia (MH) and edaravone (EDA) exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury through activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. However, whether MH and EDA exert synergistic effects against cerebral I/R injury remains unknown. The aim of the present study was to investigate the effects and mechanism of action of MH in combination with EDA in cerebral I/R injury. A rat cerebral I/R injury model was constructed by middle cerebral artery occlusion (MCAO) followed by reperfusion, and the mice were treated by MH, EDA or the inhibitor of the Nrf2 signaling pathway brusatol (Bru). It was observed that mice treated by MCAO had higher neurological deficit scores and oxidative stress levels, and low spatial learning and memory capacity; moreover, the CA1 region of the hippocampi of the mice exhibited reduced neuronal density and viability, and reduced mitochondrial dysfunction. However, MH in combination with EDA reversed the effects of MCAO, which were blocked by Bru injection. The levels of glutathione (GSH), GSH peroxidase, catalase and superoxide dismutase in rat ischemic hemisphere tissues were reduced by Bru. Western blotting demonstrated that the combined treatment with MH and EDA promoted the nuclear localization of Nrf2, and increased the levels of NAD(P)H quinone oxidoreductase and heme oxygenase (HO)-1. In conclusion, MH combined with EDA exerted synergistic neuroprotective effects against cerebral I/R injury involving changes in the Nrf2/HO-1 pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Protective effects of combined treatment with mild hypothermia and edaravone against cerebral ischemia/reperfusion injury via oxidative stress and Nrf2 pathway regulation

Wang

et al. 2020

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…Oxidative stress has been associated with different pathological processes such as neurotoxicity, neuroinflammation, ischemic stroke and neurodegenerative diseases ( 27 , 28 ). During I/R injury, the excessive production of reactive oxygen species, reactive nitrogen species, excitatory amino acid toxicity and inflammatory reaction are implicated in neuronal damage ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of Txk‑mediated activation of NF‑κB signaling pathway on neurological deficit and oxidative stress after ischemia‑reperfusion in rats

2021

Mol Med Rep

View full text Add to dashboard Cite

Ischemic stroke is an extremely mortal cerebrovascular disease, and neuroinflammation and oxidative stress emerge as important traits of ischemic stroke. However, as an inflammation-associated factor, Txk tyrosine kinases (Txk) has been poorly studied in neuroscience research. The aim of the present study was to investigate the role of Txk after ischemia-reperfusion (I/R) in vivo and in vitro , observe the association between Txk knockdown and neurological deficit and oxidative stress, and to explore whether the process was mediated by the activation of nuclear factor (NF)-κB signaling pathway. Middle cerebral artery occlusion (MCAO), oxygen and glucose deprivation/reperfusion (OGD/R) model and western blotting have been used to simulate the I/R injury to analyze the expression, and to approximate the localization of Txk, respectively. Brain infarct volume, neurological score, brain water content, apoptosis and oxidative stress assays in vivo and apoptosis, cellular viability, the LDH release and oxidative stress assays in vitro were observed using a Txk-knockdown lentivirus. Finally, NF-κB overexpression lentivirus was applied to discuss whether the role of Txk following I/R was regulated by the NF-κB signaling pathway. The results show that the Txk expression peaked at 24 h after MCAO and 6 h after OGD/R, respectively. Txk molecules gradually entered the nucleus after MCAO and OGD/R. The Txk-knockdown lentivirus resulted in decreased brain infarct volume, neurological score, brain water content, apoptosis and oxidative stress after MCAO in vivo . Besides, Txk knockdown decreased apoptosis, LDH release, oxidative stress, and increased cellular viability, after ODG in vitro . Finally, NF-κB overexpression reversed the process of neurological deficit and oxidative stress after Txk regulation in vivo and vitro . Overall, the present study suggests that Txk potentially regulates apoptosis, neurological deficit, and oxidative stress after I/R, by entering the nucleus. NF-κB maybe the downstream target factor of Txk.

show abstract

“…Finally, we sutured the skin of the rat brain and disinfect the incision with iodophor. 13 The procedure of the rats in the Sham group was the same as the above, but no ischemia model was established. During the operation, the rat’s regional cerebral blood flow (rCBF) was monitored to ensure the success of ischemia and reperfusion.…”

Section: Methodsmentioning

confidence: 99%

“…The higher the score, the more severe the nerve damage. The mNSS nerve injury classification is as follows: severe injury (score [13][14][15][16][17][18], moderate injury (score 7-12), mild injury (score 1-6) and no injury (score 0). The assessment was carried out by people who did not know the animal group.…”

Section: Modified Neurological Severity Score (Mnss) Assessmentmentioning

confidence: 99%

Sufentanil alleviates cerebral ischemia-reperfusion injury by inhibiting inflammation and protecting the blood-brain barrier in rats

Wang

et al. 2022

Eur J Histochem

View full text Add to dashboard Cite

Stroke is a brain system disease with a high fatality rate and disability rate. About 80% of strokes are ischemic strokes. Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. The purpose of this study is to investigate the effect of sufentanil (SUF) on CIRI model rats. We used middle cerebral artery occlusion (MCAO) to make the CIRI model in rats and monitored region cerebral blood flow (rCBF) to ensure that blood flow was blocked and recanalized. We used ELISA and RT-PCR to detect the expression of inflammatory factors in rat serum and brain tissue. In addition, we detected the expression of metalloproteinase (MMP) 2, MMP9 and collagen IV in brain tissues and performed Evans blue (EB) assay to determine the permeability of the blood-brain barrier (BBB). Finally, we clarified the apoptosis of brain tissue through the TUNEL staining and the detection of caspase3, Bcl2 and Bax. Various concentrations of SUF, especially 5, 10 and 25 μg/kg of SUF, all alleviated the infarct size, neurological function and brain edema of MCAO rats. SUF pretreatment also effectively reduced the expression of inflammatory cytokines in MCAO rats, including interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α. In addition, SUF also inhibited MMP2 and MMP9 and promoted the expression of collagen IV, indicating that SUF attenuated the destruction of the BBB. SUF also inhibited caspase3 and Bax rats and promoted Bcl2 in MCAO rats, thus inhibiting cell apoptosis. SUF pretreatment effectively improved the neurological function and cerebral infarction of MCAO rats, inhibited excessive inflammation in rats, protected the BBB, and inhibited cell apoptosis in brain tissue.

show abstract

Protective effects of tetramethylpyrazine analogue Z-11 on cerebral ischemia reperfusion injury

Cited by 28 publications

References 31 publications

Protective effects of combined treatment with mild hypothermia and edaravone against cerebral ischemia/reperfusion injury via oxidative stress and Nrf2 pathway regulation

Protective effects of combined treatment with mild hypothermia and edaravone against cerebral ischemia/reperfusion injury via oxidative stress and Nrf2 pathway regulation

Effects of Txk‑mediated activation of NF‑κB signaling pathway on neurological deficit and oxidative stress after ischemia‑reperfusion in rats

Sufentanil alleviates cerebral ischemia-reperfusion injury by inhibiting inflammation and protecting the blood-brain barrier in rats

Contact Info

Product

Resources

About