Thrombopoietin could protect cerebral tissue against ischemia-reperfusion injury by suppressing NF-κB and MMP-9 expression in rats

Wu, Wenjuan; Wang, Zhong; Luo, Bing; Hu, Zhiping; He, Jialin; Tang, Xiangqi

doi:10.7150/ijms.27543

Cited by 16 publications

(9 citation statements)

References 30 publications

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“…In a rat model of severe infarction and swelling after stroke induced by middle cerebral artery occlusion reperfusion, TPO significantly reduced both the infarct and the swelling in a dose-dependent manner [38]. When 0.1 μg/kg of TPO was administrated immediately or 2 hours after reperfusion, the infarct and swelling were significantly improved, and other stroke-related neurologic deficits were also ameliorated [38,39]. Treatment with TPO also reduces stroke-induced cortical MMP-9 and TIMP-1 expression and enzymatic activity.…”

Section: Agingmentioning

confidence: 95%

c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis

Xia

et al. 2020

Aging

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Thrombopoietin (TPO) is a growth factor for the megakaryocytic/platelet lineage. In this study, we investigated the expression of TPO and its receptor, c-Mpl, in the human central nervous system (CNS) and their roles after a neural insult. Our results demonstrate that both TPO and c-Mpl are expressed in the neurons of the human CNS. TPO was also detected in human cerebrospinal fluid. TPO was found to be neuroprotective in hypoxic-ischemic neonatal rat brain models. In these rat models, treatment with TPO reduced brain damage and improved sensorimotor functions. In addition, TPO promoted C17.2 cell proliferation through activation of the PI3K/Akt signaling pathway. Via the Bcl-2/BAX signaling pathway, TPO exerted an antiapoptotic effect by suppressing mitochondrial membrane potentials. Taken together, our results indicate that TPO is neuroprotective in the CNS.

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Section: Agingmentioning

confidence: 95%

c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis

Xia

et al. 2020

Aging

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“…Это согласуется с нашими данными, в соответствии с которыми концентрация ТРО коррелировала с уровнем лейкоцитов при поступлении. Кроме того, ТРО также может способствовать уменьшению повреждения миокарда в результате ишемии/реперфузии миокарда как in vitro, так и in vivo, что проявляется в уменьшении зоны некроза и ускорении восстановления функции желудочков после ишемии [26]. Поэтому повышение содержания ТРО у пациентов основной группы также может носить протективный характер, подобно увеличению уровня LIF.…”

Section: Discussionunclassified

Serum cytokines levels in patients with myocardial infarction with non-obstructive and obstructive coronary arteries

et al. 2021

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Aim. To compare the concentrations of proinflammatory and anti-inflammatory cytokines in patients with myocardial infarction with non-obstructive (MINOCA) and obstructive coronary arteries (MIOCA) in the early postinfarction period and after 1-year follow-up.Material and methods. The study included 40 patients with myocardial infarction (experimental group, 19 patients; control group, 21 patients). Three (15,7%) patients with diagnosed acute myocarditis were excluded from the final analysis. Blood samples were taken upon admission, on the 2nd, 4th and 7th days from hospitalization, and also after 1-year follow-up. Twenty-three parameters were analyzed using multiplex analysis and the Multiplex Instrument FLEXMAP 3D system (Luminex Corporation), as well as the MILLIPLEX map Human Cytokine/ Chemokine Panel II.Results. According to multiplex analysis of blood serum of the studied groups, a comparable increase in proinflammatory cytokines CCL-15, CCL-26, CCL-27 in the early postinfarction period and after 1-year follow-up, as well as antiinflammatory and regenerative cytokines CXCL-12, TPO in the early postinfarction period and after 1-year follow-up. In patients with MINOCA, higher concentrations of the following proinflammatory cytokines were determined: IL-16 upon admission (p=0,03), IL-20 on days 2 and 4 of the early postinfarction period (p=0,005 and p = 0.03), as well as CCL-15 on days 4 and 7 (p=0,05 and p=0,02). After 1-year follow-up, among the proinflammatory cytokines, a greater increase in CCL-21 (p=0,02) was noted in the patients of experimental group. Also, in patients with MINOCA, a greater increase in TPO was determined upon admission and on the 2nd day (p=0,02 and p=0,02), SCF — on the 7th day and after 1-year follow-up (p=0,04 and p=0,04), and LIF on the 4th day of early postinfarction period (p=0,007). In contrast, MIOCA patients showed a greater increase in CXCL-12 levels upon admission (p=0,04). At the same time, patients with MINOCA showed a higher level of C-reactive protein on the 1st day, as well as a higher relative monocyte count after 1-year follow-up.Conclusion. Despite a comparable increase in the cytokines CCL-8, CCL-13, CCL26, CCL-27 in patients of both groups, in patients with MINOCA there was a greater increase in proinflammatory cytokines IL-16, IL-20, CCL-15, CCL-21, and also CXCL-12, LIF, TPO, SCF, which have anti-inflammatory and regenerative activity. After 1 year follow-up, MINOCA patients showed a significant increase in CCL-21 and SCF, with a comparable increase in other proinflammatory cytokines in patients of both groups. A greater increase in proinflammatory cytokines in patients with MINOCA may indicate a more aggressive atherosclerosis course and lead to plaque destabilization followed by ischemic event.

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“…NF-κB, generally considered as the “central link” of inflammation in vivo , is an important mediator in the process of ischemia–reperfusion injury. Inhibition of NF-κB expression can reduce the inflammatory cascade and protect the structure and function of the BBB ( Wu et al, 2018 ; Howell and Bidwell, 2020 ). After cerebral ischemia, pericytes express an inflammatory phenotype (CD11b-positive), upregulate pro-inflammatory cytokine expression, and promote increased BBB permeability ( Zhou et al, 2018 ).…”

Section: Factors Associated With the Formation Of Cerebral Edemamentioning

confidence: 99%

Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

Zhou

Piao

et al. 2022

Front. Neurosci.

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Ischemic stroke is associated with increasing morbidity and has become the main cause of death and disability worldwide. Cerebral edema is a serious complication arising from ischemic stroke. It causes an increase in intracranial pressure, rapid deterioration of neurological symptoms, and formation of cerebral hernia, and is an important risk factor for adverse outcomes after stroke. To date, the detailed mechanism of cerebral edema after stroke remains unclear. This limits advances in prevention and treatment strategies as well as drug development. This review discusses the classification and pathological characteristics of cerebral edema, the possible relationship of the development of cerebral edema after ischemic stroke with aquaporin 4, the SUR1-TRPM4 channel, matrix metalloproteinase 9, microRNA, cerebral venous reflux, inflammatory reactions, and cerebral ischemia/reperfusion injury. It also summarizes research on new therapeutic drugs for post-stroke cerebral edema. Thus, this review provides a reference for further studies and for clinical treatment of cerebral edema after ischemic stroke.

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Thrombopoietin could protect cerebral tissue against ischemia-reperfusion injury by suppressing NF-κB and MMP-9 expression in rats

Cited by 16 publications

References 30 publications

c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis

c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis

Serum cytokines levels in patients with myocardial infarction with non-obstructive and obstructive coronary arteries

Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

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