Neutrophil-to-lymphocyte ratio predicts hematoma growth in intracerebral hemorrhage

Wang, Zhigang; Gong, Qingyong; Guo, Cheng; Luo, Yan; Chen, Lvan

doi:10.1177/0300060519847866

Cited by 13 publications

(17 citation statements)

References 21 publications

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“…[23][24][25][26][27] Recently, accumulating evidence supports that higher PMNs count and neutrophil to lymphocyte ratio (NLR) at early stage of ICH leads to the poorer outcome. [4][5][6][7] Thus, in a proof-of-concept experiment in rat model of ICH, we found that simvastatin effectively decreased the peripheral PMNs count, NLR and neutrophil brain-invading, as well as attenuated brain edema and neurological de cits following ICH.…”

Section: Simvastatin Exerted Pro-apoptotic Effect On Pmns In Acute Stage After Ich Via Lxa4/fpr2/p38 Mapk Signaling Pathwaymentioning

confidence: 99%

“…Recently, clinical reports indicate that early peripheral blood polymorph nuclear neutrophils (PMNs) elevation is closely related to the poor prognosis of patients with ICH, which is often accompanied by heavier brain edema and larger hematoma. [4][5][6][7] To understand the relationship between the elevated PMNs and poor prognosis among ICH patients, we performed a con rmatory experiment in a rat model of ICH. [8] The results show that the ICH rat showed a signi cant increase of PMNs in peripheral blood at an early stage, which is consistent with the clinical phenomenon.…”

Section: Introductionmentioning

confidence: 99%

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Simvastatin boosts neutrophil apoptosis and ameliorates secondary brain injury following intracerebral hemorrhage via LXA4/FPR2/p38 MAPK pathway

Chen¹

2021

Preprint

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Statins, in addition to their well-known lipid-lowering effects, have also shown a wide range of neuroprotective effects in recent years. We previously found that simvastatin effectively attenuated intracerebral hemorrhage (ICH)-induced secondary brain injury in rats. This study aims to elucidate the underlying mechanism. The animal model was established in adult male Sprague–Dawley rats by an injection of autologous blood, then randomly treated with simvastatin or vehicle. Then, a series of experiments were conducted to investigate the involvement of lipoxin A4 (LXA4) / formyl-peptide receptor 2 (FPR2) / p38 MAPK signaling pathway in simvastatin-triggered neutrophil apoptosis. Results show that simvastatin significantly elevated the level of LXA4 (an endogenous FPR2 agonist) in plasm in early stage of ICH. Exogenous LXA4 administration effectively promoted circulating neutrophil apoptosis, reduced the neutrophil count in both peripheral blood and perihematomal area, as well as ameliorated neuroinflammation and brain injury after ICH, which in line with the effect of simvastatin. Moreover, similar to simvastatin, the exogenous LXA4 markedly down-regulated the phosphorylation level of p38 and the Mcl-1/Bax ratio (the decreased ratio represents pro-apoptosis) in circulating neutrophils of ICH rat. Notably, all above effects of simvastatin on ICH were significantly abolished by Boc-2, a selective antagonist for FPR2. Moreover, simvastatin led to a similar reduction of Mcl-1/Bax ratio as SB203580 (p38 MAPK inhibitor), but it was abolished by P79350 (p38 MAPK agonist). Collectively, these results suggest that simvastatin boosts neutrophils apoptosis and alleviates subsequent neuroinflammation following ICH may via upregulating LXA4 in plasma through the FPR2/p38 MAPK signaling pathway.

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Section: Simvastatin Exerted Pro-apoptotic Effect On Pmns In Acute Stage After Ich Via Lxa4/fpr2/p38 Mapk Signaling Pathwaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Simvastatin boosts neutrophil apoptosis and ameliorates secondary brain injury following intracerebral hemorrhage via LXA4/FPR2/p38 MAPK pathway

Chen¹

2021

Preprint

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“…Accordingly, in this study we found a significant increase of microglia after ICH in mice and microglia activation peaked at 24 h after injury. Neutrophil-lymphocytes ratio (NLR) has been extensively reported as a risk factor associated with bad outcomes after ICH [23,33] Post-stroke immunological response has been extensively studied, especially in ischemia stroke [19].…”

Section: Secondary Brain Injury Such As Blood-brain Barrier (Bbb) DImentioning

confidence: 99%

“…After ischemic stroke, spleen was activated and the brainspleen cell cycling started. It is still controversial what plays the key role in the splenic response after stroke, the lymphocytes, monocytes, [22] neutrophil infiltration or the neutrophil-to-lymphocyte ratio (NLR) [23]. Moreover, it is worthwhile to elucidate the precise role of each cell type of spleen in secondary brain injury after stroke.…”

Section: Introductionmentioning

confidence: 99%

Role of C1q in spleen-derived neutrophil infiltration and neuroinflammation after ICH in mice

Tang

Luo

Geng

et al. 2019

Preprint

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Background: Neuroinflammation is a major detrimental role of secondary brain injury after spontaneously intracerebral hemorrhage (ICH). Neutrophil infiltration plays a key role in the pathophysiology of ICH, but the coming resource and mechanism is unknown. This study aims to investigate whether spleen-derived neutrophil infiltration accelerated neuroinflammation and the role of C1q classical pathway.Methods: Male C57 mice were subjected to collagenase-induced ICH. If necessary, splenectomy was performed 2 weeks prior to ICH induction or anti-C1q neutralizing antibody (50mg/kg) was injected intravenously into the tail vein 15 minutes prior. Immunohistochemistry, Propidium Iodide staining, western blotting, ELISA and qRT-PCR were used to study the change of molecular proteins, neuronal cells and inflammatory factors. 7.0T animal MRI was used to assess hydrocephalus.Results: At 0h, 6h, 12h, 24h and 48h post ICH induction, we found a significant increasing tendency of microglia activation and neutrophil infiltration around hematoma and that C1q upregulation was correlated with neuronal decrease, which peaked at 24h after ICH. Here, we demonstrated spleen atrophy and upregulation of neutrophil in spleen 24h after ICH. Splenectomy prior to ICH mice resulted in significant decrease of microglia and neutrophil infiltration compared with that in group of sham-splenectomy. Moreover, both anti-C1q antibody and splenectomy significantly attenuated neutrophil infiltration and neuron death, restored synapse VGAT, alleviated hydrocephalus and inflammatory factors, such as IL-1β, TNF-α and IL-6 after ICH.Conclusion: The study demonstrated that spleen is a major source of brain neutrophil infiltration after ICH. C1q-targeted inhibition of classic complement pathway could prevent spleen-derived neutrophil infiltration and attenuate ICH induced neuroinflammation, which provides a novel therapeutic approach for hemorrhagical stroke.

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“…In a previous study, Liu et al (2019) reported that a higher NLR level was significantly correlated with major disability at 90 days and a higher short-term mortality rate. Wang Z. et al (2019) suggested that NLR can predict hematoma expansion. Finally, Lattanzi et al (2017) indicated that NLR may be a prognostic factor for neurological deterioration.…”

Section: Introductionmentioning

confidence: 99%

Prognostic Role of the Neutrophil-to-Lymphocyte Ratio in Intracerebral Hemorrhage: A Systematic Review and Meta-Analysis

Shi

Zhang

et al. 2022

Front. Neurosci.

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The neutrophil-to-lymphocyte ratio (NLR) plays an important role in the progression of intracerebral hemorrhage (ICH). An increasing number of studies have reported that a high NLR is correlated with poor clinical outcomes among patients with ICH. Here, we conducted a systematic review and meta-analysis to evaluate the prognostic value of NLR in the setting of ICH. We performed a comprehensive search of electronic literature databases to identify all relevant studies evaluating the prognostic role of NLR in patients with ICH. Two researchers independently screened the studies and extracted relevant data. We extracted, pooled, and weighted odds ratio (OR) and 95% confidence interval (CI) values using a generic inverse-variance method, and then evaluated the heterogeneity among studies using Q test and I2 statistic. Finally, we selected a total of 26 studies including 7,317 patients for the current study. Overall, our results indicated that a high NLR was significantly associated with a poor outcome (OR, 1.32; 95% CI, 1.19–1.46; P < 0.00001), mortality (OR, 1.05; 95% CI, 1.01–1.09; P = 0.02), and neurological deterioration (OR, 1.65; 95% CI, 1.08–2.52; P = 0.02). We did not observe a significant association between NLR and hematoma expansion (OR, 1.04; 95% CI, 0.99–1.08; P = 0.09). Our study indicated that a high NLR is significantly associated with poor clinical outcomes in patients with ICH. As NLR is a simple and easily available biomarker, future studies should focus on exploring its application in the prognostic evaluation of patients with ICH.

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Neutrophil-to-lymphocyte ratio predicts hematoma growth in intracerebral hemorrhage

Cited by 13 publications

References 21 publications

Simvastatin boosts neutrophil apoptosis and ameliorates secondary brain injury following intracerebral hemorrhage via LXA4/FPR2/p38 MAPK pathway

Simvastatin boosts neutrophil apoptosis and ameliorates secondary brain injury following intracerebral hemorrhage via LXA4/FPR2/p38 MAPK pathway

Role of C1q in spleen-derived neutrophil infiltration and neuroinflammation after ICH in mice

Prognostic Role of the Neutrophil-to-Lymphocyte Ratio in Intracerebral Hemorrhage: A Systematic Review and Meta-Analysis

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