Human urinary kallidinogenase or edaravone combined with butylphthalide in the treatment of acute ischemic stroke

Qian, Yun; Lyu, Yi; Min-hai, Jiang; Tang, Bo; Nie, Tian; Lü, Shan

doi:10.1002/brb3.1438

Cited by 13 publications

(10 citation statements)

References 32 publications

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“…Alternatively, mitochondrion is an organelle that plays roles in energy conversion and metabolism, and its dysfunction is the crucial pathophysiological change in ischemic stroke due to oxygen-glucose deprivation ( 14 ). It was found that a few studies have confirmed that NLRC4 ( 15 ), NLRP1 ( 16 ) and AIM2 ( 17 ) can promote cerebral ischemic injury, but there is no evidence that mitochondria can affect the pathological process of cerebral ischemia through them.…”

Section: Introductionmentioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1β release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.

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Section: Introductionmentioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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“…It is widely used, but its clinical effect has certain limitations [ 3 , 4 ]. Butylphthalide sodium chloride can be used to improve the neurological deficit on acute ischemic stroke; in addition, it is a usual drug for curing acute ischemic stroke [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Butylphthalide Sodium Chloride Injection Combined with Edaravone Dexborneol on Neurological Function and Serum Inflammatory Factor Levels in Sufferers Having Acute Ischemic Stroke

Zhang

et al. 2022

Journal of Healthcare Engineering

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For investigating an influence on butylphthalide sodium chloride injection combined with edaravone dexborneol on neurological function and serum inflammatory factor levels in sufferers having acute ischemic stroke, 120 sufferers having acute ischemic stroke from September 2020 to September 2021 are chosen for the study subjects. In line with the diverse therapies, they took part in a control group and the study group, with 60 examples in each group. The control group is treated with edaravone dexborneol, and the study group is treated with butylphthalide sodium chloride injection, based on the control group. The posttreatment curative efficacy on the two groups is recorded, and treatment of both the two groups is compared. Before and after neurological function indexes (NIHSS and mRS), inflammatory factor indexes (IL-6, CRP, and TNF-α), life quality index (Barthel index), hemorheological indexes (plasma-specific viscosity), and neurological levels of NSE are logged and contrasted between the two groups of adverse reactions during therapy. Postcure, the overall response rate and Barthel index of the study group obviously overtop those of the control group ( p < 0.05). IL-6, CRP, TNF-α, NSE, plasma specific viscosity, and NIHSS and mRS scores obviously hypodown those of the control group ( p < 0.05), and untoward effects on the two groups during curing are lower, and the discrepancy is not obvious( p > 0.05). Butylphthalide sodium chloride injection combined with edaravone dexborneol can enhance curative efficacy on sufferers having acute ischemic stroke, improve neurological function, blood rheology, and quality of life, and decrease the secretion of cytokine, having a better effect and high medication safety.

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“…Jia et al ( 42 ) showed that butylphthalide improves the outcomes of patients with subcortical vascular cognitive impairment without dementia. Qian et al ( 43 ) showed that butylphthalide combined with kallidinogenase or edaravone enhanced the independence rate of patients with ischemic stroke. Future studies should examine those effects of butylphthalide in humans.…”

Section: Discussionmentioning

confidence: 99%

Butylphthalide Combined With Conventional Treatment Attenuates MMP-9 Levels and Increases VEGF Levels in Patients With Stroke: A Prospective Cohort Study

Xiong

Juanjuan

et al. 2021

Front. Neurol.

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Background and Purpose: Butylphtalide increases the vascular endothelial growth factor (VEGF) and decreases matrix metalloproteinase (MMP)-9 in animal models of stroke and might be of use in the management of stroke. To explore whether butylphthalide combined with conventional treatment can change the levels of MMP-9 and VEGF and the National Institutes of Health Stroke Scale (NIHSS) scores of patients with stroke.Methods: This was a prospective cohort study involving inpatients admitted to the Jiangxi Provincial People's Hospital (January–June 2019) due to acute cerebral infarction. The patients received conventional treatments with or without butylphthalide. The changes in the NIHSS scores were compared between groups. Plasma MMP-9 and VEGF were measured by enzyme-linked immunosorbent assay.Results: A total of 24 patients were included in the conventional treatment group and 46 in the butylphthalide group. The butylphthalide group showed lower MMP-9 (130 ± 59 vs. 188 ± 65, p = 0.001) and higher VEGF (441 ± 121 vs. 378 ± 70, p = 0.034) levels on day 6 compared with the conventional treatment group. The changes in MMP-9 and VEGF were significant, starting on day 3 in the butylphthalide group but on day 6 in the conventional treatment group. There were no differences between the two groups in the NIHSS scores at admission and at discharge (p > 0.05). The overall response rate was higher in the butylphthalide group compared with the conventional treatment group (63.0 vs. 37.5%, p = 0.042).Conclusion: Butylphthalide combined with conventional treatment can decrease MMP-9 levels and increase VEGF levels. The patients showed the reduced NIHSS scores, possibly suggesting some improvement in prognosis after stroke. Still, the conclusions need to be confirmed in a larger sample and in different etiological subtypes of stroke.

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Human urinary kallidinogenase or edaravone combined with butylphthalide in the treatment of acute ischemic stroke

Cited by 13 publications

References 32 publications

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Effects of Butylphthalide Sodium Chloride Injection Combined with Edaravone Dexborneol on Neurological Function and Serum Inflammatory Factor Levels in Sufferers Having Acute Ischemic Stroke

Butylphthalide Combined With Conventional Treatment Attenuates MMP-9 Levels and Increases VEGF Levels in Patients With Stroke: A Prospective Cohort Study

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