The Protective Effects of Benzbromarone Against Propofol-Induced Inflammation and Injury in Human Brain Microvascular Endothelial Cells (HBMVECs)

Huang, Zehan; Huang, Bo; Wei, Qiaosong; Su, Xiaomei; Li, Xisong; Si-ping, Qin; Huang, Wei

doi:10.1007/s12640-021-00387-1

Cited by 7 publications

(7 citation statements)

References 37 publications

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“…In human brain microvascular endothelial cells, benzbro marone inhibited propofolinduced production of mitochondrial ROS, inflammatory factors, and adhesion molecules, indicating that benzbromar one may have protective properties against endothelial injury of the brain. 40 In subgroup analysis of patients taking allopuri nol ⩾200 mg and benzbromarone ⩾50 mg, a higher aHR was found for coronary revasculariza tion in benzbromarone initiators than in allopuri nol initiators. This can be considered a result reflecting the difference in baseline characteris tics between the two groups.…”

Section: Discussionmentioning

confidence: 97%

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Cardiovascular risk associated with allopurinol or benzbromarone treatment in patients with gout

Eun

Han

Kim

et al. 2022

Therapeutic Advances in Musculoskeletal

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Background: In previous studies, cardiovascular (CV) risk was increased in patients with gout. The effects of uric acid–lowering therapy on CV risk in gout patients have been investigated in numerous studies; however, allopurinol and benzbromarone have rarely been compared. Objectives: To compare CV risk based on allopurinol and benzbromarone treatment in Korean gout patients. Design: A nationwide population-based retrospective cohort study. Methods: We used South Korea database of the Health Insurance Review and Assessment (HIRA) service to identify gout patients ⩾18 years of age who newly started allopurinol or benzbromarone between 2009 and 2015. The primary outcome of the study was the occurrence of a composite CV endpoint, which included coronary revascularization, hospitalization due to myocardial infarction, ischemic stroke, and transient ischemic attack. Cox proportional hazard regression analysis and Kaplan–Meier curves were used for analysis. Results: The study included 257,097 allopurinol initiators and 7868 benzbromarone initiators. Compared with allopurinol initiators, the adjusted hazard ratio (aHR) of the composite CV endpoint of benzbromarone initiators was 1.01 [95% confidence interval (CI): 0.83−1.21], which was not significantly different. The results did not change even when 1:3 propensity score matching was performed for baseline characteristics. In subgroup analysis of high-risk patients with CV disease, significant difference was not observed between allopurinol and benzbromarone initiators. Conclusion: In this study, significant difference was not found in CV risk between allopurinol and benzbromarone initiators. In the high-CV-risk group, the incidence of CV events did not differ between allopurinol and benzbromarone initiators.

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Section: Discussionmentioning

confidence: 97%

“…In human brain microvascular endothelial cells, benzbromarone inhibited propofol-induced production of mitochondrial ROS, inflammatory factors, and adhesion molecules, indicating that benzbromarone may have protective properties against endothelial injury of the brain. 40…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular risk associated with allopurinol or benzbromarone treatment in patients with gout

Eun

Han

Kim

et al. 2022

Therapeutic Advances in Musculoskeletal

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“…Benzbromarone is a kind of inhibiting renal tubular transporter URAT‐1 to promote uric acid excretion. In the process of ROS activation caused by high uric acid levels, benzbromarone can inhibit the activation of peroxides by reducing uric acid levels, thereby exerting an antioxidant effect (Huang et al, 2021; Muraya et al, 2018; Zhang et al, 2021). In summary, allopurinol and benzbromarone, as classic uric acid‐lowering drugs, can improve endothelial oxidative stress caused by high uric acid by reducing uric acid levels, thereby improving endothelial function and ED.…”

Section: Discussionmentioning

confidence: 99%

Hyperuricaemia is an important risk factor of the erectile dysfunction: A systematic review and meta‐analysis

et al. 2022

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Serum uric acid can affect endothelial function, and hyperuricaemia‐induced endothelial dysfunction is involved in the pathogenesis of cardiovascular diseases. As endothelial dysfunction is also a main pathogenic mechanism of erectile dysfunction (ED), the present study aims to evaluate the relationship between hyperuricaemia and ED via systemic review and meta‐analysis. Five cohort studies and six cross‐sectional studies on hyperuricaemia and ED, including a total of 454,510 participants, were recruited. Odds ratio (OR) and the 95% confidence intervals (CI) were adopted to estimate the relationship between hyperuricaemia and ED. Overall risk on effects of urate‐lowering therapy (ULT) were analysed. In addition, subgroup analyses on study design, populations, age stratification and the object were conducted. In the patients with hyperuricaemia, the risk of ED was 1.59‐fold higher than (pooled OR = 1.59, 95% CI [1.29, 1.97]) the non‐hyperuricaemia counterparts. Urate‐lowing therapy (ULT) in these hyperuricaemia patients reduced the risk of ED by 27% (OR = 1.27, 95% CI [1.14, 1.41]). After subgroup analysis, the association between hyperuricaemia and ED remained significant apart from the >60 years subgroup. Hyperuricaemia is an important risk factor of ED, while ULT can reduce the risk of ED in hyperuricaemia. This study suggests that hyperuricaemia‐associated endothelial dysfunction may also underlie the pathogenesis of ED in these patients.

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“…The antigout drugs benzbromarone and febuxostat have significant anti-inflammatory and antioxidant stress effects. , Studies found that benzbromarone can mitigate propofol-induced inflammation and oxidative stress of brain endothelial cells by downregulating the transcriptional factor Egr-1, while febuxostat can attenuate propofol-induced inflammation and oxidative stress of brain endothelial cells by upregulating the transcriptional factor Kruppel-like factor 6 (KLF6). , …”

Section: Therapeutic Strategies For Propofol-induced Neurotoxicitymentioning

confidence: 99%

Propofol-Induced Developmental Neurotoxicity: From Mechanisms to Therapeutic Strategies

Zhang

Liu

2023

ACS Chem. Neurosci.

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Propofol is the most commonly used intravenous general anesthetic in clinical anesthesia, and it is also widely used in general anesthesia for pregnant women and infants. Some clinical and preclinical studies have found that propofol causes damage to the immature nervous system, which may lead to neurodevelopmental disorders and cognitive dysfunction in infants and children. However, its potential molecular mechanism has not been fully elucidated. Recent in vivo and in vitro studies have found that some exogenous drugs and interventions can effectively alleviate propofol-induced neurotoxicity. In this review, we focus on the relevant preclinical studies and summarize the latest findings on the potential mechanisms and therapeutic strategies of propofolinduced developmental neurotoxicity.

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The Protective Effects of Benzbromarone Against Propofol-Induced Inflammation and Injury in Human Brain Microvascular Endothelial Cells (HBMVECs)

Cited by 7 publications

References 37 publications

Cardiovascular risk associated with allopurinol or benzbromarone treatment in patients with gout

Cardiovascular risk associated with allopurinol or benzbromarone treatment in patients with gout

Hyperuricaemia is an important risk factor of the erectile dysfunction: A systematic review and meta‐analysis

Propofol-Induced Developmental Neurotoxicity: From Mechanisms to Therapeutic Strategies

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