The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.

The blood-brain barrier (BBB), as a crucial gate of brain-blood molecular exchange, is involved in the pathogenesis of multiple neurological diseases. Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the scavenger system. Since oxidative stress plays a significant role in the production and maintenance of the BBB, the cerebrovascular system is especially vulnerable to it. The pathways that initiate BBB dysfunction include, but are not limited to, mitochondrial dysfunction, excitotoxicity, iron metabolism, cytokines, pyroptosis, and necroptosis, all converging on the generation of ROS. Interestingly, ROS also provide common triggers that directly regulate BBB damage, parameters including tight junction (TJ) modifications, transporters, matrix metalloproteinase (MMP) activation, inflammatory responses, and autophagy. We will discuss the role of oxidative stress-mediated BBB disruption in neurological diseases, such as hemorrhagic stroke, ischemic stroke (IS), Alzheimer’s disease (AD), Parkinson’s disease (PD), traumatic brain injury (TBI), amyotrophic lateral sclerosis (ALS), and cerebral small vessel disease (CSVD). This review will also discuss the latest clinical evidence of potential biomarkers and antioxidant drugs towards oxidative stress in neurological diseases. A deeper understanding of how oxidative stress damages BBB may open up more therapeutic options for the treatment of neurological diseases.

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Background: Ischemic stroke (IS) is a leading cause of death and long-term disability worldwide. The NaoShuanTong capsule (NSTC), a traditional Chinese patent medicine, has been extensively used in the treatment of stroke in China. However, the clinical efficacy and safety of this treatment has not been statistically and systematically verified by any comprehensive pooled analysis. We therefore performed a meta-analysis to evaluate the efficacy and safety of NSTC in the treatment of IS.Methods: Randomized controlled trials (RCTs) of NSTC in the treatment of IS conducted before September 2018 were retrieved from five databases, according to specific inclusion and exclusion criteria. Two investigators independently reviewed the included studies and extracted relevant data. The methodological quality of the included studies was assessed using criteria from the Cochrane Handbook, and analyzed using Review Manager 5.3 software.Results: Thirteen RCTs comprising a total of 1,360 participants were included in this study. NSTC was shown to significantly improve the overall response rate (OR = 3.04, 95% CI [1.76, 5.26], P < 0.00001), and neurological function (NSTC increased Modified Barthel Index (MD = 8.15, 95% CI [3.79, 12.52], P = 0.0005), Functional Independence Measure (MD = 29.61, 95% CI [10.11, 49.10], P = 0.003) and European Stroke Scale scores (MD = 8.51, 95% CI [7.00, 10.01], P = 0.03). In addition, NSTC significantly increased serum adiponectin level (MD = 0.66, 95% CI [0.23, 1.08], P = 0.002). Moreover, NSTC reduced atherosclerotic plaque area (MD = -2.24, 95% CI [-4.02, -0.46], P = 0.01) and intima-media thickness (MD = -0.09, 95% CI [-0.13, -0.05], P < 0.0001). However, there was no significant difference between NSTC treatment and conventional therapy with respect to Fugl-Meyer Assessment score (MD = 10.59, 95% CI [-1.78, 22.96], P = 0.09) or Crouse score (MD = -0.78, 95% CI [-1.79, -0.22], P = 0.13).Conclusions: The results of this meta-analysis showed that NSTC exhibits efficacy in the treatment of cerebral infarction. NSTC can improve the overall response rate and neurological function, increase blood adiponectin, reduce neurological deficits, and decrease atherosclerotic plaque area.