| Abstract Objective: To investigate the effects of nicergoline combined with early tenecteplase thrombolytic therapy on cerebral neurotransmitters, cerebrovascular reserve function, and the NOD-like receptor pyrin domain-containing protein 3 (NLRP3) signaling pathway in patients with acute stroke. Methods: A total of 384 patients with acute stroke were randomly divided into a control group and a study group, with 192 cases in each. The control group received tenecteplase, while the study group received nicergoline in addition to tenecteplase. Both groups were treated continuously for 2 weeks, and the clinical efficacy was evaluated. Before and after treatment, neurological function and cognitive function were assessed using the National Institutes of Health Stroke Scale (NIHSS) and the Mini-Mental State Examination (MMSE), respectively. Serum levels of cerebral neurotransmitters were measured by enzyme-linked immunosorbent assay (ELISA). Cerebrovascular reserve (CVR) and pulsatility index (PI) were determined using Doppler ultrasound. The relative mRNA expression levels of NLRP3, caspase-1, and apoptosis-associated speck-like protein (ASC) were measured using fluorescence quantitative detection kits. Results: The total clinical effective rate in the study group was higher than that in the control group (92.19% vs. 80.73%, P< 0.05). After treatment, NIHSS scores decreased and MMSE scores increased in both groups, with the study group showing significantly lower NIHSS scores and higher MMSE scores (all P< 0.05). After treatment, the levels of cerebral neurotransmitters (5-hydroxytryptamine, norepinephrine, dopamine, and acetylcholine) and CVR% increased in both groups, with significantly greater increases in the study group (all P <0.05). Meanwhile, the mRNA expression levels of NLRP3, caspase-1, and ASC, as well as PI, decreased in both groups, with significantly greater decreases in the study group (all P< 0.05). Conclusion: Nicergoline combined with early tenecteplase thrombolytic therapy can increase the expression levels of cerebral neurotransmitters and improve cerebrovascular reserve function. The mechanism may be related to the inhibition of the NLRP3 inflammasome signaling pathway. |
