ABSTRACT
OBJECTIVES: Higher blood pressure has been proven to be associated with poorer functional outcomes after successful reperfusion by EVT. However, the effect of intensive blood pressure-lowering regimens in these patients remains controversial and ambiguous in clinical practice. We propose further analysis aimed at determining the effect of an intensive blood pressure-lowering regimen after EVT in AIS. METHODS: The protocol registered in PROSPERO CRD42023360989. We performed a systematic search that was comprehensively executed in online databases for studies published up to June 2022. Eligibility criteria were established based on the PICOS model. The Cochrane risk of bias algorithm was used to evaluate the risk of bias. The effect models were applied to calculate the pooled ORs and CIs via Review Manager 5.4 software. RESULTS: A total of 1582 citations were identified, 3 randomized clinical trials and 2 retrospective cohort studies were included. Data from 3211 patients were analyzed. We revealed that intensive blood pressure-lowering interventions could significantly reduce symptomatic intraparenchymal hemorrhage compared with standard blood pressure lowering. Nevertheless, favorable functional outcome, poor outcome, all-cause mortality within 3 months and intraparenchymal hemorrhage in 24 hours showed no significant differences. Subgroup analysis revealed the variability of systolic blood pressure within 24 hours after EVT was not associated with odds of poor outcome and intraparenchymal hemorrhage. CONCLUSIONS: Based on the current evidence, intensive blood pressure-lowering regimen was superior to standard blood pressure-lowering regimen for a reduced risk of symptomatic intraparenchymal hemorrhage in AIS patients treated with EVT, but there was no statistically significant difference found between the 2 regimens for the other outcomes.
ABSTRACT
Hyperglycemia-induced neuronal endoplasmic reticulum (ER) stress is particularly important for the pathogenesis of diabetic encephalopathy. Spermidine (Spd) has neuroprotection in several nervous system diseases. Our current study to explore the potential protective role of Spd in hyperglycemia-induced neuronal ER stress and the underlying mechanisms. HT22 cells were treated with high glucose (HG) to establish an in-vitro model of hyperglycemia toxicity. The HT22 cells' activity was tested by cell counting kit-8 assay. RNA interference technology was used to silence the expression of growth differentiation factor 11 (GDF11) in HT22 cells. The GDF11 expression levels of mRNA were assessed using reverse transcription-PCR (RT-PCR). Western blotting analysis was applied to evaluate the expressions of GRP78 and cleaved caspase-12. Spd markedly abolished HG-exerted decline in cell viability as well as upregulations of GRP78 and cleaved caspase-12 in HT22 cells, indicating the protection of Spd against HG-induced neurotoxicity and ER stress. Furthermore, we showed that Spd upregulated the expression of GDF11 in HG-exposed HT22 cells. While, silenced GDF11 expression by RNA interference reversed the protective effects of Spd on HG-elicited neurotoxicity and ER stress in HT22 cells. These results indicated that Spd prevents HG-induced neurotoxicity and ER stress through upregulation of GDF11. Our findings identify Spd as a potential treatment for diabetic encephalopathy as well as ER stress-related neurologic diseases.
