In the present study, the expression of microRNA (miR)‑132 and the mechanism by which it modifies angiogenesis in patients with ischemic cerebrovascular disease (ICD) was investigated. RNA isolation and reverse transcription‑quantitative polymerase chain reaction were used to measure miR‑132 expression in patients with ICD. Inflammatory factors were measured using ELISA kits and western blotting measured B‑cell lymphoma‑2 (Bcl‑2)‑associated X/Bcl‑2 ratio (Bax/Bcl‑2 ratio), nuclear factor (NF)‑κB p65, matrix metalloproteinase‑9 (MMP‑9), vascular cell adhesion molecule‑1 (VCAM‑1) and protein expression of inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) protein expression. miR‑132 expression in patients with ICD was lower compared with healthy volunteers. PC12 cells were used to create an oxygen glucose deprivation (OGD) model. miR‑132 overexpression in an in vitro model was able to reduce tumor necrosis factor‑a, interleukin (IL)‑1β, IL‑6, IL‑8, cyclooxygenase‑2, caspase‑3 and caspase‑9 levels, suppress Bax/Bcl‑2 ratio, NF‑κB p65, MMP‑9, VCAM‑1, iNOS, VEGF protein expression. The results suggested that miR‑132 may modify angiogenesis in patients with ICD by suppressing the NF‑κB pathway and promoting the VEGF pathway, and may develop into a therapy for ICD in future research.

Background We aimed to investigate the risk factors of early neurological deterioration (END) after intravenous thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) and the relationship between END and poor 3-month functional outcomes. Methods Patients who accepted intravenous recombinant rt-PA were enrolled continuously. END was defined as an increase in National Institute of Health Stroke (NIHSS) score ≥ 4 points or death within 24 hours after intravenous thrombolysis. The modified Rankin Scale (mRS) score was recorded to evaluate the functional outcome of stroke, and the poor 3-month prognosis was defined as an mRS score ≥ of 3. Univariate and multivariate analyses were used to analyze the risk factors of END. The relation between END and 3-month functional outcome was analyzed by multivariate logistic regression analysis. Results A total of 1107 patients (mean age, 63.42 ± 11.33 years; 673 males) were included in the final analysis, and 81(7.32%) patients had END. In multivariate analysis, the serum glucose level was significantly associated with END; the odds ratio was 1.10 (95% CI 1.03 to 1.18, p = 0.004). The multivariate logistic analysis showed END has a notable association with the poor 3-month functional recovery even after adjusting for confounding factors; the adjusted OR was 8.25 (95% CI 3.77 to 18.03, p < 0.0001). Conclusions The initial serum glucose level might be an independent risk factor of END, and END might predict a poor 3-month prognosis.

In the present study, the aim was to investigate the function of microRNA-323 (miR-323) in cerebral infarction and its underlying mechanism. A rat model of cerebral infarction was established and hippocampal tissues were analyzed. In addition, to further understand the role of miR-323, PC12 cells were transfected with miR-323 mimics or inhibitors and subjected to hypoxia to model cerebral infarction. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression of miR-323. A luciferase reporter assay was conducted to analyze miR-323 target sites the partial sequence of the 3'-untranslated region of SMAD3 mRNA in vitro. Western blot analysis was also used to analyze transforming growth factor-β1 (TGF-β1) and SMAD3 protein expression levels. It was observed that miR-323 expression was significantly upregulated in rats with cerebral infarction compared with rats in the sham-control group. In addition, overexpression of miR-323 induced nerve cell toxicity and reduced nerve cell growth in an in vitro model of cerebral infarction, whereas downregulation of miR-323 caused the opposite effects on nerve cell toxicity and growth in this model. In addition, overexpression of miR-323 directly targeted and suppressed SMAD3 expression in the in vitro model of cerebral infarction, while inhibition of miR-323 induced SMAD3 expression. The use of a SMAD3 inhibitor suppressed the effect of anti-miR-323 on nerve cell toxicity in the in vitro model of cerebral infarction. Collectively, these findings suggested that miR-323 suppresses nerve cell apoptosis in cerebral infarction via the TGF-β1/SMAD3 signaling pathway.