
The role of blood lnc‐ZFAS1 in acute ischemic stroke: correlation with neurological impairment, inflammation, and survival profiles
Author(s) -
Wang Gang,
Zhou Ying,
Zhong Tingting,
Song Aixia,
Xue Qian
Publication year - 2022
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.24219
Subject(s) - inflammation , medicine , interleukin 6 , tumor necrosis factor alpha , gastroenterology , immunology , biology , oncology
Background Long non‐coding RNA zinc finger antisense 1 (lnc‐ZFAS1) has been reported to inhibit neuronal damage in acute ischemic stroke (AIS). However, the role of lnc‐ZFAS1 in AIS patients remains unclear. Therefore, we assessed the relationship of lnc‐ZFAS1 with neurological impairment, inflammation, and prognosis in AIS patients. Methods Totally, 241 AIS patients and 120 controls were enrolled. lnc‐ZFAS1 in peripheral blood mononuclear cells was evaluated using reverse transcription‐quantitative polymerase chain reaction. Besides, a 3‐year follow‐up was conducted to assess recurrence‐free survival (RFS) and overall survival (OS) in AIS patients. Results lnc‐ZFAS1 was reduced in AIS patients compared to that in controls ( Z = −10.693, p < 0.001). In AIS patients, lnc‐ZFAS1 was negatively correlated with National Institutes of Health Stroke Scale score ( r s = −0.335, p < 0.001), C‐reactive protein ( r s = −0.284, p < 0.001), tumor necrosis factor‐alpha ( r s = −0.293, p < 0.001), interleukin‐1β ( r s = −0.149, p = 0.021), and interleukin‐6 ( r s = −0.161, p = 0.012), but not underlying diseases (all p > 0.05). Besides, lnc‐ZFAS1 was divided into high and low levels based on the median expression in AIS patients. Indeed, high lnc‐ZFAS1 predicted better RFS ( χ 2 = 6.222, p = 0.013); the 1‐year, 2‐year, and 3‐year RFS rates were 94.2%, 88.3%, and 85.5%, respectively, in patients with high lnc‐ZFAS1, then 87.5%, 79.2%, and 71.6%, respectively, in those with low lnc‐ZFAS1. However, lnc‐ZFAS1 was not correlated with OS ( χ 2 = 1.404, p = 0.236); the 1‐year, 2‐year, and 3‐year OS rates were 98.3%, 95.8%, and 94.0%, respectively, in patients with high lnc‐ZFAS1, then 96.7%, 93.9%, and 89.6%, respectively, in those with low lnc‐ZFAS1. Conclusion Lower lnc‐ZFAS1 expression is connected with increased neurological impairment and inflammation as well as worse RFS in AIS patients.