{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T06:40:02Z","timestamp":1751524802378,"version":"3.41.0"},"reference-count":29,"publisher":"Scientific Scholar","content-domain":{"domain":["cytojournal.com"],"crossmark-restriction":true},"short-container-title":["Cytojournal"],"abstract":"<jats:sec id=\"st1\">\n<jats:title>Objective:<\/jats:title>\n<jats:p>Acute cerebral infarction (ACI) has a high incidence and complex etiology, so searching for specific diagnosis and therapeutic target molecules is highly important. This paper aimed to explore the mechanism of karyopherin alpha 4 (<jats:italic>KPNA4<\/jats:italic>) in ACI.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"st2\">\n<jats:title>Material and Methods:<\/jats:title>\n<jats:p>Four groups were established: sham group, middle cerebral artery occlusion (MCAO) group, MCAO + small interfering negative control (si-NC group), and MCAO + si-<jats:italic>KPNA4<\/jats:italic> group. The Zea-Longa scoring standard was adopted to assess the neurological impairment of ACI rats. The expression of <jats:italic>KPNA4<\/jats:italic> was verified by real-time quantity polymerase chain reaction assay and Western blot. 2,3,5-Triphenyltetrazolium chloride and hematoxylin and eosin staining were used to examine the effects of <jats:italic>KPNA4<\/jats:italic> knockdown on brain injury in ACI rats. The apoptosis of oxygen-glucose deprivation (OGD)-SH-SY5Y cells was measured by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method. Western blot analysis was performed to analyze the expression levels of apoptosis-related proteins, inflammatory factors, and nuclear factor kappa B (NF-\u03baB) pathway-related proteins.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"st3\">\n<jats:title>Results:<\/jats:title>\n<jats:p><jats:italic>KPNA4<\/jats:italic> was overexpressed in the MCAO rat brain (<jats:italic>P<\/jats:italic> &lt; 0.0001) and OGD-SH-SY5Y cells (<jats:italic>P<\/jats:italic> &lt; 0.0001). Knocking down <jats:italic>KPNA4<\/jats:italic> significantly reduced the degree of brain damage (<jats:italic>P<\/jats:italic> &lt; 0.0001) and reduced the apoptosis of OGD-SH-SY5Y cells (<jats:italic>P<\/jats:italic> &lt; 0.001). <jats:italic>KPNA4<\/jats:italic> knockdown also significantly decreased the expression levels of inflammatory factors (interleukin [IL]-1\u03b2, tumor necrosis factor-\u03b1, and IL-18; <jats:italic>P<\/jats:italic> &lt; 0.0001) and prohibited the phosphorylation of the inhibitor of NF-\u03baB and p65 (<jats:italic>P<\/jats:italic> &lt; 0.0001). However, NF-\u03baB agonist lipopolysaccharide reversed the inhibition of <jats:italic>KPNA4<\/jats:italic> knockdown.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"st4\">\n<jats:title>Conclusion:<\/jats:title>\n<jats:p>In general, <jats:italic>KPNA4<\/jats:italic> knockdown can mitigate ACI-induced damage by regulating the NF-kB pathway. This finding provides a new perspective on the treatment of ACI.<\/jats:p>\n<\/jats:sec>","DOI":"10.25259\/cytojournal_8_2025","type":"journal-article","created":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T19:23:05Z","timestamp":1751484185000},"page":"64","update-policy":"https:\/\/doi.org\/10.25259\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Preliminary investigation on the correlation between karyopherin alpha 4 and acute cerebral infarction"],"prefix":"10.25259","volume":"22","author":[{"given":"Jinzhe","family":"Chu","sequence":"first","affiliation":[{"name":"Department of Interventional Medicine, Yantaishan Hospital, Yantai, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nannan","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Neurology, Jinan Central Hospital, Jinan, 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