{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T19:54:47Z","timestamp":1775159687264,"version":"3.50.1"},"reference-count":26,"publisher":"Wiley","license":[{"start":{"date-parts":[[2022,1,15]],"date-time":"2022-01-15T00:00:00Z","timestamp":1642204800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Computational and Mathematical Methods in Medicine"],"published-print":{"date-parts":[[2022,1,15]]},"abstract":"<jats:p>Objective. To explore the effect of long noncoding RNA H19 (lncRNA H19) on brain injury in rats following experimental intracerebral hemorrhage (ICH). Methods. Rat ICH model was established with type IV collagenase. The neurological function scores were evaluated, and the water content in brain tissue was measured. The nerve injury indexes, inflammatory factors, and oxidative stress indexes were also measured. Moreover, the expression of lncRNA H19 was determined by qRT-PCR, and Western blot detected NF-\u03baB pathway-related protein expression. Results. Compared with the sham group, the neurological function scores, the water content in brain tissue, and levels of injury indicators myelin basic protein (MBP), S-100B, and neuron-specific enolase (NSE) in the ICH rats were significantly increased. Meanwhile, the levels of TNF-\u03b1, IL-6, IL-1\u03b2, ROS, and MDA were significantly increased, but the levels of SOD were significantly decreased. In addition, the expression of lncRNA H19 in the brain tissue in the ICH group was significantly higher than that in the sham group. After further interference with lncRNA H19 expression (sh-H19 group), the levels of all the above indicators were reversed and the neurological damage was improved. Western blot results showed that the expression of NF-\u03baBp65 and IKK\u03b2 was significantly higher, and I\u03baB\u03b1 expression was lower in the perivascular hematoma tissue in the ICH group compared with the sham group. Compared with the sh-NC group, NF-\u03baBp65 and IKK\u03b2 expression were significantly lower and I\u03baB\u03b1 was significantly higher in the sh-H19 group. Conclusion. lncRNA H19 exacerbated brain injury in rats with ICH by promoting neurological impairment, brain edema, and releasing inflammatory responses and oxidative stress. This may be related to the activation of NF-\u03baB signaling pathway.<\/jats:p>","DOI":"10.1155\/2022\/3017312","type":"journal-article","created":{"date-parts":[[2022,1,15]],"date-time":"2022-01-15T19:35:07Z","timestamp":1642275307000},"page":"1-7","source":"Crossref","is-referenced-by-count":7,"title":["lncRNA H19 Aggravates Brain Injury in Rats following Experimental Intracerebral Hemorrhage via NF-\u03baB Pathway"],"prefix":"10.1155","volume":"2022","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5049-1977","authenticated-orcid":true,"given":"Shuaidong","family":"Mao","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Shanghai Tenth People\u2019s Hospital Chongming Branch, Shanghai 202157, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huan","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Shanghai Tenth People\u2019s Hospital Chongming Branch, Shanghai 202157, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xianzheng","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Shanghai Tenth People\u2019s Hospital, Shanghai 200072, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(09)70025-0"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(11)70264-2"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0707534"},{"issue":"2","key":"4","first-page":"209","article-title":"The protective effect of erigeron on hemorrhagic brain injury in rats","volume":"29","author":"J. 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