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Updated: May 5, 2026
Intrastriatal Injection of Autologous Blood or Clostridial Collagenase as Murine Models of Intracerebral Hemorrhage
Published on: July 3, 2014
The LINC00968/miR-194-5p Axis Exacerbates Neurological Dysfunction After Intracerebral Hemorrhage by Regulating
Juncen Wu1, Shuo Sun2, Lihong Ren3
1Department of Neurology, People's Hospital Affiliated to Chongqing Three Gorges Medical College, Chongqing, 404100, China.
Insights
The LINC00968/miR-194-5p axis worsens secondary brain injury after intracerebral hemorrhage (ICH). LINC00968 sponges miR-194-5p, increasing neuroinflammation and oxidative stress.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Secondary neurological injury following intracerebral hemorrhage (ICH) remains a critical challenge.
- Understanding the molecular mechanisms underlying ICH progression is essential for developing effective therapies.
Purpose of the Study:
- To investigate the regulatory role of the LINC00968/miR-194-5p axis in secondary neurological injury after ICH.
- To elucidate the molecular mechanism by which this axis influences ICH outcomes.
Main Methods:
- Established rat ICH and PC12 cell models.
- Utilized RT-qPCR, CCK-8 assay, flow cytometry, and biochemical assays to measure molecular and cellular changes.
- Employed neurological deficit tests, brain edema assessment, dual-luciferase reporter, and RIP assays to validate mechanisms.
Main Results:
- LINC00968 expression was significantly upregulated in both in vivo and in vitro ICH models.
- LINC00968 knockdown improved cell proliferation, reduced apoptosis, oxidative stress, and inflammation.
- LINC00968 acts as a competing endogenous RNA (ceRNA) by sponging miR-194-5p, exacerbating ICH-induced damage.
Conclusions:
- The LINC00968/miR-194-5p axis plays a crucial role in aggravating secondary neurological injury post-ICH.
- LINC00968 exacerbates neuroinflammation and oxidative stress by competitively binding to miR-194-5p.
- Targeting this axis may offer a novel therapeutic strategy for ICH treatment.
Abstract:
This study aims to investigate the regulatory role and molecular mechanism of the LINC00968/miR-194-5p axis in secondary neurological injury after intracerebral hemorrhage (ICH). A rat ICH model was established by injecting collagenase IV. In vitro, PC12 cells were treated with hemin to mimic the ICH environment. RT-qPCR was used to detect the levels of LINC00968 and miR-194-5p. Assessment of cell proliferation and apoptosis was performed with the CCK-8 assay and flow cytometry. The levels of SOD, MDA, ROS, and inflammatory factors (IL-6, TNF-α, IL-10) were measured using commercially available detection kits. To assess neurological deficits, the mNSS, corner turn, and forelimb placement tests were employed. To evaluate brain edema, the dry-wet weight method was utilized. The direct binding between LINC00968 and miR-194-5p was verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. In both in vivo and in vitro ICH models, LINC00968 expression was significantly upregulated. Knockdown of LINC00968 significantly enhanced cell proliferation, inhibited apoptosis, and reduced oxidative stress and inflammation in vitro. In rats, it significantly improved neurological deficits and reduced brain edema. Mechanistically, LINC00968 acts as a competing endogenous RNA (ceRNA) that sponges miR-194-5p. Suppressing miR-194-5p eliminated the neuroprotection resulting from LINC00968 silencing. LINC00968 aggravates neurological deficits, neuroinflammation, and oxidative stress after ICH by competitively binding to miR-194-5p.
