Analysis of Serum VCAN-AS1 Expression Level in Patients with Cerebral Infarction Secondary Epilepsy and Its Mechanism by Regulating miR-885-3p/NTNG1
Brief intro:
- Author: Yang Lin, Kun Zhang, Meijie Zhang, Lida Yin, Zhixin Liu, Yanru Meng, Yue Li, Jinhui Meng, Xueyong Yin & Liping Wang
- Journal: Neurochemical Research
- Doi: https://www.doi.org/10.1007/s11064-026-04697-8
- Publication Date: 2026/3/4
Abstract
VCAN-AS1 is a novel long non-coding RNA that participates in diverse disease processes, but the mechanism of its action in cerebral infarction secondary epilepsy (CISE) is unclear. The potential action mechanism of VCAN-AS1 in CISE was explored by this study. VCAN-AS1 and its downstream targets, namely miR-885-3p and Netrin G1 (NTNG1), were screened by the GEO, LncRNASNP2, and miRDB databases. The epileptic mouse and cell models were constructed using pilocarpine and the Mg2+-free medium, respectively. ELISA kits or RT-qPCR was used for the measurement of TNF-α/IL-1/IL-6 levels. The levels of Fe2+, GSH, and ROS were detected by the specific biochemical kits. GPX4 expression was analyzed by RT-qPCR. Dual-luciferase reporter assay was used to detect the interactions between miR-885-3p and VCAN-AS1 or NTNG1. Meanwhile, the expression levels of VCAN-AS1, miR-885-3p, and NTNG1 were detected by RT-qPCR. Elevated serum levels of VCAN-AS1 were observed in patients with CISE, and silencing of VCAN-AS1 attenuated inflammation and ferroptosis in epilepsy-associated neurons and the hippocampus of epileptic mice. VCAN-AS1 negatively regulated miR-885-3p which subsequently repressed NTNG1 expression. Up-regulation of miR-885-3p inhibited inflammation and ferroptosis in epileptic mouse and cell models, and overexpression of NTNG1 reversed these effects of miR-885-3p. The suppression of VCAN-AS1 expression mitigated neuronal inflammation and ferroptosis in epileptic conditions by targeting the miR-885-3p/NTNG1 regulatory axis, which may be an important molecular mechanism of CISE.
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