ArticleBrain sciences2026
Notoginsenoside R1 Attenuates Oxidative Damage After Intracerebral Hemorrhage by Inhibiting LCN2 and Promoting HO-1 in Astrocytes.
Article in Brain sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesIntracerebral hemorrhage (ICH) is a devastating form of stroke characterized by high morbidity and mortality, but effective treatment strategy remains in urgent demand. Notoginsenoside R1 (NGR1), a bioactive component extracted from the traditional herb
methodsNGR1 was administrated to a collagenase-induced ICH mouse model and hemin-stimulated primary astrocytes in vitro. Hematoma volume, brain water content and neurobehavioral outcomes were assessed in the ICH mice. Cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay. In astrocytes pretreated with 25 μM NGR1 for 24 h followed by 30 μM hemin treatment for 24 h, levels of reactive oxygen species (ROS), malondialdehyde (MDA), and the glutathione (GSH)/oxidized glutathione (GSSG) ratio were measured. The expression of lipocalin-2 (LCN2), heme oxygenase-1 (HO-1), and glial fibrillary acidic protein (GFAP) was detected via immunofluorescence staining and Western blotting. Additionally, LCN2 and HO-1 were knocked down in astrocytes, using small interfering RNA (siRNA) transfection.
resultsLCN2, HO-1, and GFAP expression was upregulated in the peri-lesional area of the brain following ICH. NGR1 alleviated brain injury and improved neurological function in the collagenase-induced ICH mouse model. Specifically, administration of 20 mg/kg NGR1 suppressed the upregulation of LCN2 and increased HO-1 expression post ICH. NGR1 enhanced cell viability and reversed hemin-induced toxicity in astrocytes in vitro. Treatment with 25 μM NGR1 reduced ROS and MDA levels and upregulated the GSH/GSSG ratio in astrocytes exposed to 30 μM hemin. Furthermore, 25 μM NGR1 inhibited LCN2 and GFAP expression while promoting HO-1 expression in hemin-treated astrocytes. The inhibitory effect of NGR1 on LCN2 was reversed by the Nrf-2/HO-1 inhibitor ML385. Moreover, LCN2 knockdown promoted HO-1 expression and suppressed ROS levels in astrocytes. Conversely, HO-1 knockdown increased LCN2 and GFAP expression, thereby reversing the protective effects of NGR1.
conclusionsThis study demonstrates that NGR1 alleviates ICH-induced oxidative damage by promoting HO-1 expression and inhibiting LCN2 expression, thereby maintaining redox homeostasis.
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