ArticleNeurocritical care2025
Involvement of Periostin in Acute Neuronal Apoptosis Induced by Subarachnoid Hemorrhage in Mice and its Suppression by Clarithromycin.
Article in Neurocritical care, 2025. 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
backgroundPeriostin is an inflammation-related matricellular protein that has been reported to increase in the acute phase after subarachnoid hemorrhage (SAH) in clinical settings. However, its relationship with neuronal apoptosis, a characteristic of early brain injury, remains unknown. The purpose of this study was to investigate the involvement of periostin in SAH-induced acute neuronal apoptosis and to determine whether clarithromycin (CAM), a macrolide antibiotic known to suppress periostin expression, prevents acute neuronal apoptosis after SAH in mice.
methodsIn 141 male C57BL/6 mice undergoing endovascular perforation SAH or sham operation, vehicle or CAM (50 mg/kg) was administered subcutaneously 5 min after surgery, followed by intracerebroventricular administration of vehicle or recombinant mouse periostin (R-periostin) 30 min after surgery. The intervention effects were assessed 24 h after surgery by neurological score, Western blotting, and double immunostaining.
resultsAfter induction of SAH, neurological scores worsened, and caspase-3-dependent neuronal apoptosis was increased, which was associated with upregulation of periostin expression in the left (perforation side) cerebral hemisphere compared with sham-operated animals (p < 0.01 vs. sham + vehicle group, respectively). Administration of CAM improved neurological scores and reduced caspase-3-dependent neuronal apoptosis as well as periostin expression in SAH mice (p < 0.05, p < 0.01, p < 0.01 vs. SAH + vehicle group, respectively). The protective effects of CAM on neurological scores and neuronal apoptosis after SAH were counteracted by administration of R-periostin (SAH + CAM + vehicle group vs. SAH + CAM + R-periostin group, p < 0.05 and p < 0.001, respectively). Immunohistochemical analysis confirmed overexpression of periostin in neurons after SAH, which was attenuated by CAM treatment but re-increased by administration of R-periostin.
conclusionsThese findings indicate that periostin-driven signaling contributes to caspase-dependent neuronal apoptosis during early brain injury after SAH. This study highlights periostin as a potential therapeutic target to attenuate SAH-induced acute neuronal apoptosis and demonstrates that CAM holds promise as an antiapoptotic agent through periostin inhibition.
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