ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University
[Genistein alleviates cerebral ischemia/reperfusion-induced inflammatory injury in rats by regulating microglial polarization
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University. 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
objectivesTo investigate the mechanism of genistein for alleviating cerebral ischemia/reperfusion (I/R)-induced neuroinflammation in microglia and its protective effects on co-cultured neurons.
methodsMale SD rats were divided into control group, I/R group, and 3 genistein groups treated with 25, 50 or 100 mg/kg genistein before I/R modeling (
resultsThe rat models of I/R exhibited obvious M1 polarization of the microglia, as shown by upregulated CD86, IL‑6, IL‑8, IL‑1β, TNF‑α, PI3K, AKT, and COX‑2 expressions and downregulated IL‑4 and TGF‑β expressions. Genistein treatment effectively reversed M1 polarization of the microglia, downregulated pro‑inflammatory factors and the PI3K/AKT/COX‑2 pathway, and promoted M2 polarization of the microglia in the mouse models. The COX‑2 inhibitor celecoxib produced similar effects to genistein by decreasing the expressions of M1 markers, TNF‑α, PI3K, AKT, and COX‑2 and increasing M2 markers and TGF‑β expression. In cultured BV-2 cells, genistein significantly inhibited OGD/R‑induced M1 polarization and pro‑inflammatory responses, and such protective effects were mimicked by PI3K knockdown, whereas PI3K activation by 740Y‑P partially counteracted the effects of genistein. In the neuron‑microglia co‑culture system, genistein obviously reduced OGD/R‑induced neuronal apoptosis, enhanced cell viability, decreased cleaved caspase‑3 and Bax expressions, and increased Bcl‑2 and BDNF expressions.
conclusionsGenistein alleviates cerebral I/R-induced neuroinflammatory injury in rats by promoting M2 polarization of the microglia
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