作者: Yong-Sheng Wang , Yu-Xiang Li , Peng Zhao , Hong-Bo Wang , Ru Zhou
DOI: 10.1007/S10753-015-0211-4
关键词: Nimodipine 、 Pharmacology 、 Proinflammatory cytokine 、 Western blot 、 Prostaglandin E2 、 Nitric oxide synthase 、 Ischemia 、 Reperfusion injury 、 Medicine 、 Tumor necrosis factor alpha 、 Immunology
摘要: Oxysophoridine (OSR) is a bioactive alkaloid extracted from the Sophora alopecuroides Linn. Our aim to explore potential anti-inflammation mechanism of OSR in cerebral ischemic injury. Mice were intraperitoneally pretreated with (62.5, 125, and 250 mg/kg) or nimodipine (Nim) (6 mg/kg) for 7 days followed by ischemia. The inflammatory-related cytokines hemisphere tissue determined immunohistochemistry staining, Western blot enzyme-like immunosorbent assay (ELISA). OSR-treated groups observably suppressed nuclear factor kappa B (NF-κB), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2). group (250 mg/kg) markedly reduced protein prostaglandin E2 (PGE2), tumor necrosis alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8). Meanwhile, it dramatically increased interleukin-10 (IL-10). study revealed that protected neurons ischemia-induced injury mice downregulating proinflammatory blocking NF-κB pathway.