Anti-inflammation Effects of Oxysophoridine on Cerebral Ischemia-Reperfusion Injury in Mice
- Inflammation. 2015 Dec;38(6):2259-68. doi: 10.1007/s10753-015-0211-4.
- 1. Department of Pharmacology, Ningxia Medical University, Yinchuan, 750004, China.
- 2. College of Nursing, Ningxia Medical University, Yinchuan, 750004, China.
- 3. Ningxia Medical University, Yinchuan, 750004, China.
- 4. Medical Sci-Tech Research Center, Ningxia Medical University, Yinchuan, 750004, China.
- 5. Ningxia Key Lab of Craniocerebral Diseases of Ningxia Hui Autonomous Region, Yinchuan, 750004, China.
- 6. Department of Pharmacology, Ningxia Medical University, Yinchuan, 750004, China. [email protected].
- 7. Ningxia Hui Medicines Collaborative Innovation Center, Yinchuan, 750004, China. [email protected].
- 8. Department of Pharmacology, Ningxia Medical University and Ningxia Hui Medicines Collaborative Innovation Center, Yinchuan, Ningxia, China. [email protected].
Oxysophoridine (OSR) is a bioactive alkaloid extracted from the Sophora alopecuroides Linn. Our aim is to explore the potential anti-inflammation mechanism of OSR in cerebral ischemic injury. Mice were intraperitoneally pretreated with OSR (62.5, 125, and 250 mg/kg) or nimodipine (Nim) (6 mg/kg) for 7 days followed by cerebral ischemia. The inflammatory-related cytokines in cerebral ischemic hemisphere tissue were determined by immunohistochemistry staining, Western blot and enzyme-like immunosorbent assay (ELISA). OSR-treated groups observably suppressed the nuclear factor kappa B (NF-κB), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). OSR-treated group (250 mg/kg) markedly reduced the inflammatory-related protein prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8). Meanwhile, it dramatically increased the interleukin-10 (IL-10). Our study revealed that OSR protected neurons from ischemia-induced injury in mice by downregulating the proinflammatory cytokines and blocking the NF-κB pathway.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: ApoptosisResearch Areas: Inflammation/Immunology