Yang Zhao, Zhao Tianzhi, Zou Yongjie, Zhang John H, Feng Hua
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, Shaanxi Province, China.
Immunol Lett. 2014 Jul;160(1):89-95. doi: 10.1016/j.imlet.2014.03.005. Epub 2014 Mar 25.
Much evidence demonstrates that microglia mediated neuroinflammation is an important contributor to the inflammatory injury in intracerebral hemorrhage (ICH). Therefore, the compounds that can inhibit neuroinflammation are greatly needed. In the current study, we examined whether curcumin, present in a Chinese medicinal plant, could prevent ICH induced microglia activation and confer protection against neurotoxicity. The cytokines of microglia were measured by ELISA, p38MAPK/PKC and NF-κB were measured by Western blot and EMSA. Microglial toxicity was assessed using MTT and FACS assays. And neurological function was evaluated by animal behavioristics. We found that curcumin prevented ICH-induced inflammatory molecules through NF-κB activation via the p38MAPK/PKC pathway in vitro. In addition, curcumin protected hippocampal HT22 cells from indirect toxicity mediated by ICH-treated microglia cells. Further, curcumin also attenuated ICH-induced neurological deficit and cerebral water content in vivo. Together, our findings suggest that curcumin could suppress ICH induced inflammatory injury and represent a novel herbal sources for ICH therapeutical strategy.
大量证据表明，小胶质细胞介导的神经炎症是脑出血（ICH）炎症损伤的重要促成因素。因此，非常需要能够抑制神经炎症的化合物。在本研究中，我们检测了一种中药植物中的姜黄素是否可以预防ICH诱导的小胶质细胞活化并赋予对神经毒性的保护作用。通过ELISA检测小胶质细胞的细胞因子，通过蛋白质印迹法和电泳迁移率变动分析（EMSA）检测p38丝裂原活化蛋白激酶/蛋白激酶C（p38MAPK/PKC）和核因子κB（NF-κB）。使用MTT和流式细胞术（FACS）分析评估小胶质细胞毒性。并通过动物行为学评估神经功能。我们发现姜黄素在体外通过p38MAPK/PKC途径激活NF-κB来预防ICH诱导的炎症分子。此外，姜黄素保护海马HT22细胞免受ICH处理的小胶质细胞介导的间接毒性。此外，姜黄素在体内也减轻了ICH诱导的神经功能缺损和脑含水量。总之，我们的研究结果表明姜黄素可以抑制ICH诱导的炎症损伤，并代表了一种用于ICH治疗策略的新型草药来源。
