Curcumin inhibits microglia inflammation and confers neuroprotection in intracerebral hemorrhage

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.

Keywords: Curcumin; Intracerebral hemorrhage; Microglia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Line
  • Cell Movement / drug effects
  • Cerebral Hemorrhage / immunology
  • Cerebral Hemorrhage / metabolism
  • Cerebral Hemorrhage / pathology*
  • Curcumin / pharmacology*
  • Cytokines / metabolism
  • Disease Models, Animal
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation / pathology*
  • Inflammation Mediators / metabolism
  • Male
  • Mice
  • Microglia / drug effects*
  • Microglia / immunology
  • Microglia / metabolism
  • NF-kappa B / metabolism
  • Neuroprotective Agents / pharmacology*
  • Protein Kinase C / metabolism
  • Signal Transduction / drug effects
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Cytokines
  • Inflammation Mediators
  • NF-kappa B
  • Neuroprotective Agents
  • Protein Kinase C
  • p38 Mitogen-Activated Protein Kinases
  • Curcumin