Sinomenine inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage

• DOI: 10.1016/j.molimm.2014.03.005
• Publication Date: 2014-05-08T11:16:43Z
• Authors: Zhao Yang; Yongping Liu; Fang Yuan; Zhen Li; Shaokuan Huang; Hanchao Shen; Bangqing Yuan
• Keywords: Inflammation; Male; Interleukin-6; Tumor Necrosis Factor-alpha; Interleukin-1beta; NF-kappa B; Cell Line; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Neuroprotective Agents; 0302 clinical medicine; Morphinans; Cell Movement; Brain Injuries; Animals; Microglia; Reactive Oxygen Species; Cerebral Hemorrhage

Intracerebral hemorrhage (ICH) causes morbidity and mortality and commonly follows the reperfusion after an ischemic event. Microglial activation mediated cytokine and protease secretion contributes to brain injury in ICH. Previous studies have shown that sinomenine possesses potent immunoregulatory properties. However, little is known about its exact role in ICH. In the present study, to investigate the effect of sinomenine on microglial cells inflammation, we treated ICH-challenged BV2 microglial cells with sinomenine in vitro, and explored its neuroprotection role in intracerebral hemorrhage in vivo. Changes in inflammatory cytokines, such as TNF-α, IL-1β and IL-6, reactive oxygen species (ROS) and NF-κB activation NF-κB were observed. In addition, the neurological deficit and cerebral water content of ICH mice were studied. The results demonstrated that sinomenine could inhibit the release of these cytokines and attenuate ROS production in a dose-dependent manner, and reduce NF-κB activation. Furthermore, sinomenine markedly inhibited cerebral water content and neurological deficit. In conclusion, our findings suggest that sinomenine played the protective effects through inhibition of microglial inflammation, and the findings also provided a novel therapy to treat ICH induced brain injury.