Intracerebral hemorrhage (ICH) is a severe stroke subtype caused by the rupture of blood vessels within the brain. Increased levels of S100B protein may contribute to neuroinflammation after ICH through activation of astrocytes and resident microglia, with the consequent production of proinflammatory cytokines and reactive oxygen species (ROS). Inhibition of astrocytic synthesis of S100B by arundic acid (AA) has shown beneficial effects in experimental central nervous system disorders. In present study, we administered AA in a collagenase-induced ICH rodent model in order to evaluate its effects on neurological deficits, S100B levels, astrocytic activation, inflammatory, and oxidative parameters. Rats underwent stereotactic surgery for injection of collagenase in the left striatum and AA (2 μg/μl; weight × 0.005) or vehicle in the left lateral ventricle. Neurological deficits were evaluated by the Ladder rung walking and Grip strength tests. Striatal S100B, astrogliosis, and microglial activation were assessed by immunofluorescence analysis. Striatal levels of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) were measured by ELISA, and the ROS production was analyzed by dichlorofluorescein (DCF) oxidation. AA treatment prevented motor dysfunction, reduced S100B levels, astrogliosis, and microglial activation in the damaged striatum, thus decreasing the release of proinflammatory cytokines IL-1β and TNF-α, as well as ROS production. Taken together, present results suggest that AA could be a pharmacological tool to prevent the harmful effects of increased S100B, attenuating neuroinflammation and secondary brain damage after ICH.

脑出血 (ICH) 是一种由脑内血管破裂引起的严重中风亚型。S100B 蛋白水平升高可能通过星形胶质细胞和常驻小胶质细胞的激活导致 ICH 后的神经炎症，从而产生促炎细胞因子和活性氧 (ROS)。Arundic 酸 (AA) 抑制星形胶质细胞合成 S100B 已在实验性中枢神经系统疾病中显示出有益效果。在本研究中，我们在胶原酶诱导的 ICH 啮齿动物模型中施用 AA，以评估其对神经功能缺损、S100B 水平、星形胶质细胞激活、炎症和氧化参数的影响。大鼠接受立体定向手术，在左侧纹状体和 AA 中注射胶原酶（2 μg/μl；体重×0. 005) 或车辆在左侧侧脑室。通过梯级行走和握力测试评估神经功能缺损。通过免疫荧光分析评估纹状体 S100B、星形胶质细胞增生和小胶质细胞活化。通过ELISA测量白细胞介素1β（IL-1β）和肿瘤坏死因子α（TNF-α）的纹状体水平，并通过二氯荧光素（DCF）氧化分析ROS的产生。AA 治疗可防止运动功能障碍、降低 S100B 水平、星形胶质细胞增生和受损纹状体中的小胶质细胞活化，从而减少促炎细胞因子 IL-1β 和 TNF-α 的释放以及 ROS 的产生。总之，目前的结果表明，AA 可能是一种药理学工具，可以防止 S100B 增加的有害影响，减轻 ICH 后的神经炎症和继发性脑损伤。通过梯级行走和握力测试评估神经功能缺损。通过免疫荧光分析评估纹状体 S100B、星形胶质细胞增生和小胶质细胞活化。通过ELISA测量白细胞介素1β（IL-1β）和肿瘤坏死因子α（TNF-α）的纹状体水平，并通过二氯荧光素（DCF）氧化分析ROS的产生。AA 治疗可防止运动功能障碍、降低 S100B 水平、星形胶质细胞增生和受损纹状体中的小胶质细胞活化，从而减少促炎细胞因子 IL-1β 和 TNF-α 的释放以及 ROS 的产生。总之，目前的结果表明，AA 可能是一种药理学工具，可以防止 S100B 增加的有害影响，减轻 ICH 后的神经炎症和继发性脑损伤。通过梯级行走和握力测试评估神经功能缺损。通过免疫荧光分析评估纹状体 S100B、星形胶质细胞增生和小胶质细胞活化。通过ELISA测量白细胞介素1β（IL-1β）和肿瘤坏死因子α（TNF-α）的纹状体水平，并通过二氯荧光素（DCF）氧化分析ROS的产生。AA 治疗可防止运动功能障碍、降低 S100B 水平、星形胶质细胞增生和受损纹状体中的小胶质细胞活化，从而减少促炎细胞因子 IL-1β 和 TNF-α 的释放以及 ROS 的产生。总之，目前的结果表明，AA 可能是一种药理学工具，可以防止 S100B 增加的有害影响，减轻 ICH 后的神经炎症和继发性脑损伤。