Lu Bei-Ling, Li Jian, Zhou Jun, Li Wen-Wen, Wu Heng-Fei
aDepartment of Clinical Immunology and Microbiology, Department of Laboratory Medicine, Xiangya School of Medicine bInstitute of Medical Sciences, Xiangya Hospital, Central South University, Changsha cThe Third People's Hospital of Datong City, Datong, China.
Neuroreport. 2016 Aug 17;27(12):883-93. doi: 10.1097/WNR.0000000000000618.
To study the pathogenesis of Alzheimer's disease (AD) and explore the possible anti-inflammatory mechanism of tanshinone IIA (TanIIA), we evaluated the quantity of neurons and the expression levels of interleukin-1β (IL-1β), IL-6, glial fibrillary acidic protein, CD11b, C1q, C3c, and C3d in brain tissues of AD rats treated with TanIIA. Thirty male Sprague-Dawley rats were randomized into three groups: sham group, TanIIA treatment group, and Aβ1-42 group. Aβ1-42 treatment was performed by injecting Aβ into the hippocampus of rats and then tagged position. Brain tissue morphological structure has been observed with HE staining and the staining of exogenously injected Aβ1-42 was observed by immunohistochemistry, which confirms the success of the Aβ1-42 group. After TanIIA treatment, levels of IL-1β, IL-6, glial fibrillary acidic protein, CD11b, C1q, C3c, and C3d were measured in paraffinized brain tissue sections from all groups by immunohistochemistry staining. The results showed that no 6E10 was detected in the control group, and the difference in the expression levels of 6E10 between the Aβ1-42 group and the TanIIA treatment group was not significant (P>0.05), suggesting that both the Aβ1-42 group and the TanIIA treatment group received the same amount of Aβ. The Aβ1-42 group showed a significant increase in the expression levels of inflammatory markers compared with the sham group (P<0.05) and the TanIIA treatment group showed a partial improvement in reducing inflammation. Therefore, Aβ triggered brain inflammation and activated the complement system. TanIIA treatment reduced the number of astrocytes and microglial cells, and induced a partial decrease in complement molecules in the brain of AD rats. These findings suggested that TanIIA may represent a potential therapeutic treatment in neurodegenerative diseases such as AD to support the survival of neurons by reducing expression levels of inflammatory factors.
为研究阿尔茨海默病（AD）的发病机制并探索丹参酮IIA（TanIIA）可能的抗炎机制，我们评估了用TanIIA治疗的AD大鼠脑组织中神经元数量以及白细胞介素-1β（IL-1β）、IL-6、胶质纤维酸性蛋白、CD11b、C1q、C3c和C3d的表达水平。将30只雄性Sprague-Dawley大鼠随机分为三组：假手术组、TanIIA治疗组和Aβ1-42组。通过将Aβ注射到大鼠海马体然后标记位置来进行Aβ1-42治疗。用HE染色观察脑组织形态结构，通过免疫组织化学观察外源性注射的Aβ1-42的染色情况，这证实了Aβ1-42组造模成功。TanIIA治疗后，通过免疫组织化学染色测量所有组石蜡包埋脑组织切片中IL-1β、IL-6、胶质纤维酸性蛋白、CD11b、C1q、C3c和C3d的水平。结果显示，对照组未检测到6E10，Aβ1-42组与TanIIA治疗组之间6E10表达水平差异无统计学意义（P>0.05），表明Aβ1-42组和TanIIA治疗组接受的Aβ量相同。与假手术组相比，Aβ1-42组炎症标志物表达水平显著升高（P<0.05），TanIIA治疗组在减轻炎症方面有部分改善。因此，Aβ引发脑部炎症并激活补体系统。TanIIA治疗减少了AD大鼠脑内星形胶质细胞和小胶质细胞数量，并使脑内补体分子部分减少。这些发现表明，TanIIA可能是AD等神经退行性疾病的一种潜在治疗方法，通过降低炎症因子表达水平来支持神经元存活。
