Hu Haixia, Zhu Xiaoqin, Lin Ruhui, Li Zuanfang, Chen Lidian
Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350108, P.R. China.
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350108, P.R. China.
Mol Med Rep. 2016 Dec;14(6):5141-5147. doi: 10.3892/mmr.2016.5876. Epub 2016 Oct 21.
The present study aimed to investigate the inhibitory effects, and underlying mechanisms, of Gua Lou Gui Zhi decoction (GLGZD) in a rat model of neuroinflammation. Sprague-Dawley rats were treated with GLGZD following middle cerebral artery occlusion (MCAO). Neurological function and infarct volume were evaluated to confirm successful generation of the rat model. Subsequently, brain tissues and blood samples were collected for further analysis. Nitric oxide (NO) and prostaglandin E2 (PGE2) were evaluated in peripheral blood samples using the Griess reagent assay and an ELISA, respectively. The relative expression levels of inducible nitric oxide synthase (iNOS) and cylooxygenase‑2 (COX‑2) were detected by quantitative polymerase chain reaction and immunohistochemistry. The associated pathways, including nuclear factor‑κB (NF‑κB) and mitogen‑activated protein kinases (MAPK) signaling pathways, were detected by electrophoretic mobility shift assay and western blotting. The results demonstrated that treatment with GLGZD significantly inhibited MCAO-induced inflammation; GLGZD suppressed the production of NO and PGE2, and the expression of iNOS and COX‑2, by inhibiting NF‑κB activation and MAPK phosphorylation. These findings suggest that GLGZD, a potential agent for post‑stroke treatment, may exert anti‑inflammatory effects, thus providing neuroprotection.
本研究旨在探讨瓜蒌桂枝汤（GLGZD）对大鼠神经炎症模型的抑制作用及其潜在机制。对大脑中动脉闭塞（MCAO）后的Sprague-Dawley大鼠给予GLGZD治疗。评估神经功能和梗死体积以确认大鼠模型构建成功。随后，收集脑组织和血液样本进行进一步分析。分别使用格里斯试剂法和酶联免疫吸附测定法（ELISA）评估外周血样本中的一氧化氮（NO）和前列腺素E2（PGE2）。通过定量聚合酶链反应和免疫组织化学检测诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）的相对表达水平。通过电泳迁移率变动分析和蛋白质免疫印迹法检测包括核因子-κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号通路在内的相关信号通路。结果表明，GLGZD治疗可显著抑制MCAO诱导的炎症；GLGZD通过抑制NF-κB激活和MAPK磷酸化，抑制NO和PGE2的产生以及iNOS和COX-2的表达。这些发现表明，GLGZD作为一种潜在的中风后治疗药物，可能发挥抗炎作用，从而提供神经保护。
