Parkinson’s disease (PD) is the second most common neurodegenerative disorder mainly occurring in the elderly. MicroRNA-155-5p (miR-155-5p) plays a vital role in neurodegenerative disease and has been reported to be regulated by rosmarinic acid (RA). In our previous study, it was found that RA could improve motor function and alleviate inflammatory responses in a mice model of PD. This study aimed to investigate the role of miR-155-5p in RA-treated PD mice. The PD mice model was established by injecting mice with N-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) and treated with RA or/and miR-155-5p agomir. The effects of miR-155-5p agomir on motor function, microglial activation, inflammation, apoptosis, and oxidative stress were analyzed by performing a behavioral test, ionized calcium-binding adapter molecule 1 staining, quantitative real-time PCR, Western blot, enzyme-linked immunosorbent assay, tyrosine hydroxylase (TH)-terminal dUTP nick end labeling double staining, TH-cleaved-caspase 3 double staining, and assessment of antioxidative parameters in RA-treated PD mice. The interaction between miR-155-5p and suppressor of cytokine signaling 1/nuclear factor erythroid 2-related factor 2 was validated using dual-luciferase reporter assay. MiR-155-5p up-regulation inhibited the alleviation of motor deficits caused by RA in PD mice, as evidenced by increasing descending time, decreasing limb movement score, increasing the time crossing the beam, and decreasing the times of front limb use. MiR-155-5p up-regulation could elevate microglial activation, inflammation, apoptosis, and oxidative stress in RA-treated PD mice. In conclusion, RA was able to alleviate PD by regulating miR-155-5p, suggesting that miR-155-5p could be used as a therapeutic target for PD treatment.

中文翻译：

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迷迭香酸通过调节帕金森氏病小鼠模型中的miR-155-5p减轻炎症，细胞凋亡和氧化应激。

帕金森氏病（PD）是第二种最常见的神经退行性疾病，主要发生在老年人中。MicroRNA-155-5p（miR-155-5p）在神经变性疾病中起着至关重要的作用，据报道受迷迭香酸（RA）的调控。在我们之前的研究中，发现RA可以改善PD模型小鼠的运动功能并减轻炎症反应。这项研究旨在研究miR-155-5p在RA治疗的PD小鼠中的作用。通过向小鼠注射N来建立PD小鼠模型-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP），并用RA或/和miR-155-5p阿戈密米尔处理。通过进行行为测试，电离钙结合衔接子分子1染色，实时荧光定量PCR，蛋白质印迹，酶分析行为，分析了miR-155-5p agomir对运动功能，小胶质细胞活化，炎症，细胞凋亡和氧化应激的影响。免疫吸附试验，酪氨酸羟化酶（TH）末端dUTP缺口末端标记双染色，TH裂解的caspase 3双重染色以及RA治疗的PD小鼠的抗氧化参数评估。使用双荧光素酶报告基因分析验证了miR-155-5p和细胞因子信号抑制剂1 /核因子红系2相关因子2抑制剂之间的相互作用。MiR-155-5p上调抑制了PD小鼠中RA引起的运动功能障碍的减轻，如下降时间增加，肢体运动评分降低，横穿光束的时间增加以及前肢使用时间减少所证明。MiR-155-5p的上调可能会增加RA治疗的PD小鼠中的小胶质细胞激活，炎症，细胞凋亡和氧化应激。总之，RA能够通过调节miR-155-5p减轻PD，提示miR-155-5p可用作PD治疗的治疗靶标。