Protective Effects Of Mir-19b In Parkinson'S Disease By Inhibiting The Activation Of Inos Through Negative Regulation Of P38 Signaling Pathways

Aim: This study aimed to investigate the protective effects of microRNA-19b (miR-19b) against Parkinson's disease (PD) by targeting p38 pathways. Methods: PD mice models were dealt with through overexpression or inhabitation of miR-19b and p38 signaling pathway inhibitors, separately, and a negative control group was established. Quantitative reverse-transcription polymerase chain reaction was performed to measure miR-19b and mRNAs of p38 pathway relative genes. Western blotting was utilized to measure levels of proteins with respect to p38 relative genes and generation and apoptosis for neurons. Immunohistochemistry was used to detect the activities of inducible nitric-oxide synthase (iNOS) and tyrosine hydroxylase (TH). Nissl staining method was adopted to observe the generation of Nissl bodies. Annexin V- fluorescein isothiocyanate (FITC) and propidium iodide (PI) double staining was used to measure cell apoptosis. Results: Compared with the normal group, miR-19b in the model group was decreased, but mRNA and phosphorylated proteins of p38 were significantly increased (P < 0.05). Compared with the negative control group, iNOS in miR-19b mimic, SB203580, and miR-19b mimic + SB203580 groups was activated. Generation of neuron cells and expression of dopamine transporter (DAT), proliferating cell nuclear antigen (PCNA), and Bcl-2 in the above three groups were significantly upregulated. Also, apoptotic neurons and expression of cleaved-caspase 3, Bax were upregulated (P < 0.05). Changes in the miR-19b mimic + SB203580 group were the most obvious. Conclusion: miR-19b exerts protective effects in Parkinson's by inhibiting the activation of iNOS through regulation of p38 signaling pathways.