Abstract
Parkinson's disease (PD) is one of the most disabling diseases of the central nervous system, seriously affecting health and quality of life for the elderly. The present study aimed to explore the effects of nuclear receptor subfamily 4 group A member 2 (Nurr1) and nuclear factor‑κB (NF‑κB) on the progression of Parkinson's disease (PD). Pheochromocytoma (PC12) cells were pretreated with the NF‑κB inhibitor quinazoline (QNZ) or transfected with small interfering (si)RNA‑NF‑κB, followed by the addition of lipopolysaccharide (LPS). After culturing for 24 h, Cell Counting Kit‑8 (CCK‑8) was utilized to measure cell viability. Next, the expression levels of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α were determined using the relevant Enzyme‑linked immunosorbent assay kits. Expression levels of p65, tyrosine hydroxylase (TH), α‑Synuclein (A‑SYN) and Nurr1 were examined by immunofluorescence and western blotting. CCK‑8 results showed that the cell viability was significantly reduced in the LPS group than in the control group (P<0.05), whereas QNZ and si‑NF‑κB demonstrated significantly enhanced viability induced by LPS (P<0.05). After LPS induction, the levels of IL‑1β, IL‑6 and TNF‑α were significantly elevated when compared with those in the control group (P<0.05), whereas QNZ and NF‑κB interference partially restored their levels. Additionally, after LPS induction, the expression of p65 and A‑SYN was higher, while the expression of TH and Nurr1 was lower. However, QNZ and NF‑κB treatment significantly reversed the expression levels induced by LPS (P<0.05). Finally, it was observed that NF‑κB may be negatively associated with Nurr1. In conclusion, inhibition of NF‑κB may reduce the production of inflammatory factors by upregulating Nurr1 and TH and downregulating A‑SYN, thus relieving the inflammatory response in PD.