关键词: CD36 Gene polymorphism Inflammatory cytokines Microglia Neuroinflammation Parkinson’s disease

Mesh : CD36 Antigens / genetics Case-Control Studies China Cytokines / genetics Disease Progression Female Genetic Predisposition to Disease Genotype Humans Interleukin-6 / genetics Male Parkinson Disease / genetics Polymorphism, Single Nucleotide Tumor Necrosis Factor-alpha / genetics

来  源:   DOI:10.1016/j.neulet.2022.136736

Abstract:
This study aimed to investigate the effect of CD36 rs1761667 gene polymorphisms on the expression of CD36 and inflammatory cytokines and the progression of Parkinson\'s disease (PD).
A total of 138 patients with PD (60 men and 78 women) and 132 healthy controls (48 men and 84 women) from a northern Han Chinese population were enrolled in this case-control study. Polymerase chain reaction-restriction fragment length polymorphism was used to detect the CD36 rs1761667 genotype. An enzyme-linked immunosorbent assay was used to determine the expression of CD36, interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α in the plasma.
The frequency of the rs1761667 AA genotype was significantly higher in patients with PD than that in healthy controls, suggesting AA genotype to be a risk factor for PD. When compared with those in healthy controls, CD36 levels were significantly lower in patients with PD, whereas IL-6, IL-1β, and TNF-α levels were significantly higher in patients with PD. Furthermore, GA and AA carriers with PD showed lower levels of CD36, and GG, GA, and AA carriers showed higher levels of IL-6, IL-1β, and TNF-α than those in healthy controls. In the PD patient group, AA and GA carriers had lower expression levels of CD36 than GG carriers did, and CD36 levels were lower in AA carriers than in GA carriers. Conversely, AA carriers had elevated expression levels of IL-6 compared with that of GG and GA carriers. Logistic regression analysis revealed that IL-6, IL-1β, and TNF-α levels were risk factors for PD in a northern Han Chinese population.
The CD36 rs1761667 AA genotype may increase susceptibility to PD and the expression of inflammatory cytokines.
摘要:
本研究旨在探讨CD36rs1761667基因多态性对CD36和炎性细胞因子表达及帕金森病(PD)进展的影响。
本病例对照研究共纳入了来自中国北方汉族人群的138名PD患者(60名男性和78名女性)和132名健康对照(48名男性和84名女性)。聚合酶链反应-限制性片段长度多态性用于检测CD36rs1761667基因型。采用酶联免疫吸附试验检测CD36、白细胞介素(IL)-6、IL-1β、和血浆中的肿瘤坏死因子(TNF)-α。
PD患者的rs1761667AA基因型频率明显高于健康对照组,提示AA基因型是PD的危险因素。与健康对照组相比,CD36水平在PD患者中明显降低,而IL-6,IL-1β,PD患者的TNF-α水平明显升高。此外,患有PD的GA和AA携带者显示较低水平的CD36和GG,GA,AA携带者显示更高水平的IL-6,IL-1β,和TNF-α比健康对照组。在PD患者组中,AA和GA携带者的CD36表达水平低于GG携带者,AA携带者的CD36水平低于GA携带者。相反,与GG和GA携带者相比,AA携带者的IL-6表达水平升高。Logistic回归分析显示IL-6、IL-1β、和TNF-α水平是中国北方汉族人群PD的危险因素。
CD36rs1761667AA基因型可能增加PD的易感性和炎性细胞因子的表达。
公众号