Lipoprotein phospholipase a2

Lipoprotein phospholipase A2 is a marker of inflammation. In recent years, the incidence of cardiovascular and cerebrovascular diseases has been increasing. In order to prevent and solve such diseases, medicine has done a lot of research and developed many ways to check the pathogenic factors. Lipoprotein phospholipase, as the name implies, is composed of fat protein phospholipids. Therefore, this marker is harmless to the human body. This is also a great discovery in medicine. So what exactly is lipoprotein phospholipase A2? Next, let’s take a look together!

1. Atherosclerotic cardiovascular disease is the leading cause of death and disability. In addition to dyslipidemia, inflammation and oxidative stress are also important mechanisms in the pathophysiology and development of atherosclerosis. Currently, both domestic and international guidelines recommend the use of models based on traditional risk factors to predict the short-term and long-term risks of atherosclerotic cardiovascular disease [1,2]. However, there are still some shortcomings in using only traditional risk factors. For example, individuals with the same risk factors have different risks of cardiovascular disease events, some patients who do not have traditional risk factors still have cardiovascular disease events, and patients who receive adequate statin treatment still have residual risks. Biomarkers are considered an important supplement to traditional risk assessment. Different from C-reactive protein (CRP), lipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory marker. Studies have found that Lp-PLA2 is an independent risk factor for coronary heart disease and ischemic stroke. It was recently approved by the US FDA for predicting the risk of coronary heart disease and ischemic stroke.

Lp-PLA2 is one of the subtypes of the phospholipase superfamily, also known as platelet-activating factor acetylhydrolase, which is secreted by macrophages, T cells and mast cells in the vascular endothelium. Lp-PLA2 expression is upregulated in atherosclerotic plaques and is strongly expressed in macrophages in the fibrous cap of vulnerable plaques. Lp-PLA2 can hydrolyze oxidized phospholipids in oxidized low-density lipoprotein (ox-LDL) to generate lipid pro-inflammatory substances, such as lysolecithin and oxidized free fatty acids, which in turn produce a variety of atherogenic effects, including endothelial cell death and endothelial dysfunction, and stimulate the production of adhesion factors and cytokines. These substances can further create a self-reinforcing cycle by attracting inflammatory cells and producing more pro-inflammatory substances.

2. Lp-PLA2 released into the blood circulation mainly binds to lipoproteins rich in apolipoprotein (Apo) B, with low-density lipoprotein (LDL) accounting for 80%, and the rest binding to high-density lipoprotein (HDL), lipoprotein a [Lp(a)] and very low-density lipoprotein (VLDL). In patients with atherosclerotic disease, Lp-PLA2 levels are positively correlated with LDL subfraction levels.

Lp-PLA2 determination method

3. The level of Lp-PLA2 can be reflected by measuring the activity and mass of serum (plasma) Lp-PLA2. Clinically, it is recommended to measure the mass of serum Lp-PLA2. Currently, commercial kits are available for clinical testing. The main methods used are luminescent immunoassay and enzyme-linked immunosorbent assay (ELISA). The former is represented by luminescent immunoassay, which has the characteristics of simple operation, stable results and good repeatability. The latter is represented by the PLAC method, which is slightly complicated to operate and has many influencing factors, but as a high-throughput detection, it can meet the needs of large sample detection.

4. Lp-PLA2 is subject to little physiological variation and is basically not affected by changes in body position and daily activities. Therefore, there is no need to fix the body position and time when collecting samples, and there is no need to fast. However, strenuous exercise should be avoided 2 hours before measurement. [5] Samples for Lp-PLA2 detection can be ethylenediaminetetraacetic acid dipotassium (EDTA-K2), heparin anticoagulated plasma, sodium citrate anticoagulated plasma and serum. After blood is drawn, plasma (clear) should be separated as soon as possible and tested in time. The specimen can be stored for 1 week at 2-8°C, 3 months at -20°C, and longer at -70°C (it is best to use serum, which can be stably stored for more than 5 years).