Yin Hang, Shi Anhua, Wu Junzi
Key Laboratory of Microcosmic Syndrome Differentiation, Yunnan University of Chinese Medicine, Kunming, People's Republic of China.
Diabetes Metab Syndr Obes. 2022 Jul 8;15:2003-2030. doi: 10.2147/DMSO.S367483. eCollection 2022.
Non-alcoholic fatty liver disease (NAFLD) is a multifaceted clinicopathological syndrome characterised by excessive hepatic lipid accumulation that causes steatosis, excluding alcoholic factors. Platelet-activating factor (PAF), a biologically active lipid transmitter, induces platelet activation upon binding to the PAF receptor. Recent studies have found that PAF is associated with gamma-glutamyl transferase, which is an indicator of liver disease. Moreover, PAF can stimulate hepatic lipid synthesis and cause hypertriglyceridaemia. Furthermore, the knockdown of the PAF receptor gene in the animal models of NAFLD helped reduce the inflammatory response, improve glucose homeostasis and delay the development of NAFLD. These findings suggest that PAF is associated with NAFLD development. According to reports, patients with NAFLD or animal models have marked platelet activation abnormalities, mainly manifested as enhanced platelet adhesion and aggregation and altered blood rheology. Pharmacological interventions were accompanied by remission of abnormal platelet activation and significant improvement in liver function and lipids in the animal model of NAFLD. These confirm that platelet activation may accompany a critical importance in NAFLD development and progression. However, how PAFs are involved in the NAFLD signalling pathway needs further investigation. In this paper, we review the relevant literature in recent years and discuss the role played by PAF in NAFLD development. It is important to elucidate the pathogenesis of NAFLD and to find effective interventions for treatment.
非酒精性脂肪性肝病（NAFLD）是一种多方面的临床病理综合征，其特征是肝脏脂质过度蓄积导致脂肪变性，排除酒精因素。血小板活化因子（PAF）是一种生物活性脂质递质，与PAF受体结合后可诱导血小板活化。最近的研究发现，PAF与γ-谷氨酰转移酶有关，γ-谷氨酰转移酶是肝病的一个指标。此外，PAF可刺激肝脏脂质合成并导致高甘油三酯血症。此外，在NAFLD动物模型中敲低PAF受体基因有助于减轻炎症反应、改善葡萄糖稳态并延缓NAFLD的发展。这些发现表明PAF与NAFLD的发展有关。据报道，NAFLD患者或动物模型存在明显的血小板活化异常，主要表现为血小板黏附和聚集增强以及血液流变学改变。在NAFLD动物模型中，药物干预伴随着异常血小板活化的缓解以及肝功能和血脂的显著改善。这些证实血小板活化在NAFLD的发生和发展中可能具有至关重要的作用。然而，PAF如何参与NAFLD信号通路尚需进一步研究。在本文中，我们综述了近年来的相关文献，并讨论了PAF在NAFLD发展中所起的作用。阐明NAFLD的发病机制并找到有效的治疗干预措施很重要。
