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Toll样受体在代谢相关脂肪性肝病中的基础研究
Basic Research on Toll-Like Receptors in Metabolism-Related Fatty Liver Disease

DOI: 10.12677/ACM.2023.1361241, PP. 8877-8883

Keywords: 代谢相关脂肪性肝病(MAFLD),非酒精性脂肪性肝炎(NASH),肠道微生物群,高脂肪饮食,Toll样受体(TLR)
Metabolism-Related Fatty Liver Disease (MAFLD)
, Nonalcoholic Steatohepatitis (NASH), Gut Microbiota, High-Fat Diet, Toll-Like Receptor (TLR)

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Abstract:

代谢相关脂肪性肝病(metabolic associated fatty liver disease, MAFLD)是目前世界上最主要的肝脏疾病,对该病发病机制进行分析,能够看出其之所以会出现肝病,并非是由于酒精引起的肝损伤而是因为肝内过度沉积脂肪产生的一种临床病理综合征。流行病学研究的结果表明超重和胰岛素抵抗是MAFLD发展的关键风险因素,而临床和实验研究结果也表明,肠道微生物群组成和肠道屏障的改变可能有助于疾病的发生和发展。随着社会的逐渐发展,目前社会居民的生活质量得到显著改善,饮食习惯也发生极大变化,该病的发病率每年都在快速增长,构成了全世界肝脏纤维化的主要原因,逐渐对人体健康构成威胁,并已成为世界范围内的一大卫生问题。近年来,许多学者已经确认了固有免疫系统的活化对MAFLD的发展起到了重要的作用,Toll样受体(Toll-like receptor, TLR)途径是其中关键一环。TLR在各种肝病中均表现为异常,其作用机制是通过调节TNF-α、IL-1β的表达,从而加剧肝组织的炎症反应。
Metabolic associated fatty liver disease (MAFLD) is currently the world’s leading liver disease. By analysis of the pathogenesis of the disease, it can be seen that the reason for liver disease is not due to liver damage caused by alcohol, but because of a clinicopathological syndrome produced by ex-cessive deposition of fat in the liver. The results of epidemiological studies suggest that overweight and insulin resistance are key risk factors for the development of MAFLD, while clinical and exper-imental studies have also suggested that alterations in gut microbiota composition and intestinal barrier may contribute to the onset and progression of the disease. With the gradual development of society, the quality of life of social residents has been significantly improved, eating habits have also undergone great changes, the incidence of the disease is growing rapidly every year, constitut-ing the main cause of liver fibrosis in the world, gradually posing a threat to human health, and has become a major health problem worldwide. In recent years, many scholars have confirmed that the activation of the innate immune system plays an important role in the development of MAFLD, and the Toll-like receptor (TLR) pathway is a key part of this. TLR is abnormal in various liver diseases, and its mechanism of action is to increase the inflammatory response of liver tissue by regulating the expression of TNF-α and IL-1β.

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