ABSTRACT
Nonalcoholic fatty liver disease (NAFLD) interacts with the intestinal immune system due to enterohepatic circulation and immune cell recruitment and recirculation. Intestinal immune imbalance promotes liver inflammation and fibrosis in the process of NAFLD, and meanwhile, NAFLD can cause disorders in the number and function of immune cells in the liver and intestinal tract. This article mainly elaborates on the impact of NAFLD on intestinal immune cells and briefly summarizes the new treatment methods for NAFLD targeting at intestinal immune cells, in order to provide a new understanding of the pathogenesis and treatment of NAFLD.
ABSTRACT
Obstructive sleep apnea (OSA) may induce chronic intermittent hypoxia, which may lead to the disorders of multiple systems and organs and even sudden cardiac death in severe cases. Besides respiratory, cardiovascular, endocrine, and metabolic diseases, OSA is also closely associated with nonalcoholic fatty liver disease (NAFLD). This article briefly describes the current status of OSA and NAFLD, introduces the impact of OSA on NAFLD, and reviews the mechanisms of OSA in NAFLD. It is pointed out that clarifying the mechanisms of OSA in affecting NAFLD and discovering potential prevention and treatment targets for NAFLD from the aspect of OSA are of great significance in delaying and even blocking the progression of NAFLD.
ABSTRACT
Liver fibrosis can progress to liver cirrhosis and end-stage liver disease, which may lead to poor prognosis. In addition to pathological angiogenesis and hepatic sinusoid remodeling, hepatic lymphangiogenesis also plays an important role in the progression of liver fibrosis. This article briefly describes lymphatic vessel markers and their expression in the liver, introduces the role of lymphangiogenesis in liver fibrosis, and reviews the role of liver macrophages (Kupffer cells) and lymphatic endothelial cells in lymphangiogenesis. It is pointed out lymphangiogenesis may become a potential target for the intervention of liver fibrosis, which plays an important role in the early treatment and reversal of liver fibrosis and the prevention of liver cirrhosis and end-stage liver disease.
ABSTRACT
Objective To observe the morphologic change in rats with pulmonary fibrosis induced by bleomycin through antisense-human tissue inhibitor of metalloproteinase-1(hTIMP-1)transfection.Methods Thirty rats were divided into five groups randomly(six rats in each group),namely,hTIMP-1 transfection group,anti-sense hTIMP-1 transfection group,empty retroviral vectors transfection group,pulmonary fibrosis group,and the normal group.On the 1st,3rd,7th,14th,28th,60th,90th day of BLM administration to the hTIMP-1,anti-sense hTIMP-1 and retroviral vectors transfection group,the hTIMP-1 cDNA retroviral vectors containing sense and anti-sense ones and the empty vectors were conducted into the lungs of rats with pulmonary fibrosis,which were sacrificed on the 28th days.The pulmonary fibrosis group was given just BLM for the same period of time.The rats in the normal control groups were sacrificed on the same day.Observe the role of anti-sense hTIMP-1 transfection and the change of hydroxyproline.Results The degree of fibrosis and content of HYP were extenuated by antisense hTIMP-1 transfection on 1st and 3rd day after BLM exposure compared with the same time of fibrosis and transfection by empty retroviral vectors group,morphologically.Conclusion Transfection with antisense-TIMP-1 on the first and third day can suppress the process of pulmonary fibrosis induced by BLM to some extent.