Involvement of hypertension in nonalcoholic fatty liver disease via the kininogen fragment peptide

非酒精性脂肪性肝病（NAFLD）与生活方式相关的疾病如高血压有关。在之前的一项研究中，我们在NAFLD患者的血清中发现了与高血压相关的激肽原片段。在这项研究中，我们检查了NAFLD的病理状况与高血压或激肽原片段的存在之间的关系。对盐敏感型高血压大鼠给予高盐饮食和缺乏胆碱的L氨基酸饮食，发现高血压通过抑制HO-1和IL-10的表达加重肝炎和肝纤维化，但不影响脂肪肝的程度。另一方面，NAFLD促进激肽原降解，但NAFLD患者高血压与激肽原片段浓度之间无相关性。因此，高血压是NAFLD的加速因素，而激肽原与NAFLD与高血压的相互作用无关。

Nonalcoholic fatty liver disease (NAFLD) is associated with lifestyle-related diseases such as hypertension. In a previous study, we identified kininogen fragments, which are associated with hypertension, in the serum of patients with NAFLD. In this study, we examined the relationship between the pathological conditions of NAFLD and the presence of hypertension or kininogen fragments. Administration of a high-salt diet, in addition to a choline-deficient L amino-acid-defined diet, to salt-sensitive hypertensive rats revealed that hypertension aggravated hepatitis and liver fibrosis by suppressing the expression of HO-1 and IL-10, but did not affect the degree of fatty liver. On the other hand, kininogen degradation was promoted in NAFLD, but there was no association between hypertension and kininogen fragment concentration in NAFLD patients. Therefore, hypertension is an accelerating factor of NAFLD, but kininogen is not associated with the interaction between NAFLD and hypertension.