Departamento de Medicina, Facultad Evangélica Mackenzie de Paraná, Curitiba, Paraná, Brazil; Instituto de Investigación Denton Cooley, Ciencia y Tecnología, Curitiba, Paraná, Brazil.
Departamento de Medicina, Facultad Evangélica Mackenzie de Paraná, Curitiba, Paraná, Brazil; Instituto de Investigación Denton Cooley, Ciencia y Tecnología, Curitiba, Paraná, Brazil.
Rev Gastroenterol Mex (Engl Ed). 2022 Apr-Jun;87(2):159-169. doi: 10.1016/j.rgmxen.2022.03.004. Epub 2022 May 21.
Cirrhosis is the common outcome of liver diseases. It can be decompensated and lead to the development of complications, such as encephalopathy. Hyperammonemia that develops due to liver dysfunction is etiopathologically related to hepatic encephalopathy. Caffeine increases the activity of the urea cycle in the liver, augmenting ammonia degradation. By antagonizing adenosine receptors, it also has a hepatoprotective effect, impeding the formation of fibrosis, as well as having a stimulating effect on the central nervous system. The present study analyzed the effects of caffeine on the progression of cholestatic liver fibrosis and hepatic encephalopathy.
An experimental model of cholestatic liver fibrosis, through common bile duct ligature, and of hepatic encephalopathy, through the administration of a high-protein diet, was constructed. Male Wistar rats (n=32) were equally divided into 4 groups. The experiment lasted 28 days, with the administration of 50mg/kg/day of caffeine. Laboratory tests, histologic analyses of the liver and encephalon, open field tests (OFTs), and daily behavioral analyses were carried out.
The ligated animals treated with caffeine had lower mean transaminase levels and improved histologic aspects of the liver and encephalon. The untreated ligated animals were clearly lethargic and apathetic at the last week of the experiment, confirmed by reduced exploratory activity during the OFT.
Caffeine improved the microarchitecture of the liver and encephalon of the cirrhotic animals and prevented the decrease in exploratory behavior of the animals during the OFT.
肝硬化是肝脏疾病的常见结局。它可能会失代偿并导致并发症的发展，如肝性脑病。由于肝功能障碍而产生的高氨血症与肝性脑病在病因学上有关。咖啡因可增加肝脏尿素循环的活性，从而增强氨的降解。通过拮抗腺苷受体，它还具有肝保护作用，阻碍纤维化的形成，并对中枢神经系统具有刺激作用。本研究分析了咖啡因对胆汁淤积性肝纤维化和肝性脑病进展的影响。
通过胆总管结扎构建胆汁淤积性肝纤维化的实验模型，通过高蛋白饮食构建肝性脑病模型。雄性 Wistar 大鼠（n=32）被平均分为 4 组。实验持续 28 天，给予 50mg/kg/天的咖啡因。进行了实验室检查、肝脏和大脑的组织学分析、旷场试验（OFT）和日常行为分析。
用咖啡因治疗的结扎动物的平均转氨酶水平较低，肝脏和大脑的组织学方面得到改善。未治疗的结扎动物在实验的最后一周明显昏睡和冷漠，通过 OFT 期间探索活动减少得到证实。
咖啡因改善了肝硬化动物的肝脏和大脑的微观结构，并防止了动物在 OFT 期间探索行为的减少。
