The mRNA levels of PPAR alpha, HIF-1 alpha, and VEGF in the liver tissues of rats with alcoholic liver disease

Objective: To investigate the mRNA levels of peroxisome proliferator-activated receptor alpha (PPAR alpha), hypoxiainducible factor-1 alpha (HIF-1 alpha), and vascular endothelial growth factor (VEGF) in the liver tissues of rats with alcoholic liver disease. Methods: A total of 50 Wistar rats were randomly divided into a 4-week model group (n = 10), an 8-week model group (n = 10), a 12-week model group (n = 10), a 16-week model group (n = 10), and a control group (n = 10). The control group got the same volume of distilled water, and the rats in the model groups were given ethanol to establish alcoholic liver disease model. The mRNA levels of PPAR alpha, HIF-1 alpha, and VEGF in the rats' liver tissues, the fatty liver degree, and the inflammation degree in each group were examined and compared. Results: The liver tissues in 4 model groups showed a more worsened fatty liver degree and inflammation degree than those in control group (P < 0.05). With the extension of the modeling time, the fatty liver degree and inflammation levels were significantly increased (P < 0.05). All the model groups showed lower mRNA level of PPAR alpha, and higher levels of HIF-1 alpha and VEGF than the control group (P < 0.05). With the extension of the modeling time, the relative mRNA level of PPAR alpha was decreased, while the mRNA levels of HIF-1 alpha and VEGF increased (all P < 0.05). The fatty liver degree and inflammation level were negatively correlated with the PPAR alpha mRNA level (r = -0.899,-0.893, P < 0.05) and positively correlated with the HIF-1 alpha and VEGF mRNA levels (r = 0.791, 0.679, 0.744, 0.597, P < 0.05). The PPAR alpha mRNA level was negatively correlated with HIF-1 alpha and VEGF mRNA levels (r = -0.732,-0.681, P < 0.05). Conclusion: High PPAR alpha mRNA levels and low HIF-1 alpha and VEGF mRNA levels in the liver tissues of rats with alcoholic liver disease may be closely related to fatty liver and inflammation reactions.