Recent data indicate that peripheral, as well as hypothalamic pro-inflammatory
cytokines play an important role in the development of
cancer cachexia. However, there are only a few studies simultaneously investigating the expression of inflammatory molecules in both the periphery and hypothalamic structures in animal models of
cancer cachexia. Therefore, using the Yoshida
ascites hepatoma rat's model of
cancer cachexia we investigated the gene expression of inflammatory markers in the spleen along with the paraventricular and arcuate nuclei, two hypothalamic structures that are involved in regulating energy balance. In addition, we investigated the effect of intracerebroventricular administration of
PS-1145 dihydrochloride (an Ikβ inhibitor) on the expression of selected inflammatory molecules in these hypothalamic nuclei and spleen. We observed significantly reduced food intake in
tumor-bearing rats. Moreover, we found significantly decreased expression of
IL-6 in the spleen as well as decreased NF-κB in the paraventricular nucleus of rats with Yoshida
ascites hepatoma. Similarly, expression of TNF-α, IL-1β, NF-κB, and COX-2 in the arcuate nucleus was significantly reduced in
tumor-bearing rats. Administration of
PS-1145 dihydrochloride reduced only the gene expression of COX-2 in the hypothalamus. Based on our findings, we suggest that the growing Yoshida
ascites hepatoma decreased food intake by mechanical compression of the gut and therefore this model is not suitable for investigation of the
inflammation-related mechanisms of
cancer cachexia development.