Effects of aspirin on dendritic cells in the inflammatory microenvironment of rabbit buccal VX-2 squamous cell carcinoma / 华西口腔医学杂志

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of aspirin and inflammation on the maturation and function of dendritic cells (DC) on the supernatant of VX-2 squamous cell carcinoma.</p><p><b>METHODS</b>The rabbit buccal VX-2 squamous cell carcinoma models with inflammation were established by tumor particle implantation, mechanical trauma, and high sugar diet. The rabbits were divided into three groups. For the experimental group (rabbit buccal VX-2 squamous cell carcinoma with local inflammation), aspirin were given by gavage for three consecutive days. For the control group (rabbit buccal VX-2 squamous cell carcinoma with local inflammation), normal saline was given by gavage for three consecutive days. For the blank group (tumor without inflammation), normal saline was given by gavage for three consecutive days. Each tumor specimens were collected in three days and made into tissue homogenate. The supernatant was collected after centrifugation. Normal rabbit peripheral blood mononuclear cells were separated and co-cultured with different states of supernatant. The expression of DC surface markers CD83, CD86, and human leukocyte antigen-DR (HLA-DR) were detected by flow cytometry. The state of function of DC was tested by mixed lymphocyte reaction.</p><p><b>RESULTS</b>The positive rate of CD83, CD86, and HLA-DR of the experimental and control groups were both lower than that of the blank group (P<0.05). In addition, the ability to stimulate T cell proliferation of the experimental and control groups were weaker than that of the blank group (P<0.05). No significant difference was observed between the experi- and HLADR of DC. The short-term administration of aspirin is not conducive to the phenoty and function of DC in a rabbit mental and control groups (P>0.05).</p><p><b>CONCLUSION</b>Inflammation may inhibit the function and expression of CD83, CD86, buccal VX-2 squamous cell carcinoma inflammatory environment</p>