RESUMO
<p><b>OBJECTIVE</b>To observe the effects of scorpion and centipede on interleukin (IL)-2, IL-4, IL-10 in the small intestinal mucosa and joint injury of rats with collagen induced arthritis (CIA).</p><p><b>METHODS</b>Sixty Wistar rats were randomly divided into 6 groups: the normal control group, the model group, the low dose scorpion and centipede group, the middle dose scorpion and centipede group, the high dose scorpion and centipede group, and the type II collagen treatment group. The joints' volume was measured 40 days after type II collagen (CII) induced rheumatoid arthritis model was established. The joint injury was observed by naked eyes. The expression levels of IL-2, IL-4, and IL-10 in the small intestine tissue homogenate were detected by enzyme linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>The joint injury score and volume of two hind limbs were obviously higher in the model group than in the normal control group since the 23rd day (P < 0.01). Rats were accompanied with red, swollen, and deformed foot toes and ankle joints. Walking was even affected. Meanwhile, the joint injury score and volume of two hind limbs were obviously lowered by medicated with 0.4, 0.2, 0.1 g/kg scorpion and centipede, as well as CII on the 32nd day after medication (P <0.05, P < 0.01). The expression levels of IL-2, IL-4, and IL-10 in the small intestine tissue homogenate were obviously lower in the model group than in the normal control group (P < 0.05, P < 0.01). Compared with the model group, only the expression levels of IL-2 and IL-4 in the small intestine tissue homogenate of the high dose scorpion and centipede group and the type II collagen treatment group significantly increased. The expression level of IL-10 significantly increased in the high and middle dose scorpion and centipede groups, as well as the type II collagen treatment group, showing statistical difference (P < 0.05, P < 0.01).</p><p><b>CONCLUSIONS</b>Scorpion and centipede could effectively release the joint injury of rats with CIA. Its mechanism might be correlated with increased expression levels of IL-2, IL-4, and IL-10 in the small intestine mucosa.</p>
