Effect of paclitaxel on the expression of CD28, CTLA-4 and BAFF in rats with experimental autoimmune encephalomyelitis

  OBJECTIVE: To investigate the effect of paclitaxel on the expression of CD28 and CTLA-4 in brain tissue of experimental autoimmune encephalomyelitis (EAE) rats and the content of B cell stimulating factor (BAFF) in the supernatant of spleen tissue and its significance.

  Methods: According to the random number method, 50 Wistar rats were divided into 5 groups: paclitaxel (PTX) small, medium and large dose groups (PTX doses were 1 mg/kg, 2 mg/kg, 4 mg/kg) , Normal control group, EAE control group, 10 animals in each group. The guinea pig spinal cord was used to make GPSCH and mixed with CFA in equal volumes to make immune antigens, and injected into the foot pads (2 mL/kg) of both feet of rats for EAE modeling. After self-building, each dose group of PTX was intraperitoneally injected with paclitaxel. 10 d. Both the normal control group and the EAE control group were given an intraperitoneal injection of 0.9% NaCl 2 mL. The brain histology score was used to evaluate the inflammation and infiltration of the experimental rat brain tissue. The rat brain tissue was taken to determine the content of CD28 and CTLA-4 in the brain tissue by flow cytometry. The spleen tissue was taken and made into supernatant, and the spleen tissue was measured by ELISA Medium BAFF content.

  Results: The brain tissue scores of each dose of PTX were lower than those of the EAE control group, and the differences between the groups were significant (P<0.01); the expression of CD28 in the brain tissue of the rats in each dose group of PTX was lower than that of the EAE control group. The difference was significant (P<0.01); the expression of CTLA-4 was higher than that of the EAE control group, and the difference between the groups was significant (P<0.01); the content of BAFF in the supernatant of spleen tissue was lower than that of the EAE control group. The difference between the groups was significant (P<0.01).

  Conclusion: PTX can reduce the neurological dysfunction score of EAE rats, and its mechanism may involve regulating the expression of CD28 and CTLA-4 in rat brain tissue and the content of BAFF in the supernatant of spleen tissue, thereby exerting a preventive effect on EAE.