OBJECTIVE: This study aimed to observe the therapeutic effect of pentapeptide PLNPK on systemic lupus erythematosus (SLE) in mice, and to study the inhibitory effect of PLNPK on activation of T cells in vivo. METHODS: Murine SLE-like chronic graft-versus-host disease (cGVHD) was induced. After treatment with PLNPK (100, 200, 400 μg/kg per day) for 70 days, serum blood urea nitrogen, creatine, total cholesterol, triglyceride and albumin were tested, and serum levels of anti-dsDNA and anti-histone antibodies were detected by ELISA. The pathological damage and IgG deposition in the kidney were identified. Concanavalin A (ConA)-induced T lymphocyte proliferation in SLE mice was also tested. RESULTS: PLNPK can reduce serum blood urea nitrogen, creatine, total cholesterol, triglyceride, and elevate serum albumin, and reduce levels of anti-dsDNA and anti-histone antibodies in the murine SLE model. Pathological damage and IgG deposition in the kidney were reduced in the PLNPK-treated group. PLNPK inhibited T lymphocyte infiltration in kidney tissues and ConA-induced T lymphocyte proliferation in SLE mice. CONCLUSION: Our results demonstrate that PLNPK can suppress T cell function and reduce the production of autoantibodies, and may be a feasible and effective therapy in the SLE model.
OBJECTIVE: This study aimed to observe the therapeutic effect of pentapeptide PLNPK on systemic lupus erythematosus (SLE) in mice, and to study the inhibitory effect of PLNPK on activation of T cells in vivo. METHODS:MurineSLE-like chronic graft-versus-host disease (cGVHD) was induced. After treatment with PLNPK (100, 200, 400 μg/kg per day) for 70 days, serum blood ureanitrogen, creatine, total cholesterol, triglyceride and albumin were tested, and serum levels of anti-dsDNA and anti-histone antibodies were detected by ELISA. The pathological damage and IgG deposition in the kidney were identified. Concanavalin A (ConA)-induced T lymphocyte proliferation in SLEmice was also tested. RESULTS: PLNPK can reduce serum blood ureanitrogen, creatine, total cholesterol, triglyceride, and elevate serum albumin, and reduce levels of anti-dsDNA and anti-histone antibodies in the murineSLE model. Pathological damage and IgG deposition in the kidney were reduced in the PLNPK-treated group. PLNPK inhibited T lymphocyte infiltration in kidney tissues and ConA-induced T lymphocyte proliferation in SLEmice. CONCLUSION: Our results demonstrate that PLNPK can suppress T cell function and reduce the production of autoantibodies, and may be a feasible and effective therapy in the SLE model.
Authors: H Tamamura; T Murakami; S Horiuchi; K Sugihara; A Otaka; W Takada; T Ibuka; M Waki; N Yamamoto; N Fujii Journal: Chem Pharm Bull (Tokyo) Date: 1995-05 Impact factor: 1.645
Authors: Haixiang Yu; Karen Sliedregt-Bol; Herman Overkleeft; Gijs A van der Marel; Theo J C van Berkel; Erik A L Biessen Journal: Arterioscler Thromb Vasc Biol Date: 2006-05-04 Impact factor: 8.311
Authors: Hidehiko Shogomori; Adam T Hammond; Anne G Ostermeyer-Fay; Daniel J Barr; Gerald W Feigenson; Erwin London; Deborah A Brown Journal: J Biol Chem Date: 2005-03-07 Impact factor: 5.157
Authors: Bernd Wollscheid; Priska D von Haller; Eugene Yi; Samuel Donohoe; Kelly Vaughn; Andrew Keller; Alexey I Nesvizhskii; Jimmy Eng; Xiao-jun Li; David R Goodlett; Ruedi Aebersold; Julian D Watts Journal: Subcell Biochem Date: 2004