Mechanism of triptolide in treating ankylosing spondylitis through the anti‑ossification effect of the BMP/Smad signaling pathway.

The present study aimed to examine the mechanism of triptolide in the treatment of ankylosing spondylitis (AS) through the anti‑ossification effect of bone morphogenetic protein (BMP)/small mothers against decapentaplegic (Smad) pathway. Male rats were randomly divided into five groups: Normal rat group; model group; triptolide low dose group (10 mg/kg); triptolide middle dose group (20 mg/kg); triptolide high dose group (40 mg/kg). The spinal joint capsules of each group of rats were collected to perform primary cell culture to determine the levels of cell proliferation. Western blot and reverse transcription‑polymerase chain reaction analyses, and ELISA were used to detect the mRNA and protein expression levels of core‑binding factor α1 (Cbfal), BMP receptor type II (BMPRII), Smad1, Smad4, Smad5 and Smad6, the protein expression of phosphorylation indicators, including phosphorylated (p)Smad1 and pSmad5, the mRNA expression of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑6 in rat plasma, and the mRNA expression of BMP/Smads in fibroblasts induced by recombinant human (rh)BMP‑2. The effects on AS in the rats were also examined. The results revealed that, following intervention with triptolide, inflammation was suppressed, and the mRNA expression levels of TNF‑α, IL‑1β and IL‑6 were reduced. The expression levels of Cbfal, BMPRII, Smad1, Smad4 and Smad5 were also reduced, whereas the expression of Smad6 was increased. Following induction by rhBMP‑2, the effects of triptolide weakened, with the most marked effects observed at the highest concentration, suggesting that triptolide functions through the BMP/Smad signaling pathway. Taken together, the results suggested that triptolide may be used to treat AS, the mechanism of which may be through the BMP/Smad pathway.