Effects of Triptolide on Periodontal Inflammation and Osteoclasts in Orthodontic Tooth Movement Model Rats through p38 MAPK/ERK/JNK Signaling Pathway

doi:10.13701/j.cnki.kqyxyj.2024.11.007

Abstract

Abstract: Objective: To explore the effects of triptolide on periodontal inflammation and osteoclasts in orthodontic tooth movement model rats through regulating p38 mitogen-activated protein kinase (p38 MAPK)/extracellular signal-regulated kinase (ERK)/c-Jun amino-terminal kinase (JNK) signaling pathway. Methods: The rat orthodontic tooth model was established and totally 48 rats were randomly equally divided into model group, triptolide low dose (50 μg/kg) group, high dose (100 μg/kg) group, and triptolide high dose (100 μg/kg) + p38 MAPK activator (25 μg) group. Twelve healthy rats were set as control group. Each group was given corresponding intervention methods for 2 weeks. The distance of orthodontic tooth movement was measured. Osteoclasts in periodontal tissue were stained with tartrate resistant acid phosphatase and counted. The expression of bone morphogenetic protein-2 (BMP-2) in periodontal tissue was detected with immunohistochemical staining. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), prostaglandin E2 (PGE2), osteoprotegerin (OPG), and receptor activator of nuclear factor-κB ligand (RANKL) were detected by enzyme linked immunosorbent assay. The expressions of p38 MAPK/ERK/JNK pathway related proteins in periodontal tissues were detected by western blot. Results: Compared with control group, the movement distance of orthodontic teeth, the number of osteoclasts in periodontal tissue, the expression intensity of BMP-2, the levels of serum TNF-α, IL-1β, PGE2, RANKL, phosphorylated (p)-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2, and p-JNK/JNK protein ratio in the model group were significantly increased, however, the serum OPG level was significantly decreased (P<0.05). Compared with model group, the movement distance of orthodontic teeth, the expression intensity of BMP-2 in periodontal tissue, and the level of serum OPG in triptolide low dose and high dose groups were increased successively, the number of osteoclasts in periodontal tissue, serum TNF-α, IL-1β, PGE2, RANKL levels, p-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2, and p-JNK /JNK protein ratio were decreased (P<0.05). p38 MAPK activator could reverse the effect of high dose triptolide on orthodontic tooth movement model rats (P<0.05). Conclusion: Triptolide can reduce periodontal inflammation, decrease the number of osteoclasts, improve bone resorption, and accelerate orthodontic tooth movement in orthodontic model rats. Its mechanism is related to the inhibition of p38 MAPK/ERK/JNK signaling pathway activation.

Key words: triptolide, orthodontic tooth movement, rats, periodontal tissue, p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, c-Jun amino-terminal kinase

CAI Yehua, LI Xing, ZHAO Yanxia, WANG Li, LI Hang. Effects of Triptolide on Periodontal Inflammation and Osteoclasts in Orthodontic Tooth Movement Model Rats through p38 MAPK/ERK/JNK Signaling Pathway[J]. Journal of Oral Science Research, 2024, 40(11): 978-984.

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