Journal of ethnopharmacology · 2025
Astilbin from Smilax china L. remarkably inhibits LPS-induced endometritis in rats via blocking positive feedback between TLR4 and IL-6R signalling pathways in a PPAR-γ-dependent manner.
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Feng Haixing, Li Chunni, Chen Jingyao, Li Zhiwen, Ye Xuan, Hou Lianbing, Wang Chunxia, Hou Chuqi, Liu Wenqin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Astilbin (ATB), a natural flavonoid compound with anti-inflammatory bioactivities, can be isolated from Smilax china L., which has been used in traditional Chinese medicine to treat pelvic inflammatory disease (PID) (including endometritis). Our previous studies reported that flavonoids from Smilax china rhizome (FSCR) have therapeutic effects in rats with PID. However, the effects of ATB, the main active component of FSCR, against endometritis remain unknown.
AIM OF THE STUDY: We aim to investigate the role of ATB on endometritis induced by lipopolysaccharide (LPS) in rats and elucidate the mechanisms underlying anti-inflammatory action of ATB on LPS-stimulated endometrial epithelial cells (EECs).
METHODS: The effects and action mechanisms of ATB on LPS-induced endometritis in rats and LPS-induced EECs were systematically assessed using H&E staining, immunohistochemistry, ELISA, RT-PCR, western blotting, immunofluorescence, molecular docking and siRNA knockdown technology.
RESULTS: ATB significantly alleviated typical uterine pathological damages in endometritis, decreased inflammatory cytokine levels in both serum and uterus, and also inhibited the excessive release of inflammatory cytokines in EECs induced by LPS. Mechanistically, ATB markedly upregulated PPAR-γ levels and suppressed the overexpression of TLR4 and IL-6R proteins and their downstream signals, MyD88, and phosphorylation of NF-κB P65, JAK2, and STAT3, in vivo. Further, the effects of ATB on PPAR-γ protein expression, and NF-κB and STAT3 signalling activation in LPS-induced EECs were consistent with the results of in vivo experiments. Furthermore, both PPAR-γ-specific siRNA transfection and a selective PPAR-γ antagonist abolished ATB-induced inhibition of NF-κB and STAT3 signalling activation and production of inflammatory cytokines. Molecular docking and in vitro experiments further proved that ATB can target PPAR-γ binding.
CONCLUSION: Overall, our results demonstrated that ATB can significantly inhibit endometritis in rats, presumably through interfering with NF-κB and STAT3 signal transduction in a PPAR-γ-dependent manner, blocking the positive feedback between NF-κB and STAT3 signalling. Our findings provide new evidences for developing the ATB, the main compound identified from FSCR, as a potential therapeutic agent for endometritis.
AIM OF THE STUDY: We aim to investigate the role of ATB on endometritis induced by lipopolysaccharide (LPS) in rats and elucidate the mechanisms underlying anti-inflammatory action of ATB on LPS-stimulated endometrial epithelial cells (EECs).
METHODS: The effects and action mechanisms of ATB on LPS-induced endometritis in rats and LPS-induced EECs were systematically assessed using H&E staining, immunohistochemistry, ELISA, RT-PCR, western blotting, immunofluorescence, molecular docking and siRNA knockdown technology.
RESULTS: ATB significantly alleviated typical uterine pathological damages in endometritis, decreased inflammatory cytokine levels in both serum and uterus, and also inhibited the excessive release of inflammatory cytokines in EECs induced by LPS. Mechanistically, ATB markedly upregulated PPAR-γ levels and suppressed the overexpression of TLR4 and IL-6R proteins and their downstream signals, MyD88, and phosphorylation of NF-κB P65, JAK2, and STAT3, in vivo. Further, the effects of ATB on PPAR-γ protein expression, and NF-κB and STAT3 signalling activation in LPS-induced EECs were consistent with the results of in vivo experiments. Furthermore, both PPAR-γ-specific siRNA transfection and a selective PPAR-γ antagonist abolished ATB-induced inhibition of NF-κB and STAT3 signalling activation and production of inflammatory cytokines. Molecular docking and in vitro experiments further proved that ATB can target PPAR-γ binding.
CONCLUSION: Overall, our results demonstrated that ATB can significantly inhibit endometritis in rats, presumably through interfering with NF-κB and STAT3 signal transduction in a PPAR-γ-dependent manner, blocking the positive feedback between NF-κB and STAT3 signalling. Our findings provide new evidences for developing the ATB, the main compound identified from FSCR, as a potential therapeutic agent for endometritis.