Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026
Therapeutic effect and anti-inflammatory mechanism of modified Shoutai pills against lipopolysaccharide-induced miscarriage in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Junwei L I, Xinyue Liu, Xuan Mou, Hongliang Xie, Yating Gao, Aolin Zhang, Tao H E, Tszching Yeung, Chao Tang, Xiaoke W U, Xiaohui Fan, Chichiu Wang, Lu L I
Аннотация
OBJECTIVE: To elucidate the anti-inflammatory mechanisms of modified Shoutai pills (, MSTP) in miscarriages, we performed transcriptome sequencing on the decidua and placental tissues of pregnancy mice.
METHODS: The therapeutic effects and anti-inflammatory mechanisms of MSTP were studied in mice with lipopolysaccharide (LPS)-induced miscarriage. First, the effects of MSTP on pregnancy outcomes and the maternal-fetal interface, in LPS-induced miscarriage mice were examined. RNA sequencing was used to further investigate gene expression changes in LPS-induced miscarriage mice and to assess the effects of MSTP intervention. Finally, the expression levels of inflammation-related genes in the decidua and placental tissues were determined using quantitative real-time polymerase chain reaction (qRT-PCR).
RESULTS: A high dose of MSTP significantly decreased the resorption rate (P < 0.05) and reduced apoptosis of the decidua and placental tissues in mice. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that inflammatory and immune-related signals were enriched. qRT-PCR results confirmed that in decidual and placental tissues, MSTP reduced the gene expression levels of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), c-Jun N-terminal kinase 1, p38, and tumor necrosis factor-α.
CONCLUSIONS: In this study, we demonstrated that MSTP effectively prevented embryo loss with an anti-inflammatory mechanism through downregulation of the TLR4-NF-κB/ MAPK signaling pathway, in LPS-induced miscarriage mice model. To our knowledge, this is the first study to reveal the therapeutic mechanism of MSTP in LPS-induced miscarriage in mice.
METHODS: The therapeutic effects and anti-inflammatory mechanisms of MSTP were studied in mice with lipopolysaccharide (LPS)-induced miscarriage. First, the effects of MSTP on pregnancy outcomes and the maternal-fetal interface, in LPS-induced miscarriage mice were examined. RNA sequencing was used to further investigate gene expression changes in LPS-induced miscarriage mice and to assess the effects of MSTP intervention. Finally, the expression levels of inflammation-related genes in the decidua and placental tissues were determined using quantitative real-time polymerase chain reaction (qRT-PCR).
RESULTS: A high dose of MSTP significantly decreased the resorption rate (P < 0.05) and reduced apoptosis of the decidua and placental tissues in mice. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that inflammatory and immune-related signals were enriched. qRT-PCR results confirmed that in decidual and placental tissues, MSTP reduced the gene expression levels of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), c-Jun N-terminal kinase 1, p38, and tumor necrosis factor-α.
CONCLUSIONS: In this study, we demonstrated that MSTP effectively prevented embryo loss with an anti-inflammatory mechanism through downregulation of the TLR4-NF-κB/ MAPK signaling pathway, in LPS-induced miscarriage mice model. To our knowledge, this is the first study to reveal the therapeutic mechanism of MSTP in LPS-induced miscarriage in mice.