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| Mechanism of Jingui Wenjing Decoction in improving uterine injury in rats with deficiency-cold syndrome based on NLRP3 inflammasome-mediated macrophage polarization |
| Hits 26 Download times 9 Received:June 05, 2026 |
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| DOI
10.11656/j.issn.1673-9043.2026.09.09 |
| Key Words
NLRP3 inflammasome;macrophage polarization;Jingui Wenjing Decoction;cold stress;uterine injury |
| Author Name | Affiliation | E-mail | | ER Jiali | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | ZHANG Jiayu | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | BING Xiangnan | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | ZHAO Shu | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | DU Chenguang | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | QI Feng | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | ZHANG Biwei | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | | | XU Dingjie | Traditional Chinese Medicial College, North China University of Science and Technology, Tangshan 063210, China | xudingjie@163.com |
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| Abstract
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| [Objective] To investigate the effects of Jingui Wenjing Decoction（JGWJD）on cold stress-induced uterine inflammation and vascular injury in rats，and to elucidate its molecular mechanism based on NOD-like receptor family pyrin domain-containing 3（NLRP3）inflammasome-mediated macrophage polarization. [Methods] A rat model of uterine inflammatory injury was established by combined ice-water immersion and freezing exposure. Rats were randomly divided into control group，model group，JGWJD-H group，JGWJD-M group，and JGWJD-L group，with 12 rats in each group. Rats were treated with JGWJD at doses of 16.4，8.2，and 4.1 g/（kg·d），respectively. Vaginal smears were performed to evaluate estrous cycle stages. Laser speckle contrast imaging was used to assess blood perfusion in the plantar skin and uterine surface. Transabdominal ultrasonography was employed to detect uterine structural changes. Serum levels of IL-1β，TNF-α，IL-10，E2，P，LH，and FSH were determined by ELISA. Uterine morphological alterations were observed using HE staining and TEM. Immunofluorescence staining was performed to detect the localization and expression intensity of iNOS and Arg-1. Protein expression levels of NLRP3，caspase 1，IL-1β，iNOS，IL-6，TNF-α，Arg-1，TGF-β，and IL-10 in uterine tissues were measured by Western blot. [Results] In the model group，rats exhibited mental depression，disrupted estrous cycles，and significantly reduced blood perfusion in the plantar skin and uterine surface. Ultrasonography revealed irregular hypoechoic areas，with uterine swelling and deformation. Histological and ultrastructural examination showed endometrial thinning，reduced glandular counts，inflammatory cell infiltration，sparse microvilli，mitochondrial swelling，and dilated endoplasmic reticulum. Serum levels of IL-1β and TNF-α were markedly elevated，whereas IL-10 and reproductive hormone levels were significantly decreased. Western blot analysis demonstrated upregulated expression of NLRP3，caspase-1，IL-1β，iNOS，IL-6，and TNF-α，along with downregulated expression of Arg-1，TGF-β，and IL-10 in uterine tissues. Compared with the model group，JGWJD treatment dose-dependently restored general behavioral status，increased abdominal temperature as well as plantar and uterine blood perfusion，and ameliorated uterine morphological damage，as evidenced by increased endometrial thickness，attenuated inflammation，and repaired local injury. Moreover，JGWJD significantly reduced serum IL-1β and TNF-α levels，elevated IL-10 and reproductive hormone levels，suppressed NLRP3 inflammasome activation and downstream pro-inflammatory cytokine production，while promoting the release of anti-inflammatory and tissue-repair factors. [Conclusion] JGWJD attenuates cold stress-induced uterine inflammation and vascular injury by inhibiting NLRP3 inflammasome priming and activation，thereby reducing the generation and release of downstream effector proteins and pro-inflammatory cytokines. Concurrently，it modulates macrophage polarization-related protein expression by suppressing M1 phenotype-associated factors and enhancing M2 phenotype associated factors，which restores the M1/M2 immune homeostasis，alleviates uterine inflammatory responses，and repairs vascular damage. |
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