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        <datestamp>2026-09-22T13:47:18Z</datestamp>
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          <dc:title>Table 1_Kaempferol ameliorates gestational diabetes mellitus by regulating STAT3-associated AIM2 inflammasome activation and ferroptotic injury in trophoblasts.docx</dc:title>
          <dc:creator>Ronghui Liu (1638166)</dc:creator>
          <dc:creator>Qiqi Liu (381557)</dc:creator>
          <dc:creator>Lanjie Yi (25090279)</dc:creator>
          <dc:subject>Physiology</dc:subject>
          <dc:subject>AIM2 inflammasome</dc:subject>
          <dc:subject>ferroptosis</dc:subject>
          <dc:subject>gestational diabetes mellitus</dc:subject>
          <dc:subject>kaempferol</dc:subject>
          <dc:subject>STAT1/IRF1</dc:subject>
          <dc:subject>STAT3</dc:subject>
          <dc:description>Introduction&lt;p&gt;To investigate the protective effects of kaempferol (KPF) against gestational diabetes mellitus (GDM) and elucidate its underlying molecular mechanisms.&lt;/p&gt;Methods&lt;p&gt;A GDM rat model was established to assess metabolic abnormalities, inflammation, oxidative stress, and placental injury following KPF treatment. In vitro, high glucose (HG)-stimulated HTR-8/SVneo trophoblast cells were used to investigate the protective mechanisms of KPF. Mitochondrial dysfunction, lipid peroxidation, ferroptosis-related alterations, and AIM2 inflammasome activation were evaluated. STAT3 knockdown and AIM2 overexpression were further performed to determine their roles in HG-induced trophoblast injury.&lt;/p&gt;Results&lt;p&gt;KPF significantly improved glucose and lipid metabolism, reduced inflammatory cytokine levels, alleviated placental injury, and decreased oxidative stress in GDM rats. In HG-stimulated trophoblasts, KPF attenuated mitochondrial dysfunction, lipid peroxidation, and ferroptosis-related alterations by restoring GPX4 and SLC7A11 expression and inhibiting AIM2 inflammasome activation. Mechanistically, KPF suppressed STAT3 activation, while STAT3 knockdown reduced STAT1/IRF1 activation and AIM2 expression under hyperglycemic conditions. AIM2 overexpression aggravated ferroptosis-related changes and inflammatory responses.&lt;/p&gt;Conclusion&lt;p&gt;KPF alleviates GDM-associated placental dysfunction by modulating STAT3-associated signaling and AIM2 inflammasome activation, thereby reducing ferroptosis-related injury and inflammatory activation in trophoblasts. These findings provide new insights into the mechanisms of GDM and support KPF as a potential therapeutic candidate.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-22T13:47:18Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fphys.2026.1857741.s001</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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