Gastrodin Ameliorates Maternal-Fetal Interface Injury in Gestational Diabetes Mellitus Rats by Activating the GPR120/AMPK Pathway

Nan LI; Ziyi NIU; Lan SHAO

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Nan LI, Ziyi NIU, Lan SHAO. Gastrodin Ameliorates Maternal-Fetal Interface Injury in Gestational Diabetes Mellitus Rats by Activating the GPR120/AMPK Pathway[J]. Journal of Kunming Medical University.

Citation:

Nan LI, Ziyi NIU, Lan SHAO. Gastrodin Ameliorates Maternal-Fetal Interface Injury in Gestational Diabetes Mellitus Rats by Activating the GPR120/AMPK Pathway[J]. Journal of Kunming Medical University.

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Gastrodin Ameliorates Maternal-Fetal Interface Injury in Gestational Diabetes Mellitus Rats by Activating the GPR120/AMPK Pathway

Department of Obstetrics，Shijiazhuang Maternal and Child Health Hospital，Shijiazhuang Hebei 050000，China

Received Date: 2025-07-04
Available Online: 2025-10-02

Abstract

Abstract

Objective To investigate the effects and mechanisms of gastrodin on lipotoxicity damage at the maternal-fetal interface in rats with gestational diabetes mellitus （GDM）. Methods A GDM rat model was established using intraperitoneal injection of streptozotocin. Thirty pregnant rats were randomly divided into three groups: model group, gastrodin group （100 mg/kg）, and gastrodin （100 mg/kg） + G protein-coupled receptor 120 （GPR120） antagonist AH7614 （25 mg/kg） group. An additional 10 pregnant rats were used as a control group. Each group received intraperitoneal injection or gavage of corresponding drugs once daily until the 20th day of pregnancy. Serum fasting blood glucose （FBG）, free fatty acids （FFA）, total cholesterol （TC）, and triglycerides （TG） levels, as well as maternal body weight and fetal survival rate, were measured. ELISA and immunohistochemistry were used to measure serum and maternal-fetal interface tissue TNF-α and IL-1β levels. Flow cytometry was used to detect cell apoptosis in maternal-fetal interface tissue. Immunofluorescence was used to detect GPR120 and adenosine monophosphate-activated protein kinase （AMPK） protein distribution and expression. Western blot was used to detect GPR120, AMPK, and phosphorylated AMPK （p-AMPK） protein expression in maternal-fetal interface tissue. Results Compared with the control group, the model group showed significantly increased serum FBG, FFA, TC, TG, TNF-α, and IL-1β, maternal body weight, maternal-fetal interface tissue TNF-α, IL-1β, and cell apoptosis levels （P < 0.05）, while fetal rat survival rate and maternal-fetal interface tissue GPR120 and p-AMPK/AMPK levels were significantly decreased （P < 0.05）. Compared with the model group, the gastrodin group showed significantly decreased serum FBG, FFA, TC, TG, TNF-α, and IL-1β, maternal body weight, maternal-fetal interface tissue TNF-α, IL-1β, and cell apoptosis levels（P < 0.05）, while fetal rat survival rate and maternal-fetal interface tissue GPR120 and p-AMPK/AMPK levels were significantly increased （P < 0.05）. AH7614 reversed the intervention effect of gastrodin on GDM rats （P < 0.05）. Conclusion Gastrodin can improve glucose and lipid metabolism, obesity, and adverse pregnancy outcomes in GDM rats, inhibit inflammation and apoptosis at the maternal-fetal interface, and its mechanism may be related to the activation of the GPR120/AMPK pathway.
- Gastrodin,
- Gestational diabetes mellitus,
- Maternal-fetal interface,
- Glucose and lipid metabolism,
- Lipotoxicity,
- GPR120/AMPK signaling pathway,
- Rats

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References(20)

References

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