ArticleMolecular biology reports2026
Co-supplementation of fructooligosaccharide with soy isoflavone restores the gut-brain axis dysfunction via modulation of gut microbiome in estrogen-deprived rat model.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe gut-brain axis (GBA) plays a critical role in regulating neurocognitive and gastrointestinal functions through integrated neuronal, immune, endocrine, and microbial pathways. Estrogen deficiency causes gut dysbiosis and associated GBA dysfunction. Strategies that may modulate GBA dysfunction in the postmenopausal phase need to be explored. Our present research aimed to examine the synergistic effect of soy isoflavone (SIF) and fructooligosaccharide (FOS) in combination on GBA dysfunction in an estrogen-deprived rat model.
methodsTo induce similar postmenopausal complications, female SD rats were bilaterally ovariectomized (OVX) and were orally administered a combination of FOS (50 mg/kg) & SIF (40 mg/kg) and 17β-estradiol (10 μg/kg) for 28 days. At the end, the uterus, hippocampus, & proximal colon health was measured.
resultsCo-supplementation of FOS with SIF in estrogen-deprived rats synergistically improves body weight, neurobehavior, brain-derived neurotrophic factor levels, and monoamine neurotransmission. We also observed marked restoration of oxidative stress, inflammation, and apoptosis in the hippocampus and colon. With this, we also observed restoration of gut health as indicated by increased mucosal layer integrity, promoting tight junction (TJ) genes, and rebalancing the gut microbiome (GM). The combination approach also selectively activates ER-β expression in the hippocampus without affecting serum estradiol levels & uterine weight. Collectively, the combination approach acts as a selective estrogen receptor modulator and improves GBA functioning.
conclusionThus, the combination approach may attenuate GBA dysfunction in estrogen-deprived rats by selectively activating the ER-β receptor and modulating oxidative stress, inflammation, and apoptosis while preserving the mucosal layer, TJ genes, and GM.
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