International journal of biological macromolecules · 2026
Lycium barbarum polysaccharides ameliorate diabetes-associated cognitive impairment through modulation of peripheral glycemic homeostasis and inflammation in mice.
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Qianqian Yang, Shanqiang Xu, Kai Li, Rong Song, Yuxing Tang, Xiaohui Yang, Xiahui, Huizhen Cai
Аннотация
BACKGROUND AND PURPOSE: Diabetes-associated cognitive impairment (DCI) is a devastating complication of type 2 diabetes mellitus (T2DM), driven by abnormal glucose metabolism and chronic systemic inflammation. Lycium barbarum polysaccharide (LBP), a macromolecular bioactive component, has shown neuroprotective potential despite limited blood-brain barrier (BBB) permeability. We hypothesized that LBP ameliorates DCI through peripheral glycemic regulatory and anti-inflammatory mechanisms.
METHODS: KKAy mice (a spontaneous polygenic T2DM model) were used. Cognitive function was assessed by the Morris water maze (MWM). Fasting blood glucose was monitored throughout the study. Serum cytokines (TNF-α, IL-1β, IL-6, IL-10) were measured by ELISA. Hippocampal ultrastructure was examined by transmission electron microscopy (TEM). The TLR4/MyD88/NF-κB pathway was evaluated in peritoneal macrophages and RAW264.7 cells by Western blot and immunofluorescence.
RESULTS: LBP (20-80 mg/kg, 3 months) improved spatial learning efficiency (P < 0.05) without fully normalizing memory retention, and attenuated hippocampal neuronal damage in KKAy mice. LBP reduced fasting blood glucose and improved systemic glycemic control, with the low dose (20 mg/kg) showing pronounced efficacy in glycemic control. LBP upregulated insulin signaling proteins (IRS, PDX1, ISLET1) and protected β-cell function. Systemically, LBP suppressed pro-inflammatory cytokines (TNF-α, IL-1β) partially and elevated IL-10 by inhibiting the TLR4/MyD88/NF-κB pathway.
CONCLUSION: LBP ameliorates DCI primarily through dual peripheral actions, suggesting a peripheral-central axis mechanism: (1) stabilizing glycemic homeostasis via enhanced insulin/β-cell signaling; (2) suppressing systemic inflammation via inhibition of the TLR4/MyD88/NF-κB pathway. These findings provide a novel mechanistic framework for the clinical translation of LBP in managing DCI.
METHODS: KKAy mice (a spontaneous polygenic T2DM model) were used. Cognitive function was assessed by the Morris water maze (MWM). Fasting blood glucose was monitored throughout the study. Serum cytokines (TNF-α, IL-1β, IL-6, IL-10) were measured by ELISA. Hippocampal ultrastructure was examined by transmission electron microscopy (TEM). The TLR4/MyD88/NF-κB pathway was evaluated in peritoneal macrophages and RAW264.7 cells by Western blot and immunofluorescence.
RESULTS: LBP (20-80 mg/kg, 3 months) improved spatial learning efficiency (P < 0.05) without fully normalizing memory retention, and attenuated hippocampal neuronal damage in KKAy mice. LBP reduced fasting blood glucose and improved systemic glycemic control, with the low dose (20 mg/kg) showing pronounced efficacy in glycemic control. LBP upregulated insulin signaling proteins (IRS, PDX1, ISLET1) and protected β-cell function. Systemically, LBP suppressed pro-inflammatory cytokines (TNF-α, IL-1β) partially and elevated IL-10 by inhibiting the TLR4/MyD88/NF-κB pathway.
CONCLUSION: LBP ameliorates DCI primarily through dual peripheral actions, suggesting a peripheral-central axis mechanism: (1) stabilizing glycemic homeostasis via enhanced insulin/β-cell signaling; (2) suppressing systemic inflammation via inhibition of the TLR4/MyD88/NF-κB pathway. These findings provide a novel mechanistic framework for the clinical translation of LBP in managing DCI.