ArticleMolecular biology reports2026
Berberine attenuates hyperglycemia induced neurodegeneration in mice by modulation of Nrf2 expression.
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
introductionCognitive impairment is one of the complication associated with type 2 diabetes mellitus (T2DM), and patients with T2DM are more likely to develop memory-related neurodegenerative disorders. Berberine (BBR), a natural compound used in the treatment of diabetes and diabetes-associated cognitive dysfunction (DACD), although the underlying mode of action remains largely unknown. Herein, we investigated whether nuclear factor erythroid 2-related factor 2 (Nrf2), a redox-associated factor, is essential to the neuroprotective action of BBR.
methodsStreptozotocin (STZ; 100 mg/kg IP, single shot) was used for induction of T2DM in mice. BBR was administered before STZ administration in Pre-treatment group and after STZ administration in Post-treatment group for 4 weeks. Learning and memory was assessed using Y-maze test and Step through passive avoidance task. The impact of BBR on tight junction proteins, VEGF, GLUT receptors and Nrf2/HO-1 signaling in the hippocampus was analyzed using qPCR. Using standard biochemical tests, the activity of AChE and ChAT were assessed in the hippocampus of T2DM mice.
resultsOur findings indicate that BBR significantly improved cognition in T2DM mice. It significantly increased the gene expression of tight junction proteins and VEGF in the hippocampus of T2DM mice. Also, BBR improved glucose uptake by upregulating GLUT receptors. Furthermore, a marked elevation of AChE activity and decreased activity of ChAT was seen in STZ treated mice which upon treatment with BBR was reversed. Moreover, the expression of Nrf2 and its downstream genes was reduced in the diabetic group and was significantly reversed upon BBR treatment.
conclusionTaken together, our results demonstrate that BBR may exerts protective effects against cognitive decline, by decreased BBB permeability, enhanced glucose uptake, enhanced neurogenesis and activation of Nrf2/HO-1 signaling in the hippocampus of T2DM mice. Our study may signify a new mode of action and a novel therapeutic target for DACD.
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