Molecular biology reports · 2026
Berberine attenuates hyperglycemia induced neurodegeneration in mice by modulation of Nrf2 expression.
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Gupta Mrinal, Rumman Mohammad, Ubaid Saba, Mahdi Abbas Ali, Pandey Shivani
Аннотация
INTRODUCTION: Cognitive 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.
METHODS: Streptozotocin (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.
RESULTS: Our 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.
CONCLUSION: Taken 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.
METHODS: Streptozotocin (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.
RESULTS: Our 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.
CONCLUSION: Taken 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.