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<p>Diabetes-associated cognitive impairment is a recognized complication of chronic hyperglycemia affecting learning and memory. We investigated whether <i>Tamarindus indica</i> seed extract (TSE) and Diabecon, a marketed herbal formulation (MHF), could reverse diabetes-associated cognitive decline in a high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic rat model. Diabetic rats were treated with pioglitazone (standard), TSE (250&#xa0;mg/kg), or MHF (500&#xa0;mg/kg) for four weeks. Antioxidant activity and phenolic content of TSE and MHF were evaluated using DPPH radical scavenging and ferric-reducing antioxidant power (FRAP) assays, and animals were assessed for learning and memory using the Barnes maze and novel object recognition tests. Hippocampal biochemical analysis revealed reduced antioxidant levels, decreased BDNF and insulin levels, and increased oxidative stress and inflammatory cytokines in diabetic rats. Behavioral assessments demonstrated significant cognitive impairment in HFD–STZ diabetic rats, evidenced by increased escape latency time and reduced preference index. Treatment with MHF significantly improved cognitive performance compared with untreated diabetic animals, whereas TSE showed limited effects. Biochemical analysis revealed that diabetes induction reduced hippocampal BDNF and insulin levels and increased oxidative stress and inflammatory cytokines. MHF treatment significantly restored BDNF and insulin levels, reduced lipid peroxidation, enhanced endogenous antioxidant enzyme activity, and suppressed inflammatory mediators. Western blot analysis further demonstrated modulation of NF-κB and Nrf2 signaling pathways in the hippocampus following MHF treatment. These findings suggest that the marketed herbal formulation Diabecon may alleviate diabetes-associated cognitive decline by reducing oxidative stress and inflammation while improving neurotrophic signaling.</p>

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Reversal of diabetes-associated cognitive impairment through modulation of BDNF, insulin, and NF-κB pathways by a marketed herbal formulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Nabeel Kinattingal,
  • Venugopal Bovilla,
  • Seema Mehdi,
  • Mahadevaswamy G. Kuruburu,
  • K. Nandakumar,
  • Santhepete N. Manjula

摘要

Diabetes-associated cognitive impairment is a recognized complication of chronic hyperglycemia affecting learning and memory. We investigated whether Tamarindus indica seed extract (TSE) and Diabecon, a marketed herbal formulation (MHF), could reverse diabetes-associated cognitive decline in a high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic rat model. Diabetic rats were treated with pioglitazone (standard), TSE (250 mg/kg), or MHF (500 mg/kg) for four weeks. Antioxidant activity and phenolic content of TSE and MHF were evaluated using DPPH radical scavenging and ferric-reducing antioxidant power (FRAP) assays, and animals were assessed for learning and memory using the Barnes maze and novel object recognition tests. Hippocampal biochemical analysis revealed reduced antioxidant levels, decreased BDNF and insulin levels, and increased oxidative stress and inflammatory cytokines in diabetic rats. Behavioral assessments demonstrated significant cognitive impairment in HFD–STZ diabetic rats, evidenced by increased escape latency time and reduced preference index. Treatment with MHF significantly improved cognitive performance compared with untreated diabetic animals, whereas TSE showed limited effects. Biochemical analysis revealed that diabetes induction reduced hippocampal BDNF and insulin levels and increased oxidative stress and inflammatory cytokines. MHF treatment significantly restored BDNF and insulin levels, reduced lipid peroxidation, enhanced endogenous antioxidant enzyme activity, and suppressed inflammatory mediators. Western blot analysis further demonstrated modulation of NF-κB and Nrf2 signaling pathways in the hippocampus following MHF treatment. These findings suggest that the marketed herbal formulation Diabecon may alleviate diabetes-associated cognitive decline by reducing oxidative stress and inflammation while improving neurotrophic signaling.