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KR-20260063495-A - PHARMACEUTICAL COMPOSITION AND HEALTH FUNCTIONAL FOOD FOR COGNITIVE FUNCTION IMPROVEMENT

KR20260063495AKR 20260063495 AKR20260063495 AKR 20260063495AKR-20260063495-A

Abstract

The present invention relates to a pharmaceutical composition and a health functional food that exhibit an excellent cognitive ability improvement effect by including a compound of Formula 1 or a salt thereof.

Inventors

  • 이동성
  • 이형규
  • 이환
  • 윤치수
  • 유지명

Assignees

  • 조선대학교산학협력단

Dates

Publication Date
20260507
Application Date
20241030

Claims (4)

  1. A pharmaceutical composition for improving cognitive ability comprising a compound of the following chemical formula 1 or a salt thereof: [Chemical Formula 1] .
  2. A composition for improving cognitive ability according to claim 1, wherein the cognitive ability is attention, memory, language comprehension and expression ability, problem-solving ability, decision and judgment ability, or planning and organization ability.
  3. A pharmaceutical composition for improving cognitive ability comprising a compound of the following chemical formula 1 or a salt thereof: [Chemical Formula 1] .
  4. A health functional food for improving cognitive ability according to claim 3, wherein the cognitive ability is attention, memory, language comprehension and expression ability, problem-solving ability, decision and judgment ability or planning and organization ability.

Description

Pharmaceutical composition and health functional food for cognitive improvement The present invention relates to a pharmaceutical composition for improving cognitive ability and a health functional food. Neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis, are defined by the destruction of nerve cells. The progression of neurodegenerative diseases is generally accompanied by mitochondrial dysfunction, which leads to the excessive production of reactive oxygen species (ROS) and oxidative stress in the central nervous system (CNS). Oxidative damage caused by ROS can cause severe damage to cellular structures and promote the release of inflammatory mediator proteins such as inducible nitric oxide (iNOS) and cyclooxygenase-2 (COX-2). These proteins induce neuroinflammation by regulating the secretion of nitric oxide (NO) and prostaglandin E2 (PGE2). Microglia are important immune cells in neuroinflammation and change their morphology and function in response to environmental signals. In response to stimuli such as the endotoxin lipopolysaccharide (LPS), microglia assume the M1 morphology and exhibit inflammatory effects. Therefore, LPS-induced M1 microglia play a role in exacerbating oxidative stress and inflammation in the nervous system. M1 microglia release various inflammatory markers, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which can cause direct damage to the CNS and induce neurodegenerative diseases. Recently, there has been significant interest in finding new natural substances capable of treating or preventing neuroinflammation by regulating microglia activation. The loss of functional neurons is a significant cause of neurodegenerative diseases, and glutamate is an excitatory neurotransmitter that plays a crucial role in synaptic plasticity in the brain. However, glutamate imbalance (excessive levels) can damage cellular components, particularly mitochondria, and promote ROS production, potentially leading to neurotoxicity and neuronal damage. Therefore, glutamate plays a critical role in the pathogenesis of various neurodegenerative diseases, particularly AD and PD. Consequently, inhibiting glutamate-induced oxidative stress is an important strategy for protecting neurons. Fig. 1. Cytotoxicity of 18 compounds on HT22 cells. HT22 cells were treated with various concentrations of compounds for 24 hours, and cell viability (AF) was evaluated using the MTT test. Values are reported as % of the control group and are expressed as the mean ± standard deviation (SD) of at least three independent experiments. ** p < 0.01, *** p < 0.001 Control group vs. Treatment group. Fig. 2. Protective effects of 18 compounds on glutamate-induced HT22 cytotoxicity. HT22 cells were pretreated with various concentrations of compounds for 2 hours, followed by treatment with glutamate for 24 hours. Cell viability (AF) was measured using the MTT assay. Values are reported as % of the control group and expressed as the mean ± standard deviation (SD) of at least three independent experiments. * p < 0.05, *** p < 0.001. Glutamate treatment group vs. control group. Fig. 3. Cytotoxicity of dihydropashanone in HT22 cells. (A) Structure of dihydropashanone. (B) HT22 cells were treated with dihydropashanone (10-40 μM) and cell viability was evaluated using the MTT test. Values are reported as % of the control group and are expressed as the mean ± standard deviation (SD) of at least three independent experiments. Fig. 4. Antioxidant effect of dihydropashanone in glutamate-induced HT22 cells. HT22 cells were pretreated with various concentrations of dihydropashanone for 2 hours and then exposed to glutamate for 24 hours. Cell viability was subsequently evaluated using the MTT test (A). Cells were pretreated with dihydropashanone for 2 hours and then exposed to glutamate for 8 hours. ROS (B, C) levels were measured using the dichlorodihydrofluorescein diacetate (DCFDA) test. Values are expressed as the mean ± standard deviation (SD) of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001. Glutamate treatment group vs. control group. Fig. 5. Dihydropashanone induced HO-1 expression in HT22 cells. HO-1 expression was confirmed by Western blot analysis after 12 hours of treatment with dihydropashanone (A). CoPP was used as a positive control. Cells were pretreated with dihydropashanone or SnPP for 2 hours and then exposed to LPS for 24 hours. Cells were pretreated with dihydropashanone or SnPP for 2 hours and then exposed to glutamate for 24 hours. Cell viability (B) was evaluated using the MTT test. Values are expressed as the mean ± standard deviation (SD) of at least three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 control group vs. LPS or glutamate treatment group; ?? p < 0.05 dihydropashanone treatment group vs. LPS or glutamate treatment group. Fig. 6. Dihydropashanone induced Nrf2 activation in HT22 cells