Application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving neurotoxicity caused by glutamic acid

A technology of trimethoxybenzene and neurotoxicity, applied in the fields of biology and medicine, can solve the problems of mitochondrial function damage, mitochondrial membrane permeabilization, cell death, etc., achieve significant neuroprotective function, inhibit neurotoxicity, and have good application prospects Effect

Active Publication Date: 2021-05-07
XI AN JIAOTONG UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Excess reactive oxygen species and Ca in cells 2+ It will promote the translocation of tBid to mitochondria, resulting in damage to mitochondrial function and mitochondrial membrane permeabilization, causing rapid loss of ATP and release of cytochrome c, allowing AIF to enter the nucleus and induce DNA fragmentation, eventually leading to cell death

Method used

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  • Application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving neurotoxicity caused by glutamic acid
  • Application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving neurotoxicity caused by glutamic acid
  • Application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving neurotoxicity caused by glutamic acid

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0083] (1,2,3-Trimethoxybenzene)-propenone has no toxic and side effects on mouse hippocampal neurons and human neuroblastoma cells

[0084] Use (1,2,3-trimethoxybenzene)-propenone to act on mouse hippocampal neuron cells and human neuroblastoma cells for 12h or 24h, and detect cell viability. figure 2 A and figure 2 B shows that (1,2,3-trimethoxybenzene)-propenone at concentrations below 5 μM has no effect on cell viability of mouse hippocampal neurons, and (1,2,3-trimethoxybenzene)-propenone at concentrations above 5 μM Acrylone can slightly reduce the viability of mouse hippocampal neurons, but (1,2,3-trimethoxybenzene)-propenone does not affect the viability of human neuroblastoma cells. results from the cell cycle figure 2 C and figure 2 D It can be seen that high concentration of (1,2,3-trimethoxybenzene)-propenone can arrest the cell cycle of mouse hippocampal neurons in the S phase, thereby inhibiting cell proliferation and reducing cell viability.

Embodiment 2

[0086] (1,2,3-Trimethoxybenzene)-propenone improves mitochondrial function

[0087] Use (1,2,3-trimethoxybenzene)-propenone to act on mouse hippocampal neuron cells and human neuroblastoma cells for 12h or 24h, and detect the mitochondrial membrane potential. image 3 A and 3B show that (1,2,3-trimethoxybenzene)-propenone can significantly increase the mitochondrial membrane potential of mouse hippocampal neuron cells and human neuroblastoma cells. image 3 C is the result graph of mitochondrial respiration oxygen consumption rate in mouse hippocampal neuron cells treated with (1,2,3-trimethoxybenzene)-propenone, and the mitochondrial respiration oxygen consumption rate represents the ability of mitochondria to carry out aerobic metabolism. Such as image 3 C shows the basal oxygen consumption, oxidative phosphorylation oxygen consumption for ATP synthesis, maximal respiratory oxygen consumption and non-mitochondrial oxygen consumption in the (1,2,3-trimethoxybenzene)-propeno...

Embodiment 3

[0089] (1,2,3-Trimethoxybenzene)-propenone is an antioxidant targeting mitochondria

[0090] Intracellular reactive oxygen species are mainly produced by the mitochondrial respiratory chain as well as NADPH oxidase and peroxidase. As the main site of reactive oxygen species generation, mitochondria with high aerobic capacity will generate more reactive oxygen species. Therefore, the ability of (1,2,3-trimethoxybenzene)-propenone to scavenge reactive oxygen species was detected by using the reactive oxygen species probe DCFH-DA and the mitochondrial reactive oxygen species probe MitoSOX. Figure 4 A shows that compared with the control, 5 μM (1,2,3-trimethoxybenzene)-propenone can significantly reduce the level of reactive oxygen species in cells, suggesting that it has antioxidant effect. Simultaneously, Figure 4 B shows that compared with the control, the weakening of the red fluorescence intensity proves that (1,2,3-trimethoxybenzene)-propenone can obviously remove the mi...

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Abstract

The application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving the neurotoxicity caused by glutamate, by increasing the mitochondrial membrane potential and mitochondrial aerobic metabolism, enhancing mitochondrial function, and activating biphasic Enzyme system, up-regulate the expression of biphasic enzyme genes, scavenge mitochondrial reactive oxygen species, (1,2,3-trimethoxyphenyl)-propenone, as an antioxidant targeting mitochondria, can regulate PI3K / Akt signaling pathway, restore Mitochondrial function damage and oxidative stress caused by glutamate, exert anti-oxidation and protect mitochondrial function, restore oxidative stress and mitochondrial damage caused by glutamate, thereby preventing acute neurotoxicity caused by glutamate Onset and progression of chronic brain injury.

Description

technical field [0001] The invention belongs to the fields of biology and medicine, and particularly relates to the application of (1,2,3-trimethoxybenzene)-propenone in the preparation of drugs for improving neurotoxicity caused by glutamic acid. Background technique [0002] Glutamate is an abundant and important excitatory neurotransmitter in the mammalian central nervous system. Under normal physiological conditions, glutamate can regulate many important physiological functions of neurons and glial cells, including synaptic transmission, synaptic plasticity, interaction between synapses, non-synaptic neurotransmission, neuronal cell survival, and neurotransmitter release from glial cells. Although the neural excitation caused by glutamate plays a vital role in the structure and function of the brain, excessive glutamate in the synaptic cleft can cause excitotoxicity, leading to neuronal death, which in turn triggers a variety of central Neurological and psychiatric dis...

Claims

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Application Information

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Patent Type & Authority Patents(China)
IPC IPC(8): A61K31/12A61P25/00
CPCA61K31/12A61P25/00
Inventor 刘健康崔玉婷冯智辉曹瑞军黄娜
Owner XI AN JIAOTONG UNIV
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