Eucommia ulmoides leaf lignan compound, preparation method and application of eucommia ulmoides leaf lignan compound in neuroprotection

Abstract

The invention discloses a folium cortex eucommiae lignan compound, a preparation method and application of the folium cortex eucommiae lignan compound in neuroprotection, the folium cortex eucommiae lignan compound generates antioxidant protein by regulating a PI3K / AKT / GSK3beta / Nrf2 signal channel, nerve cells are protected from being influenced by oxidative stress, and the chemical structural formula of the folium cortex eucommiae lignan compound and corresponding nuclear magnetic data are obtained. The compound is separated from folium cortex eucommiae. In the compounds, (+)-7-epi-pinoresin mr1 (1) is a new lignan separated from eucommia ulmoides, and (2) is a new lignan separated from eucommia ulmoides. Through determination of cell activity, the enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), the level of reactive oxygen species (ROS) and the level of lactic dehydrogenase (LDH), 6 compounds in the 12 lignans show good neuroprotective activity; wherein the compound 1, the compound 2 and the compound 4 have the best activity, and the protein expression quantity of antioxidant proteins HO-1, NQO-1 and Cat is increased by adjusting a PI3K / AKT / GSK-3beta / Nrf2 signal channel, so that the compound 1, the compound 2 and the compound 4 have a remarkable neuroprotective effect.

Description

technical field [0001] The invention belongs to the field of biomedicine, and relates to a eucommia leaf lignan compound, a preparation method and an application for neuroprotection. Background technique [0002] Parkinson's disease (PD) is a chronic neurodegenerative movement disorder caused primarily by the death of dopaminergic neurons in the substantia nigra and characterized by the degeneration of specific populations of central and peripheral neurons, including dopaminergic neurons in the substantia nigra . The mechanisms underlying neuronal death in PD are not fully understood and current therapies focus on symptoms rather than neuronal loss [1] . Activation of pro-apoptotic genes is often required for neuronal death, regardless of its cause. Studies have shown that DNA damage, oxidative stress, hypoxia, ER stress, and energy depletion are all causes of neuronal degeneration in PD [2] . A large number of in vivo and in vitro experiments have shown that the oxidat...

AI Technical Summary

Problems solved by technology

Currently, drugs for the treatment of PD cannot stop or delay the degeneration of dopaminergic neurons, so discovering drugs with anti-oxidation and anti-apoptosis effects is of great significance for the prevention and treatment of PD.

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