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Application of Epimedin B to preparation of medicines for treating neuroinflammation

A technology of neuroinflammation and epimedin, applied in the fields of cell biology and pharmacology, can solve the problems of epimedin B neuroinflammation and neurodegenerative diseases that have not yet been seen, achieve high clinical application value and development prospects, reduce Expression, reducing the effect of dopaminergic neuron damage

Inactive Publication Date: 2019-12-31
QINGDAO UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

At present, there are very few reports on the pharmacological activity of Epimedin B, and there is no report on the use of Epimedin B in the treatment of neuroinflammation and neurodegenerative diseases

Method used

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  • Application of Epimedin B to preparation of medicines for treating neuroinflammation
  • Application of Epimedin B to preparation of medicines for treating neuroinflammation
  • Application of Epimedin B to preparation of medicines for treating neuroinflammation

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0033] Example 1. Real-time fluorescence quantitative PCR technology detects the inhibitory effect of different concentrations of Epimedin B on the inflammatory response of primary astrocytes induced by LPS

[0034] 1. Materials and methods

[0035] (1) Culture of primary microglia and astrocytes in the midbrain

[0036] Select newborn SD rats (SPF grade) within 1-2 days after birth, immerse them in 75% alcohol for disinfection for 15 seconds, take out the whole brain in an aseptic operating table, separate the midbrain, wash 3 times with sterilized PBS, and Gently peel off the meninges and blood vessels, avoiding damage to the brain tissue. Cut the tissue into small pieces, blow the tissue gently with 1000 μL, 200 μL, and 10 μL pipette tips in turn to disperse the cells, collect the cell suspension into a large centrifuge tube, and centrifuge at 1000 rpm for 5 min. Discard the supernatant, then add DMEM / F12 complete medium (containing 10% fetal bovine serum, 100IU / mL penici...

Embodiment 2

[0060] Example 2. Real-time fluorescence quantitative PCR technology detects the mechanism of action of Epimedin B in inhibiting the inflammatory response of primary astrocytes

[0061] G protein-coupled estrogen receptor (GPER), as a new type of membrane estrogen receptor, plays an important role in the treatment of inflammation. GPER-specific blocker G15 and Epimedin B co-treated cells to detect its Effects on astroglial inflammatory factors TNF-α and IL-1β as well as iNOS and COX-2 gene expression.

[0062] After culturing the rat midbrain astrocytes by the same method as in Example 1, when the cell density in the six-well plate reaches 80%-90%, the drug can be added for treatment. Experimental groups 4 and 5 were pretreated with 10 μM Epimedin B for 1 hour, and then added LPS (final concentration 1 μg / ml) to act together for 6 hours; G15 was added 1 hour before Epimedin B pretreatment, and then added LPS together Works for 6 hours. Total mRNA was extracted according to t...

Embodiment 3

[0069] Example 3. Detection of the inhibitory effect of Epimedin B on the inflammatory response of primary microglial cells induced by LPS and the blocking effect of G15 on this effect by real-time fluorescent quantitative PCR technology

[0070] The inflammatory response caused by excessive activation of microglia can invade dopaminergic neurons, causing progressive damage and loss of neurons. The inflammatory factors released by microglia can also activate astrocytes, promote the aggravation of the inflammatory response, and damage neurons. The distribution density of microglia in the substantia nigra is very high, and inflammatory factors can damage dopaminergic neurons in the substantia nigra over time, so inflammation plays an important role in the pathogenesis of PD.

[0071] In this example, cells were co-treated with GPER-specific blocker G15 and Epimedin B, and their effects on gene expression of microglial inflammatory factors TNF-α and IL-1β were detected.

[0072]...

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Abstract

The invention belongs to the fields of cell biology and pharmacology, relates to an application of a natural medicine herba epimedii extract namely Epimedin B, in particular to an application of the Epimedin B to preparation of medicines for treating neuroinflammation. The Epimedin B can reduce the release of inflammatory factors, can reduce damage of dopaminergic neurons, has a certain preventionand protection effect on Parkinson's disease caused by damage of dopaminergic neurons, and can be used for preparing the medicines for preventing and / or treating neuroinflammation and relevant diseases thereof. The application has high clinical application value and high development prospects.

Description

technical field [0001] The invention belongs to the field of cell biology and pharmacology, and relates to the use of epimedin B, which is an extract of epimedium, a natural medicine, and in particular to the application of epimedin B in preparing a medicine for treating neuroinflammation. Background technique [0002] Parkinson's disease (PD) is a degenerative disease of the central nervous system characterized by the progressive degeneration and loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of Lewy bodies. Motor symptoms such as tremor, bradykinesia, muscle rigidity, and postural disturbance, and non-motor symptoms such as depression, anxiety, sleep disturbance, and cognitive impairment. Parkinson's disease is a serious brain disease that endangers the health of the elderly. With the aging of the population, the incidence of Parkinson's disease is increasing year by year. The total number of patients with Parkinson's disease in my co...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K31/7048A61K36/296A61P25/00A61P29/00A61P25/28A61P25/16
CPCA61K31/7048A61K36/296A61P25/00A61P25/16A61P25/28A61P29/00
Inventor 陈文芳王皓田张梅谷雨
Owner QINGDAO UNIV
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