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Use of beta-nicotinamide mononucleotide or precursor thereof in preparation of medicament for delaying lung aging

A single nucleotide, nicotinamide technology, applied in the field of biomedicine, can solve problems such as no lung disease, and achieve the effect of delaying the reduction of lung function, delaying lung aging, and delaying lung aging

Pending Publication Date: 2019-04-26
SICHUAN UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0006] However, there is no research report on the relationship between the supplementation of β-nicotinamide mononucleotide or its precursor on the age-related decrease in lung function and lung diseases

Method used

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  • Use of beta-nicotinamide mononucleotide or precursor thereof in preparation of medicament for delaying lung aging
  • Use of beta-nicotinamide mononucleotide or precursor thereof in preparation of medicament for delaying lung aging
  • Use of beta-nicotinamide mononucleotide or precursor thereof in preparation of medicament for delaying lung aging

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0035] Example 1 Effect of β-nicotinamide mononucleotide on mouse alveolar epithelial cells

[0036] 1. Materials

[0037] 1.1 Experimental animals SPF grade C57BL / 6 mice (female, 8-10 months or 6-8 weeks old, <28-30g and 19-21g), purchased from Beijing Weitong Lihua Experimental Animal Technology Co., Ltd., raised in SPF level animal room.

[0038]1.2 Experimental drugs Fetal bovine serum, PRMI1640 (gibico), SA-β-Gal staining kit (Beiyuntian Biotechnology Company), calf serum, petri dish, normal saline, absolute ethanol, antibody, (Abcam, USA), sa-β-gal antibody (Beta galactosidase Antibody, American Proteintech Company), nicotinamide riboside (nicotinamide riboside, Shanghai Hanxiang Company), FITC-labeled mouse fluorescent secondary antibody (American AbD Serotec Company), IL-6 (American CST Company) ), TNF-α (USA CST Company), IL-1β (USA CST Company). Hematoxylin staining solution (Guangzhou Xiuwei Trading Co., Ltd.), H2DCF-DA (Sigma Company of the United States), sodiu...

Embodiment 2

[0053] Example 2 NMN delays the aging of primary alveolar epithelial cells

[0054] On the basis of in vivo experiment Example 1, we further explored the direct effect of NMN on alveolar epithelial cells, and investigated whether NMN can alleviate the replicative senescence of alveolar epithelial cells and the aging induced by external stimuli.

[0055] The experimental process is as follows:

[0056] The primary alveolar epithelial cells of mice were isolated and cultured in vitro. When the cells were passed to the 7th and 8th passages, the cells showed a senescent phenotype, that is, the cell shape became significantly larger and rounder, the nucleus increased like a fried egg, and the cell proliferation ability was also significant. reduce. One of the causes of cellular aging is stress aging caused by NAD+ reduction, oxidation / antioxidation system imbalance, and increased oxidative stress. When the cells were subcultured to the 4th passage, NMN was added (at a dose of 500...

Embodiment 3

[0058] Example 3 NMN relieves bleomycin-induced alveolar aging in mice

[0059] NMN can alleviate the replicative aging of alveoli with age, so whether it can alleviate the alveolar aging caused by stress. Bleomycin belongs to the family of glycopeptide antibiotics and has potent antitumor activity. Its main side effect is to cause pulmonary fibrosis, and the main mechanism is to cause genome instability and ROS generation.

[0060] Existing studies have found that bleomycin-induced pulmonary fibrosis is based on the aging of alveolar epithelial cells, thereby impairing the regeneration of alveolar epithelial cells. Cellular senescence exists in the process of lung fibrosis, and by inducing apoptosis, the secretion of senescence-associated SASP can be reduced, as well as markers of extracellular matrix fibrosis, while increasing markers of alveolar epithelial cells. Therefore, we used bleomycin-induced senescence of primary lung epithelial cells as a model to investigate whe...

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Abstract

The invention belongs to the technical field of biomedicine, and particularly relates to a use of a beta-nicotinamide mononucleotide or a precursor thereof in the preparation of a medicament for delaying lung aging. In the prior art, there is no study of supplementation of the beta-nicotinamide mononucleotide or the precursor thereof and reduction of an age-related lung function. In the invention,a mouse model of lung aging is constructed to find, for the first time, that lung aging, especially alveolar epithelial cell aging, can be delayed by adding the beta-nicotinamide mononucleotide or the precursor thereof, and the use of the beta-nicotinamide mononucleotide or the precursor thereof in the preparation of the medicament for delaying the lung aging is provided. The invention provides anew way for delaying the lung aging and delaying the reduction of the lung function, and provides a new treatment basis for preventing or treating related lung diseases caused by the lung aging, which has a broad prospect.

Description

technical field [0001] The invention belongs to the technical field of biomedicine, and in particular relates to the use of β-nicotinamide mononucleotide or its precursor in the preparation of medicines for delaying lung aging. Background technique [0002] As the body ages, the physiological functions, resistance and adaptability of cells, tissues and organs gradually decline. Lung function gradually decreases with age, leading to an increased incidence of aging-related lung diseases, such as lung cancer, chronic structural lung disease, and chronic pulmonary fibrosis. The process of reducing the function of these organs is based on the occurrence of cell senescence, that is, cell senescence is the basis of body aging. [0003] One of the most significant changes in the body's cells as the body ages is NAD + The level of NAD is reduced, thereby the NAD + Decreased levels have been linked to age-related lung disease. NAD + Can form NADH, is a reducing agent and electron...

Claims

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Application Information

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IPC IPC(8): A61K31/706A61P11/00
CPCA61K31/706A61P11/00
Inventor 魏霞蔚魏于全
Owner SICHUAN UNIV
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