CN117357510A - Application of atractylone as Sirt3 gene activator - Google Patents

Application of atractylone as Sirt3 gene activator Download PDF

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CN117357510A
CN117357510A CN202311052390.2A CN202311052390A CN117357510A CN 117357510 A CN117357510 A CN 117357510A CN 202311052390 A CN202311052390 A CN 202311052390A CN 117357510 A CN117357510 A CN 117357510A
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atractylone
sirt3
cells
gene
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黄智慧
孙闪闪
王永杰
徐佳韵
石家莉
黄榆茜
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Hangzhou Normal University
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Abstract

The present invention relates toSirt3The field of gene activator, discloses application of atractylone as Sirt3 gene activator, in particular relates to the preparation of atractyloneSirt3Use of gene activators to up-regulate intracellular in vitroSirt3Use of gene expression and a method for up-regulating intracellular expression in vitroSirt3Methods of gene expression. The invention discovers that atractylone can be effectively up-regulatedSirt3Expression of the Gene asSirt3The active ingredients in the gene activator areSIRT3Treatment of related diseases provides a new option.

Description

Application of atractylone as Sirt3 gene activator
The present application is a divisional application of patent application with application number 202111334909.7 and creative name of "application of atractylone as Sirt3 gene activator" of 2021, 11/the application date.
Technical Field
The invention relates to the field of Sirt3 gene activators, in particular to application of atractylone as a Sirt3 gene activator.
Background
SIRT3 is a member of the sirtuin (silent information regulator, sirtuin) family, a highly conserved, nicotine-dependent adenine dinucleotide (NAD) + ) Is a deacetylase of (a). The human Sirt3 gene is located on chromosome 11 pl5.5 (11p15.5) and consists of 21902 bases. The cellular localization of mature SIRT3 is not specific, it is distributed in mitochondria or cytoplasm, and even occurs in the nucleus. However, SIRT3 distribution has obvious tissue specificity and is related to organ metabolic activity, and the higher the metabolic activity, the higher the SIRT3 expression of organs such as liver, brown adipose tissue, heart, kidney and the like.
SIRT3 is used as main deacetylase in mitochondria, can regulate cell energy synthesis and mitochondrial physiological activity, and simultaneously participates in regulating and controlling synthesis of biomolecules (such as proteins, lipids and the like) required by cell survival maintenance. SIRT3 is involved in the regulation of almost all signal paths related to the cellular metabolism of organisms, such as ROS production and elimination, tricarboxylic acid cycle (Tricarboxylic acid cycle, TAC), fatty acid oxidation (Fatty acid metabolism, FAM), urea Cycle (UC), ketogenesis, protein synthesis, cell growth and apoptosis and the like, plays an important role in regulating and controlling cell growth, cell apoptosis, cell aging, metabolism, inflammation and oxidative stress, becomes a treatment target of various diseases, and has very important scientific research value and clinical application prospect.
Atractylone (ATR) is a sesquiterpenoid compound isolated from the traditional Chinese medicine asteraceae plant atractylis lancea Atractylodes lancea (thunder.) dc or atractylis japonica Atractylodes chinensis (dc.) Koidz, and has a long history in china. Modern pharmacological research shows that atractylone can be used for treating rheumatic diseases, digestive system diseases, protecting liver, influenza, etc. In early 80 s of 20 th century, atractylone was found to have remarkable liver protecting activity, and was able to prevent liver injury caused by carbon tetrachloride and inhibit hepatocyte DNA injury caused by t-butyl hydroperoxide. In recent years, studies have reported that atractylone also has anti-inflammatory, antinociceptive, antiviral, antiulcer and sodium/potassium-atpase inhibitory activities. However, no study has been reported on the effect of atractylone on SIRT3 signaling.
Disclosure of Invention
In order to solve the technical problems, the invention provides application of atractylone as an Sirt3 gene activator. The atractylone can effectively up-regulate the expression of the Sirt3 gene, can be used as an active ingredient in Sirt3 gene activators, and provides a new choice for treating SIRT3 related diseases.
The specific technical scheme of the invention is as follows:
in a first aspect, the invention provides the use of atractylone for the preparation of a Sirt3 gene activator.
Preferably, the Sirt3 gene activator is in a solid preparation or a liquid preparation.
Preferably, the Sirt3 gene activator is administered orally or by injection in vivo and is administered in vitro by adding to a cell culture medium.
Preferably, the Sirt3 gene activator comprises a pharmaceutically acceptable carrier or excipient.
Further, the excipient includes one or more of a solvent, a binder, a filler, a stabilizer, and an emulsifier.
In a second aspect, the invention provides the use of atractylone for up-regulating intracellular Sirt3 gene expression in vitro.
In a third aspect, the present invention provides a method of up-regulating Sirt3 gene expression in a cell in vitro comprising the steps of: in vitro, the cells were treated with atractylone.
Preferably, the method of treating the cells with atractylone is to add atractylone to a culture solution of the cells and culture the cells.
Compared with the prior art, the invention has the following advantages:
the research of the inventor shows that atractylone can up-regulate the expression of Sirt3 gene, plays the role of Sirt3 gene activator, and provides a new choice for treating SIRT3 related diseases.
Drawings
FIG. 1 shows the effect of atractylone on expression of SIRT3 in glioma cells. Wherein: panel A shows protein levels of SIRT3 and Lamin B1 detected by Western blot after C6 cells were treated with atractylone at 100. Mu.M for 24 h; panels B and C are statistical plots of SIRT3 and Lamin B1 proteins, respectively, in panel a; panel D shows the fluorescence intensity levels of SIRT3 detected by immunofluorescence after C6 cells were treated with atractylone at 100. Mu.M for 24 h; FIG. E is a statistical plot of FIG. D; panel F shows the mRNA levels of SIRT3 by qPCR after 24h treatment of C6 cells with atractylone at 100. Mu.M.
FIG. 2 shows the effect of atractylone on glioma cell and glioblastoma cell proliferation. Wherein: panel A and B show the viability of cells tested using CCK8 kit after C6 and DBTRG cells were treated with atractylone at 0, 25, 50, 100. Mu.M for 0, 24, 48 hours, respectively; panel C shows the results of cell cloning after C6, DBTRG cells were treated with atractylone at 100. Mu.M for 7 d; FIG. D is a statistical plot of FIG. C; panel E shows that PH3 detects proliferation of C6, DBTRG cells after 24h treatment with atractylone at 100. Mu.M; figure F is a statistical plot of figure E.
FIG. 3 shows the effect of atractylone on glioma cell and glioblastoma cell migration. Wherein: panel A shows the migration ability of C6, DBTRG cells after treatment with atractylone at 100. Mu.M for 0, 24, 48 h; panels B and C are statistical plots of C6 and DBTRG cells, respectively, in panel a; panel D shows the migration ability of C6, DBTRG cells after 24h treatment with atractylone at 100. Mu.M, as measured by transwell; panel E and F are statistical plots of C6 and DBTRG cells, respectively, in panel D.
Fig. 4 is the effect of atractylone on glioma cell cycle and apoptosis. Wherein: panel A shows the effect of flow cytometry on the cell cycle of C6 cells treated with atractylone at 100. Mu.M for 24 h; FIG. B is a statistical plot of FIG. A; panel C shows the effect of flow cytometry on apoptosis of drug after C6 cells were treated with atractylone at 100. Mu.M for 24 h; FIG. D is a statistical plot of the plot of FIG. C; panel E shows the effect of PI staining on apoptosis of drug tested after C6 cells were treated with atractylone at 100. Mu.M for 24 h; FIG. F is a statistical plot of FIG. E; panel G shows protein levels of p53, clear-caspase 3 and Cyclin D1 detected by Western blot after C6 cells were treated with atractylone at 100. Mu.M for 24 h; panel H, panel I and panel J are statistical plots of the p53, clear-caspase 3 and Cyclin D1 proteins, respectively, in panel G.
FIG. 5 shows the effect of atractylone on glioma cell growth. Wherein: panel A is a representative of C6 xenograft tumors following atractylone treatment; panel B is a weight statistic of the tumors in panel A; panel C shows the Western Blot detection of changes in P53, bcl-2, clear-caspase 3 and SIRT3 expression levels in xenograft tumors after 23d atractylone treatment; panel D, E, F and G are statistical plots of P53, bcl-2, clear-caspase 3 and SIRT3 proteins, respectively, in panel C; panel H shows the immunostaining of xenograft tumors at pH3 after 23d atractylone treatment.
Detailed Description
The invention is further described below with reference to examples.
Example 1: effect of atractylone on SIRT3 expression
To examine the effect of atractylone on SIRT3 expression, we detected by Western Blot, immunofluorescence and RT-PCR. The specific operation is as follows:
1) Western Blot detection of changes in SIRT3 protein expression in atractylone-treated gliomas: inoculating cell suspension into 6-well plate, adding culture solution containing 100 μm atractylone, and culturing in incubator for 24 hr. Protein extraction, electrophoresis with 10% SDS-PAGE, transfer membrane (320 mA,70 min), blocking at room temperature for 1h, and incubation at 4℃overnight. The next day was washed 3 times with TBST for 5min each. After incubation of the secondary antibody for 1h at room temperature, TBST was washed 3 times for 15min each. And (5) developing.
2) Immunofluorescence detection of SIRT3 localization and change in fluorescence intensity in atractylone-treated glioma cells: a cell slide of 14mm was spread in a 24-well plate, and a cell suspension (10 4 Individual cells/well), adding a culture medium containing 100. Mu.M atractylone, and placing in an incubatorCulturing for 24h. The plates were fixed with 4% PFA for 15min and then washed 3 times with PBS for 5min each. After blocking with blocking solution (5% bsa+0.1% triton) for 1 hour, the primary antibody was incubated overnight at 4 ℃. The next day was washed 3 times with PBS for 5min each. After incubation for 1h at room temperature, the secondary antibody was washed 3 times with 5min each with PBS. And (5) after sealing, the film can be photographed and analyzed under a confocal microscope.
3) RT-PCR detects the effect of atractylone on SIRT3 transcript levels: after C6 cells (glioma cells) and DBTRG cells (glioblastoma cells) were grown to appropriate densities on 6cm plates, they were cultured for 24h using control and atractylone-containing medium, resuspended and collected cells were blown off using Trizol, left at room temperature for 5min, centrifuged at 12000rpm,4℃for 10min, the supernatant was aspirated, 200. Mu.L of chloroform was added to the supernatant, gently inverted for 2min to mix, left at room temperature for 5min,12000g, centrifuged at 4℃for 15min, 400-500. Mu.L of the upper aqueous phase was carefully aspirated, pre-chilled 500. Mu.L of isopropanol was added, left at-20℃for 20min, centrifuged at 12000g,4℃for 10min, at which time a white pellet was seen at the bottom, the supernatant was discarded, 1mL of 75% ethanol was added, 12000g, centrifuged at 4℃for 5min, the supernatant was discarded, the open EP nozzle was dried for 10min, and after drying the pellet was added 30. Mu.L of DEPC water, and dissolved at 55℃for 6min. Removing genome DNA by using a kit, performing reverse transcription, performing RT-PCR analysis by using a SYBR two-step method, wherein each of three cells of a control group and an experimental group corresponds to one sample, each sample corresponds to SIRT3 primer and internal reference Actin primer to make three compound holes, performing on-machine RT-PCR, and calculating 2 according to Ct values -ΔΔCt Values were taken and analyzed statistically for changes in the transcription level of SIRT 3.
As shown in FIG. 1, it was found that atractylone can up-regulate SIRT3 expression by Western Blot, immunofluorescence and RT-PCR (after color image is converted into gray pattern in panel D, fluorescence is difficult to see, and from original image and panel E, fluorescence intensity after atractylone treatment is significantly increased compared with control).
Example 2: influence of atractylone on glioma cell proliferation
In order to detect whether atractylone has an effect on glioma proliferation, we examined atractylone proliferation effect on glioma by CCK8 assay, clonogenic assay, PH3 immunofluorescence. The specific operation is as follows:
1) Cell suspensions (100. Mu.L/well, 3000 cells/well) were seeded in 96-well plates. The plates were pre-incubated in an incubator for 24h (37 ℃,5% CO) 2 ). The culture medium was changed to one containing atractylone at different concentrations, and 10. Mu.LCCK 8 solution was added to each well (note that bubbles were not generated in the wells). The plates were incubated in an incubator for 1-4h. The absorbance at 450nm was measured with a microplate reader.
2) Inoculating cell suspension (500 cells/well) into 6-well plate, adding culture solution containing 100 μm atractylone, culturing in incubator for 5 days (37deg.C, 5% CO) 2 ) PFA was immobilized, crystal violet stained and photographed.
3) A cell slide of 14mm was spread on a 24-well plate, and the cell suspension (10000 cells/well) was inoculated, and a culture solution containing 100. Mu.M atractylone was added and cultured in an incubator for 24 hours. The sections were fixed with 4% PFA for 15min and then washed 3 times with PBS for 5min each. After blocking with blocking solution (5% bsa+0.1% Triton) for 1 hour, the primary antibody was incubated overnight at 4 ℃. The next day was washed 3 times with PBS for 5min each. After incubation of the secondary antibody for 1 hour at room temperature, PBS was washed 3 times for 5min each. And (5) after sealing, the film can be photographed and analyzed under a confocal microscope.
As shown in fig. 2, it can be seen from cck8 experiment, cell cloning experiment, and PH3 immunofluorescence that atractylone can inhibit proliferation of glioma cells (after color image is converted into gray pattern in fig. E, fluorescence intensity is different from that of original image, and as can be seen from original image and fig. F, fluorescence intensity of C6 and DBTRG cells after atractylone treatment is significantly reduced compared with control group).
Example 3: influence of atractylone on glioma cell migration
In order to detect whether atractylone has influence on glioma migration, the migration effect of atractylone on glioma is detected through scratch experiments and transwell. The specific operation is as follows:
1) A1 mL gun head is used for uniformly scribing transverse lines along the 6-hole plate cover, scratches of the transverse lines are perpendicular to the back as much as possible, and the gun head is perpendicular and cannot incline. The cells were washed 3 times with PBS, the scraped cells were removed, and serum-free medium was added. Placing at 37deg.C, 5% CO 2 And (5) culturing in an incubator. Samples were taken at 0, 24, 48h and photographed.
2) 200. Mu.L of cell suspension (containing 10) 4 Individual cells, serum-free) was added to the transwell chamber and 500 μl of serum-containing medium was added to the 24-well plate chamber. Culturing for 24h. PFA was immobilized, crystal violet stained and photographed.
As shown in FIG. 3, atractylone was found to inhibit glioma cell migration by scratch and transwell experiments.
Example 4: influence of atractylone on glioma cell cycle and apoptosis
To examine whether atractylone affects glioma cell cycle and apoptosis, we examined atractylone's effects on glioma cell cycle and apoptosis by flow cytometry, western Blot and PI staining. The specific operation is as follows:
1) Western Blot-coupled flow cytometry to detect atractylone effect on cell cycle arrest: after C6 and DBTRG cells grow to a proper density on a 6cm dish, respectively culturing for 24 hours by using a control and a culture solution containing 100 mu M atractylone, adding a proper amount of RIPA lysate containing a protease inhibitor to collect cells, carrying out protein quantification by using a BCA method, preparing a sample by using a protein Loading Buffer, running a gel by SDS-PAGE, transferring a PVDF film under the condition of 20% methanol, sealing 5% skim milk for 1 hour at room temperature, incubating an antibody cyclin D1 at 4 ℃, incubating a corresponding species source coupling HRP secondary antibody the next day, washing TBST, incubating by using ECL luminous solution, carrying out band gray calculation by using Image J, and carrying out statistical analysis difference;
2) Flow cytometry analysis using pancreatin digested cells, cell mass greater than 30 ten thousand, after centrifugation, PBS wash, 300g,2min centrifugation to remove supernatant, 500 μl70% ethanol re-suspension, fixation for 2h, storage at 4deg.C, centrifugation to remove supernatant, PBS wash, centrifugation to remove supernatant, addition of 100 μl RNase A, incubation at 37deg.C for 30min, addition of 400 μl PI, light-shielding at 4deg.C for 30min, filtration, and cycle-blocking analysis by flow tube bench;
3) Detecting the influence of atractylone on apoptosis by Western Blot combined flow cytometry; extracting protein, detecting the expression level change of apoptosis-related proteins C-caspase 3, bcl-2, bax, P53 and the like under the action of atractylone by using a Western Blot technology, and carrying out statistical analysis; flow cytometry analysis was performed using pancreatin digested cells, cell numbers were greater than 30 ten thousand, after centrifugation, PBS was washed, 300g,2min centrifuged to remove supernatant, binding Buffer 500 μl resuspended cells, mixed-level-dyeing with FITC and PI, incubation at room temperature for 5min in the dark, filtration and apoptosis analysis by flow tube bench.
As shown in FIG. 4, atractylone can promote apoptosis of glioma cells and arrest glioma cells in the G1/S phase as found by flow cytometry, western Blot and PI staining.
Example 5: effect of atractylone on in vivo glioma growth
To examine the effect of atractylone on glioma growth in vivo, we examined by subcutaneous oncological model. The specific operation is as follows: 1) Subcutaneous oncological model establishment: will be 3X 10 6 The individual C6 cells were suspended in serum-free DMEM medium and inoculated subcutaneously into nude mice. When the injection site is observed to grow to 50-100mm 3 At this time, mice were randomly divided into two groups: drug control group and rhizoma Atractylodis group.
2) The atractylone is dissolved in corn oil and respectively administered by 5 mg/kg and 10mg/kg of stomach, and the obtained mixture is respectively administered by 0.1mL/10g of stomach for 18d, and the corn oil with the same amount is used as a control. Tumor volume was measured every three days, and the calculation formula was: tumor volume (mm) 3 )＝0.5×L×W 2 L is long and W is wide. Finally, mice were sacrificed by cervical dislocation and tumors, hearts, livers, lungs and kidneys were excised. The tumors were photographed immediately and weighed. Tumors and organs were then fixed with 4% pfa and HE analysis was performed.
As shown in fig. 5, the atractylone can inhibit the growth of glioma in vivo through a subcutaneous tumor formation model (after the color image is converted into a gray pattern in fig. H, the fluorescence intensity is different from that of the original image, and as can be seen from the original image, the fluorescence intensity after the atractylone treatment is obviously reduced compared with that of the control group.
The raw materials and equipment used in the invention are common raw materials and equipment in the field unless specified otherwise; the methods used in the present invention are conventional in the art unless otherwise specified.
The foregoing description is only a preferred embodiment of the present invention, and is not intended to limit the present invention, and any simple modification, variation and equivalent transformation of the above embodiment according to the technical substance of the present invention still fall within the scope of the technical solution of the present invention.

Claims (8)

1. Preparation of atractyloneSirt3Use of gene activators.
2. The use according to claim 1, wherein theSirt3The gene activator is in the form of solid preparation or liquid preparation.
3. The use according to claim 1, wherein theSirt3The gene activator is taken orally or injected in vivo and added into cell culture liquid in vitro.
4. The use according to claim 1 or 2, wherein theSirt3The gene activator comprises a pharmaceutically acceptable carrier or excipient.
5. The use of claim 4, wherein the excipient comprises one or more of a solvent, a binder, a filler, a stabilizer, and an emulsifier.
6. Atractylone up-regulates intracellular in vitroSirt3Use in gene expression.
7. Up-regulating intracellular in vitroSirt3A method of gene expression comprising the steps of: in vitro, the cells were treated with atractylone.
8. The method of claim 7, wherein the cells are treated with atractylone by adding atractylone to a culture solution of the cells and culturing the cells.
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