CN114452280B - Application of atractylone in preparation of glioma treatment drug - Google Patents

Application of atractylone in preparation of glioma treatment drug Download PDF

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CN114452280B
CN114452280B CN202111334909.7A CN202111334909A CN114452280B CN 114452280 B CN114452280 B CN 114452280B CN 202111334909 A CN202111334909 A CN 202111334909A CN 114452280 B CN114452280 B CN 114452280B
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atractylone
sirt3
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glioma
gene
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CN114452280A (en
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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 the preparation of atractyloneSirt3Use of gene activators. The saidSirt3The dosage form of the gene activator can be solid preparation or liquid preparation, and the administration route can be oral administration or injection. 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 in preparation of glioma treatment drug
Technical Field
The present invention relates toSirt3The field of gene activators, in particular to the preparation of atractyloneSirt3Use of gene activators.
Background
SIRT3Is a member of the family of silencing information modulators (silent information regulator, sirtuins), a highly conserved, dependent on Nicotinamide Adenine Dinucleotide (NAD) + ) Is a deacetylase of (a). Human bodySirt3The gene is located on chromosome 11 pl5.5 (11p15.5) and consists of 21902 bases. Mature typeSIRT3Is not specific, and is distributed in mitochondria or cytoplasm, and even appears in nucleus. However, the process is not limited to the above-mentioned process,SIRT3the distribution has obvious tissue specificity and is related to the metabolic activity of organs, such as liver, brown adipose tissue, heart, kidney and the like, the stronger the metabolic activity isSIRT3The higher the expression.
SIRT3As the main deacetylase in mitochondria, the deacetylase can regulate the energy synthesis of cells and the physiological activity of mitochondria, and simultaneously participate in regulating and controlling the cell growthMaintaining synthesis of desired biomolecules (e.g., proteins, lipids, etc.), and the like.SIRT3Takes part in the regulation of almost all signal paths related to the cellular metabolism of organisms, such as ROS generation and removal, tricarboxylic acid cycle (Tricarboxylic acid cycle, TAC), fatty acid oxidation (Fatty acid metabolism, FAM), urea cycle (Urea cycle, UC), ketogenesis, protein synthesis, cell growth and apoptosis, plays an important role in the aspects of cell growth, cell apoptosis, cell aging, metabolism, inflammation and oxidative stress, becomes a treatment target point of various diseases, and has very important scientific research value and clinical application prospect.
Atractylone (ATR) is rhizoma Atractylodis belonging to CompositaeAtractylodes lancea (Thunb.)DC.Or rhizoma AtractylodisAtractylodes chinensis(DC.)KoidzSesquiterpenoids isolated from the above have 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, regarding atractylone pairsSIRT3The influence of the signal pathway has not been reported.
Disclosure of Invention
In order to solve the technical problems, the invention provides the preparation of atractyloneSirt3Use of gene activators. Atractylone can be effectively up-regulatedSirt3Expression of the Gene asSirt3The active ingredients in the gene activator areSIRT3Treatment of related diseases provides a new option.
The specific technical scheme of the invention is as follows:
in a first aspect, the present invention provides a process for the preparation of atractyloneSirt3Use of gene activators.
Preferably, the method comprisesSirt3The gene activator is in the form of solid preparation or liquidA body preparation.
Preferably, the method comprisesSirt3The administration route of the gene activator is oral or injection.
Preferably, the method comprisesSirt3The gene activator also contains 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 present invention provides a method ofSirt3A gene activator comprising atractylone.
Preferably, the method comprisesSirt3The gene activator is in the form of solid preparation or liquid preparation.
Preferably, the method comprisesSirt3The administration route of the gene activator is oral or injection.
Preferably, the method comprisesSirt3The gene activator also contains a pharmaceutically acceptable carrier or excipient.
Preferably, the excipient comprises one or more of a solvent, a binder, a filler, a stabilizer, and an emulsifier.
Compared with the prior art, the invention has the following advantages:
as a result of the research of the inventor, atractylone can be up-regulatedSirt3Expression of Gene and expression of GeneSirt3The gene activator acts asSIRT3Treatment of related diseases provides a new option.
Drawings
FIG. 1 shows the pair of atractylone-to-glioma cellsSIRT3Influence of expression. Wherein: panel A shows Western blot detection of C6 cells treated with atractylone at 100. Mu.M for 24 hSIRT3And protein levels of Lamin B1; FIG. B and FIG. C are respectively in FIG. ASIRT3Statistical plots of protein and Lamin B1 protein; panel D shows immunofluorescence assay after C6 cells were treated with atractylone at 100. Mu.M for 24 hSIRT3Is a fluorescent intensity level of (2); FIG. E is a statistical plot of FIG. D; FIG. F is a qPCR assay after C6 cells were treated with atractylone at 100. Mu.M for 24 hSIRT3Is a target for the expression of mRNA levels of (2).
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, 0, 24, 48, h, 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 the pH3 assay of cell proliferation after C6, DBTRG cells were treated with atractylone at 100. Mu.M for 24 h; 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 of 0, 24, 48, h with atractylone at 100. Mu.M; 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 24 h 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 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 detection of P53, bcl-2, clear-caspase 3 and Western Blot in xenograft tumors after atractylone treatment 23 dSIRT3Variation in expression level; panel D, E, F and G are P53, bcl-2, clear-caspase 3 and, respectively, in panel CSIRT3A statistical map of proteins; FIG. H is a xenograft tumor treated with atractylone 23 dImmunostaining of tumor at PH 3.
Description of the embodiments
The invention is further described below with reference to examples.
Example 1: atractylone pairSIRT3Effect of expression
To detect atractylone pairsSIRT3The effect of expression, we detected by Western Blot, immunofluorescence and RT-PCR. The specific operation is as follows:
1) Western Blot detection of atractylone-treated gliomaSIRT3Expression change of protein: the cell suspension was inoculated in a 6-well plate, a culture medium containing 100. Mu.M atractylone was added, and the mixture was cultured in an incubator for 24. 24 h. Protein extraction, electrophoresis with 10% SDS-PAGE, transfer membrane (320 mA,70 min), blocking 1h at room temperature, and incubation at 4℃overnight. The next day was washed 3 times with TBST for 5min each. After incubation of the secondary antibody at room temperature for 1h, TBST was washed 3 times for 15min each. And (5) developing.
2) Immunofluorescence detection of atractylone-treated glioma cellsSIRT3Positioning and change in fluorescence intensity: a cell slide of 14 mm was spread in a 24-well plate, and a cell suspension was inoculated (10 4 Cells/well), a culture medium containing 100. Mu.M atractylone was added, and the mixture was cultured in an incubator for 24. 24 h. 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 of the secondary antibodies at room temperature for 1h, PBS was washed 3 times for 5min each. And (5) after sealing, the film can be photographed and analyzed under a confocal microscope.
3) RT-PCR detection of atractylone pairsSIRT3Effect of transcription level: after C6 cells (glioma cells) and DBTRG cells (glioblastoma cells) were grown to an appropriate density on 6 cm plates, the cells were collected by resuspension with Trizol blow, centrifugation at 5min,12000 rpm,4 ℃for 10 min, aspiration of the supernatant, addition of 200. Mu.L of chloroform to the supernatant, gentle inversion for 2 min, mixing, standing at room temperature for 5min,12000 g, centrifugation at 4℃for 15min, careful aspiration of 400-500. Mu.L of the upper aqueous phase, addition of pre-chilled 500. Mu.L, and the like, respectively, were cultured under control and atractylone-containing medium culture conditionsL isopropyl alcohol, after 20 min of standing at-20 ℃,12000 g of the solution is centrifuged for 10 min at 4 ℃, at the moment, white precipitate is seen at the bottom of the tube, the supernatant is discarded, 1 mL of 75% ethanol is added, 12000 g of the solution is centrifuged for 5min at 4 ℃, the supernatant is discarded, an open EP tube orifice is dried for 10 min, 30 mu L of DEPC water is added to the precipitate after drying, and the precipitate is dissolved for 6 min at 55 ℃. Removing genome DNA by using a kit, performing reverse transcription, performing RT-PCR analysis by using SYBR two-step method, wherein each of three cells of a control group and an experimental group corresponds to one sample, and each sample corresponds toSIRT3Three compound holes are made by the primer and the internal reference Actin primer, the RT-PCR is carried out on the machine, and 2 is calculated according to the Ct value -ΔΔCt Values were statistically analyzedSIRT3Is a change in the level of transcription of (a).
As shown in FIG. 1, it was found that atractylone was up-regulated by Western Blot, immunofluorescence and RT-PCRSIRT3The fluorescence is difficult to see after the color pattern is converted into gray pattern in panel D, and it can be seen from the original pattern and panel E that the fluorescence intensity after atractylone treatment is significantly increased compared to the control group.
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 24 h (37 ℃,5% CO) 2 ). The culture medium was changed to one containing atractylone at different concentrations, and 10. Mu.L of CCK8 solution was added to each well (note that no bubbles were generated in the wells). The plates were incubated in an incubator for 1-4 h. The absorbance at 450 nm 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) The cell slide of 14 mm was spread on a 24-well plate, the cell suspension (10000 cells/well) was inoculated, a culture solution containing 100. Mu.M atractylone was added, and the mixture was cultured in an incubator for 24 h. 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) The 1 mL gun head is used for uniformly scribing transverse lines along the 6-hole plate cover, scratches are vertical to the transverse lines at the back as much as possible, and the gun head is vertical and cannot be inclined. 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, 48 and h, and photographs were taken.
2) Cell suspension 200 [ mu ] L (containing 10 4 Individual cells, serum-free) was added to a transwell chamber and 500 μl of serum-containing medium was added to a 24-well plate lower chamber. Culture 24 h. 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 6 cm disc, respectively culturing for 24 h under the culture conditions of 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 protein Loading Buffer sample, carrying out SDS-PAGE gel running, transferring a PVDF membrane under the condition of 20% methanol, sealing 5% skim milk at room temperature for 1h, 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 luminescent 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, centrifugation, PBS washing, 300g,2 min centrifugation to remove supernatant, 500 μl70% ethanol resuspension, fixation for 2 h, storage at 4deg.C, centrifugation to remove supernatant, PBS washing, centrifugation to remove supernatant, adding 100 μl RNase A, incubation at 37deg.C for 30 min, adding 400 μl PI,4 ℃ light shielding for 30 min, 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 using pancreatin digested cells, cell mass greater than 30 ten thousand, centrifugation, PBS washing, 300g,2 min centrifugation to remove supernatant, binding Buffer 500 μl resuspension cells, FITC and PI mixing, 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 50-100 mm 3 At this time, mice were randomly divided into two groups: drug control group and rhizoma Atractylodis group.
2) Atractylone was dissolved in corn oil and administered by gavage at 5 and 10 mg/kg, respectively, and by gavage at 0.1 mL/10 g of body weight, respectively, for 18 d, with equal amounts of corn oil as 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 (3)

1. Application of atractylone in preparing glioma therapeutic drug is provided.
2. The use of claim 1, wherein the glioma-treating agent is for inhibiting glioma growth.
3. The use according to claim 1 or 2, wherein the glioma therapeutic agent is for inhibiting proliferation or migration of glioma cells, or for promoting apoptosis of glioma cells, or for blocking glioma cells in the G1/S phase.
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