CN116637097A - Application of allicin in improving skeletal muscle disorder - Google Patents

Application of allicin in improving skeletal muscle disorder Download PDF

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CN116637097A
CN116637097A CN202310897296.0A CN202310897296A CN116637097A CN 116637097 A CN116637097 A CN 116637097A CN 202310897296 A CN202310897296 A CN 202310897296A CN 116637097 A CN116637097 A CN 116637097A
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allicin
prdx5
skeletal muscle
cell
muscle disorder
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沈胜楠
谷丽维
张珺哲
张昕炜
朱永平
刘艳青
郭秋岩
王继刚
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    • A61K31/255—Esters, e.g. nitroglycerine, selenocyanates of sulfoxy acids or sulfur analogues thereof
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Abstract

The invention relates to the field of biotechnology, in particular to application of allicin in improving skeletal muscle disorder, and discovers that the allicin can obviously improve cell survival rate, reduce ROS content and H 2 O 2 The content improves the cell oxidative damage caused by TBHP, reconstructs the oxidative balance steady state, clarifies the stability of the allicin in the PRDX5, suggests that the PRDX5 is a specific target protein of the allicin, and Cys100 is a main binding site of the allicin and the PRDX5, and provides experimental basis for further popularization and application of the allicin in improving oxidative stress state and skeletal muscle disorder.

Description

Application of allicin in improving skeletal muscle disorder
Technical Field
The invention relates to the field of biotechnology, in particular to application of allicin in improving skeletal muscle disorder.
Background
Skeletal muscle is the largest organ of the human body, accounting for 40% of the total mass in adults, whose primary function is to generate mechanical forces to support body posture and promote various movements, and plays a key role in glycemic control and metabolic homeostasis. Studies have shown that a variety of disease states, such as aging, obesity, cachexia, etc., cause significant physiological changes in skeletal muscle, including a decrease in muscle strength, myogenesis rate, and an increase in muscle fatigue, ultimately leading to decline in skeletal muscle function such as insulin resistance, muscle atrophy, etc.
Mitochondrial dysfunction due to oxidative damage is a recognized primary causative agent of skeletal muscle dysfunction. The Peroxiredoxins (Prdxs) family of peroxidases has a highly conserved cysteine dependence and has been of great interest in scavenging peroxides, improving oxidative stress, and maintaining redox balance. Among the 6 subtypes of Prdxs family, PRDX5 exists mainly in mitochondria and cytoplasm, is a key hydrogen peroxide scavenging enzyme, and research shows that the overexpression of PRDX5 can directly reduce the generation of ROS, and forms an antioxidant system of mitochondria together with SOD2, TRX and PRDX 3. PRDX5 may also co-act with other factors, SIRT1 promoting expression of PRDX5 by interacting with FOXO3a and PGC-1 a, while modulating expression of other antioxidant enzymes. In addition, PRDX5 can interact with proteins such as NRF2, SIRT2-P53, STAT3 and the like to initiate signal transduction and corresponding biological effects.
Allicin is a bioactive substance extracted from garlic bulb of Liliaceae, its chemical name is diallyl trisulfide, and a large number of researches prove that allicin has various pharmacological effects of resisting apoptosis, preventing cardiovascular diseases, resisting aging, improving immunity, etc.
At present, allicin is studied for improving oxidative stress, but less in the skeletal muscle field. In conclusion, PRDX5 is taken as a target protein, and has broad prospect on diseases related to skeletal muscle dysfunction. The specific action mechanism of the allicin is unknown aiming at the further development of the pharmacological activity of the allicin, and the target protein is still to be elucidated. However, there is currently no report of improving skeletal muscle dysfunction by allicin targeting PRDX5.
Disclosure of Invention
The invention aims to improve skeletal muscle dysfunction, clarify the action targets and provide experimental basis for further popularization and application in subsequent drug and product development.
In a first aspect the invention provides the use of allicin for improving skeletal muscle disorders.
In some embodiments, the skeletal muscle disorder is a skeletal muscle disorder caused by oxidative damage.
In some embodiments, the allicin is at least one of allicin, or a garlic metabolite.
In some embodiments, the allicin targets PRDX5.
In some embodiments, the allicin is bound to PRDX5 at a stoichiometric 1:1 ratio.
In a second aspect the invention provides the use of allicin in the manufacture of a medicament and/or dietary supplement for the prevention and treatment of skeletal muscle disorders.
In some embodiments, the allicin is present at an effective concentration of 25-100 μm.
In a third aspect, the invention provides a pharmaceutical composition comprising allicin and a pharmaceutically acceptable carrier.
In some embodiments, the dosage form of the medicament comprises a tablet, capsule, oral liquid, oral granule, or oral powder.
In some embodiments, the allicin is the only active ingredient or one of the active ingredients.
Compared with the prior art, the invention has the following beneficial effects:
1. the invention discovers that the allicin can obviously improve the cell survival rate,Reducing ROS content and H 2 O 2 The content improves the cell oxidative damage caused by TBHP and rebuilds the oxidative balance steady state.
2. According to the invention, a large number of experiments prove that the stability of the allicin can be enhanced, and the PRDX5 is a specific target protein of the allicin, so that an experimental basis is provided for further popularization and application of the allicin in improving oxidative stress and skeletal muscle disorder.
3. The present invention further found that Cys100 is the primary binding site for allicin and PRDX5.
Drawings
FIG. 1 shows the cell viability (FIG. 1A), ROS content (FIG. 1B), and cell H of the C2C12 myotube cells of example 1 2 O 2 Content (fig. 1C) graph.
FIG. 2 shows Western blot detection of C2C12 cell differentiation regulatory factors (MyoD, myogenin, muRF-1, atrogin 1) in example 2;
FIG. 3 is a graph showing ROS content, H2O2 content (FIG. 3B) in model, control, and dosing groups of the PRDX5 silenced C2C12 cell line of example 3 (FIG. 3A);
FIG. 4A is a graph of the experimental results of example 4 on ITC, the upper graph showing the thermodynamic effect titration curve of the interaction of PRDX5 with allicin, and the lower graph showing the parameters of the model of PRDX5 binding to allicin; FIG. 4B is a graph of CETSA experiment results of example 5, wherein the upper graph shows the relative expression level of PRDX5 detected by western-blot at 37-73 ℃, and the lower graph shows the thermal melting curve of PRDX5 protein;
FIG. 5A is a graph of the results of the molecular docking experiments of example 6, and FIG. 5B is a graph of the effect of allicin on ROS content in a C2C12 point mutant cell line of example 7.
Detailed Description
The invention is based on the fact that allicin improves oxidative stress and improves skeletal muscle dysfunction to clarify an action target, and combines virtual screening and experimental verification, and discovers that PRDX5 is the action target of allicin which plays pharmacological activity for the first time, and the allicin activates PRDX5 to improve oxidative stress state and improve skeletal muscle dysfunction through cys100 of a cysteine binding site of the PRDX5, so that the allicin has positive treatment effect on related diseases caused by PRDX5 defects.
The following description of the technical solutions in the embodiments of the present invention will be clear and complete, and it is obvious that the described embodiments are only some embodiments of the present invention, but not all embodiments. All other embodiments, which can be made by those skilled in the art based on the embodiments of the invention without making any inventive effort, are intended to be within the scope of the invention.
Example 1
Establishment of a TBHP-induced C2C12 myotube cell oxidative damage model.
Obtaining cells: growing good-growth C2C12 myoblasts in DMEM medium containing 10% fetal calf serum, and placing at 37deg.C and 5% CO 2 Culturing in a constant-temperature closed incubator with saturated humidity, after cells were confluent at 70-80%, digested with 0.05% trypsin at 37℃and 10% 5 The individual/well cell density was inoculated into 96 well plates, and after 70-80% of the cells were fused, they were replaced with DMEM cell induction medium containing 2% horse serum, cultured for 4 days, and differentiated into myotube cells, which were grouped.
And (3) drug administration molding treatment:
a: blank control group: adding serum-free culture medium DMEM for culturing 24 h;
b: group of individual doses: adding serum-free culture medium DMEM containing allicin (100 μm) for culturing 24 h;
c: model group: 200. mu M TBHP treated cells for 6h, and then replaced by serum-free culture medium DMEM for 24 h;
drug administration group: 200. mu M TBHP treated cells for 6h, and then replaced with serum-free medium DMEM containing allicin at different concentrations for 24 h, (groups D, E and F, with allicin concentrations of 25. Mu.M, 50. Mu.M and 100. Mu.M respectively);
all the cells were placed at 37℃with 5% CO 2 Culturing in a constant temperature closed incubator with saturated humidity.
Detection of CCK-8 of model, control, and dosing group C2C12 myotube cells cell viability, 90 μl of culture broth and 10 μl of CCK-8 reagent (CCK 8, bi yun, C0038) were added to each well, and after incubation of 1.5. 1.5 h in the cell incubator, absorbance values (a 450) were measured with a fluorescent microplate reader at a wavelength of 450 nm according to the formula:cell viability (%) = cell viability was calculated for treatment group a 450/control group a450 x 100%. ROS content detection (reactive oxygen species detection kit, bi yun tian, S0033S): 1 mL of a medium containing DCFH-DA probe at a concentration of 10. Mu.M was added to each well, and after incubation at 37℃for 20 min, quantitative analysis was performed using a flow cytometer to detect the ROS content. Cell H 2 O 2 Content detection: (Hydrogen peroxide detection kit, biyundian, C0038), operating according to the reagent instructions, measuring absorbance value (A560) with a fluorescent microplate reader at a wavelength of 560 nm, calculating H using a standard curve based on protein concentration 2 O 2 Horizontal.
Experimental results referring to fig. 1, TBHP in the model group resulted in decreased C2C12 myotube cell viability (fig. 1A), ROS content (fig. 1B) and H compared to the control group 2 O 2 The content is increased (figure 1C), and allicin with different concentrations can remarkably improve the cell survival rate, reduce the ROS content and H 2 O 2 The content improves the cell oxidative damage caused by TBHP and rebuilds the oxidative balance steady state.
Example 2
Establishment of a model of TBHP-induced oxidative damage to C2C12 myotube cells was performed as in example 1. The cells were lysed using protein lysates, and the A-F group protein lysates were collected, followed by Western blot detection of C2C12 cell differentiation regulatory factors (MyoD, myogenin, muRF-1, atrogin 1) to evaluate C2C12 myoblast injury related factors.
Referring to fig. 2, compared with the blank control group (group a), TBHP in the model group (group C) causes C2C12 myotube cell injury, thereby affecting skeletal muscle function, inhibiting the expression of skeletal muscle differentiation regulation related factor MyoD, myogenin, promoting the expression of myoprotein degradation related factors MuRF-1 and atrogin1, and simultaneously, allicin with different concentrations can significantly promote the expression level of MyoD, myogenin, inhibit the expression of MuRF-1 and atrogin1, improve skeletal muscle injury caused by TBHP, and reestablish oxidative balance steady state.
The above results indicate that allicin may be able to improve skeletal muscle cell oxidative stress conditions in a dose-dependent manner including increasing cell survival, decreasing ROS content and H 2 O 2 Content, reestablishing oxidation balance steady state; downregulation of skeletal muscle related proteins by oxidative damage at all times improves skeletal muscle function.
Example 3
Constructing a PRDX5 gene silencing expression C2C12 cell line by utilizing a si-RNA technology: C2C12 was inoculated into 6-well plates as cells, respectively, and after 24 hours, the cells were divided into a negative control group (scrambled group (sc-37007, santa Cruz) and a siRNA interference technique silencing PRDX5 group (si-Prdx5Group, (sense: GCUACCCAGAUAACUUUCUTT; anti: AGAAAGUUAUCUGGGUAGCTT) (# 1080, santa Cruz)), cells were transfected with Lipofectamine3000 (Invitrogen), 80 nM siRNA per 6-well plate, and after 6h of transfection, the medium was changed to continue culture, and subsequent experiments were performed after cell differentiation was complete. Cell culture and establishment of a model of TBHP-induced oxidative damage to C2C12 myotube cells were performed as in example 1.si-Prdx5The components are a model group and an administration group. The scrambled component is a model building block and a dosing block. Model group: 200. mu M TBHP treated cells for 6h, and then replaced by serum-free culture medium DMEM for 24 h; drug administration group: 200. mu M TBHP treated cells for 6h, and then replaced with serum-free medium DMEM containing 100 mu M allicin for 24 h; control group: serum-free medium DMEM was cultured for 24 h. All the cells were placed at 37℃with 5% CO 2 Culturing in a constant temperature closed incubator with saturated humidity. To detect cellular ROS and H 2 O 2 The content was the same as in example 1.
Experimental results indicate that allicin cell protective activity is greatly reduced, and allicin cannot be purified by promoting ROS (FIG. 3A) and H 2 O 2 To enhance the resistance of the cells to oxidative damage (fig. 3B).
Example 4
CETSA-WB：
Cytothermal transition analysis (CETSA) explored the binding affinity of allicin to PRDX 5: differentiated and mature C2C12 myotube cells were cultured in a culture dish with a diameter of 10cm, and after the differentiation of the cells was completed, the specific culture method was the same as in example 1, and the cells were grouped: the control group: serum-free medium DMEM; drug administration group: adding 100 μm allicin, placing cells at 37deg.C, and 5% CO 2 Constant temperature of saturated humidityCulturing in a closed incubator for 24 hours, and then digesting with pancreatin to collect cells. Cells were suspended in 50mM HEPES lysis buffer, and after repeated freeze thawing for 3 times, they were mechanically sheared with a needle to lyse proteins. Collecting soluble proteins, equally dividing the soluble proteins into 10 PCR tubes, and respectively carrying out heat treatment at different temperatures of 37-73 ℃ for 3 minutes to collect the soluble proteins; the method is used for subsequent Western blot detection and is used for confirming that allicin is combined with PRDX5 under different temperature treatment conditions and forms a heat-stable protein complex.
CETSA-WB experimental results show that allicin can enhance the stability of PRDX5, suggesting that PRDX5 is a specific target protein of allicin (FIG. 4A).
Example 5
Isothermal titration calorimetry ITC method analysis of allicin affinity assay for PRDX5 protein:
purifying PRDX5 protein, diluting the PRDX5 protein solution to 200 mu M with PBS, and taking 200 mu L of the solution into a centrifuge tube; garlicin PBS solution was taken at a concentration of 200. Mu.M and an experimental volume of 60. Mu.L. ITC detection was performed at constant temperature of 25 ℃. The rotation speed is 750 r/min, 13 drops are titrated together, and the interval is 150 s. The remaining 12 drops were 2. Mu.L in volume except for the first drop of 0.4. Mu.L. Each result was processed using ITC Analysis software and KD and related thermodynamic constants were fitted by subtracting the background signal.
ITC experimental results showed that allicin bound to PRDX5 at a stoichiometric 1:1 ratio, KD value of 1.08±0.30 μm, Δg= -8.51 kcal/mol, -tΔs= -15.4 kcal/mol, Δh= -80 kcal/mol, indicating that allicin and PRDX5 may interact through hydrogen bonding and electrostatic interactions (fig. 4B).
Example 6
To further explore the mode of action of allicin with PRDX5, a molecular docking experiment was used to prepare a PRDX5 structural file (PDB ID: 3 MNG), and in AutoDock's visualization tool Python Molecular Viewer (PMV), the ligand and receptor files were converted to pdbqt format using ADT tools. During ligand conversion, all of the hydrogen on the ligand needs to be added to ensure that the Gasteiger charge is calculated correctly. The rotatable bond of the ligand was detected and set up in the ADT tool using a Torsion Tree. In the PRDX5 conversion process, the file format is saved after hydrogenation. And importing the PRDX5 in the pdbqt format, setting the size and the center position of a Grid in a Grid module of the ADT by using a Grid box tool, obtaining gpf parameter files after setting, operating autoprid 4, obtaining glg Grid point energy recording files and recording map files of a series of acting forces such as electrostatic force, van der Waals force and the like after calculation. Setting search parameters in the ADT module, setting 100 docking generating conformations by using a Ramahk genetic algorithm, storing dpf docking parameter files, and operating autodock4 to obtain dlg docking record files.
Experimental results indicate that the binding pocket of allicin and PRDX5 is very identical and conformationally stable, involving hydrogen bonding and hydrophobic interactions, wherein Cys100 is the primary binding site for allicin and PRDX5 (fig. 5A).
Example 7
PRDX5 overexpression and establishment of a point mutant C2C12 cell line. Functional amino acid identified by molecular butt joint is used as mutation site, and in order to further explore the interaction mode of allicin and PRDX5, an over-expression cell line of PRDX5 wild type (PRDX 5-WT, amino acid sequence is shown as SEQ ID NO. 1) and the mutation of Cys100 amino acid residue in PRDX5 into Ala (PRDX 5-C100A, amino acid sequence is shown as SEQ ID NO. 2) is respectively constructed. One-step PCR was performed to amplify the target gene of the mutant, after confirming the mutant, pSFFV. Neo vectors linking PRDX5 to different mutants were transferred into C2C12 cells by electroporation transfection, and G418 was used to select cell lines stably expressing PRDX5 and mutants thereof. The overexpressed C2C12 cells were seeded into 6-well plates, respectively, and were divided into PRDX5 wild-type overexpressing cell line control (PRDX 5-WT) and PRDX5 mutant (PRDX 5 OV-C100A) groups, followed by cell culture as in example 1. The PRDX5-WT component was a model group and an administration group. The PRDX5OV-C100A composition was used as a model and drug administration composition in the same manner as in example 4.
According to molecular docking experimental results, a point mutation cell line is constructed, and experimental results show that Cys100 mutation leads allicin not to exert cytoprotective activity by promoting ROS clearance (figure 5B), and that Cys100 amino acid residues are critical to interaction of allicin and PRDX5, and Cys100 in PRDX5 can be selectively combined through hydrophobic interaction, so that the antioxidant activity of the allicin can be enhanced.
While the foregoing is directed to the preferred embodiments of the present invention, it will be appreciated by those skilled in the art that various modifications and adaptations can be made without departing from the principles of the present invention, and such modifications and adaptations are intended to be comprehended within the scope of the present invention.

Claims (10)

1. Use of allicin for improving skeletal muscle disorders.
2. The use according to claim 1, wherein the skeletal muscle disorder is a skeletal muscle disorder caused by oxidative damage.
3. The use according to claim 1, wherein the allicin is at least one of allicin, allicin or a garlic metabolite.
4. The use according to claim 1, wherein the allicin targets PRDX5.
5. The use of claim 4, wherein the allicin is bound to PRDX5 in a stoichiometric 1:1 ratio.
6. Use of allicin in the preparation of a medicament and/or dietary supplement for the prevention and treatment of skeletal muscle disorders.
7. The use according to claim 6, wherein the allicin has an action concentration of 25-100 μm.
8. A pharmaceutical composition comprising allicin and a pharmaceutically acceptable carrier.
9. The pharmaceutical composition of claim 8, wherein the dosage form of the drug comprises a tablet, a capsule, an oral liquid, an oral granule, or an oral powder.
10. The pharmaceutical composition of claim 9, wherein the allicin is the only active ingredient or one of the active ingredients.
CN202310897296.0A 2023-07-21 2023-07-21 Application of allicin in improving skeletal muscle disorder Pending CN116637097A (en)

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