CN107233338A - Climb application of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared - Google Patents
Climb application of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared Download PDFInfo
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- A61K31/35—Heterocyclic compounds having oxygen as the only ring hetero atom, e.g. fungichromin having six-membered rings with one oxygen as the only ring hetero atom
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Abstract
The invention provides climb new opplication of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared, the structural formula for climbing trifoliate jewelvine isoflavones is as follows, the suppression cervical cancer cell for climbing trifoliate jewelvine isoflavones selectivity that the present invention is provided, composition is safe and reliable, and in time-dose dependence, possess larger application prospect in terms of drug development.
Description
Technical field
The invention belongs to compound applied technical field, more particularly, to climb trifoliate jewelvine isoflavones prepare prevention and/
Or the application in treatment uterine neck cancer drug.
Background technology
Cervical carcinoma is to endanger one of major malignant tumor of women's health, and the incidence of disease in female tumor is only second to mammary gland
Cancer, and existing antineoplastic still has that toxicity is big, the more low drawback of curative effect, therefore develop a kind of good effect and poison is secondary makees
Had very important significance with small medicament for resisting cervical cancer.
Phytochemicals production occupies an important position always in new treatment malignant tumor medicine is developed all the time, climbs
Trifoliate jewelvine isoflavones (English name is Warangalone) is stepped on for tricuspid cudrania fruit (Fructus Maclurae Tricuspidatae)
In isolated isoflavonoid, early-stage Study finds that it has preferable antioxidation activity, and to breast cancer cell
MDA-MB-231 and MCF-7 have good inhibiting effect, but the molecular mechanism for suppressing tumour cell is not known.And not
Understand whether it has preferable effect to other tumour cells.
The content of the invention
The invention provides climb application of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared.
To achieve these goals, the present invention is adopted the following technical scheme that：
Climb application of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared, the different Huang of climbing trifoliate jewelvine
The structural formula of ketone is as follows：
Preferably, the medicine includes pharmaceutically acceptable salt or carrier.
The present invention optionally suppresses the suppression mechanism research that cervical cancer cell has carried out correlation for Warangalone,
It can suppress the transfer ability of tumour by suppressing the invasion and attack and migration of tumour cell, 1 μ Μ Warangalone with sun
The inhibition of property control group cis-platinum (1 μ Μ) is suitable.It is to induce HeLa by mitochondria pathway to demonstrate Warangalone
Apoptosis.Meanwhile, being accumulated in Warangalone induction HeLa Apoptosis paths for ROS plays very important effect,
After Warangalone processing HeLa cells cellular antioxidant or Antioxidant Enzymes may be caused to be oxidized so that ROS can not
Removed and largely accumulated in time, finally have activated mitochondrial apoptosis path and MAPK signal paths.
Compared with prior art, the invention has the advantages that and beneficial effect：
The invention provides new opplication of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared is climbed, originally
The suppression cervical cancer cell for climbing trifoliate jewelvine isoflavones selectivity that invention is provided, and m- dose dependent when being in, composition safety
Reliably, possesses larger application prospect in terms of drug development.
Brief description of the drawings
Fig. 1 is life of the climbing trifoliate jewelvine isoflavones (Warangalone) in time and the suppression HeLa cells of dose dependent
It is long.
Fig. 2 is the cellular morphology change (200 ×) that Warangalone handles HeLa cells after 24h and 48h.
Fig. 3 is that Hoechst 33342 dyes influences (200 ×) of the observation Warangalone to HeLa karyomorphisms.
Fig. 4 is Warangalone to HeLa cell invasions and the inhibitory action of migration.
Fig. 5 is Warangalone to HeLa cell scratch experiment results.
Fig. 6 is influences of the Flow cytometry Warangalone to HeLa cell cycle distributions.
Fig. 7 is the effect that the double dye detection Warangalone of Annexin V-FITC/PI induce HeLa Apoptosis.
Fig. 8 is that Flow cytometry various concentrations Warangalone is handled after HeLa cells 24h and 48h, to cell line
The influence of mitochondrial membrane potential.
Fig. 9 is that Warangalone influences on HeLa cells ROS.
Figure 10 is that Western blot methods detect that Warangalone is expressed Bcl-2 family proteins and endochylema cromoci
Influence.
Figure 11 is that Warangalone induces the intracellular caspases-3 of HeLa, caspase-8 and caspase-9 activation.
Figure 12 is that various concentrations Warangalone is handled after HeLa cells 48h, Western bolting detection cells
Caspases-3, caspase-8, caspase-9 and PARP expression.
Figure 13 is influences of the Warangalone to apoptosis-related protein in cervical cancer cell.ERK in MAPK signal paths,
The influence (A-C) of Akt dephosphorylations and p38, JNK phosphorylation；P53 phosphorylation (D).
Embodiment
The present invention is further illustrated below in conjunction with specific embodiments and the drawings, and embodiment is illustrated and later in the accompanying drawings
It is illustrated, gives the detailed embodiment in part and specific operating process.Unless stated otherwise, the examination that the present invention is used
Agent, method and apparatus are the art conventional reagent, method and apparatus.
Embodiment 1Warangalone anti tumor activity in vitro
503nhibiting concentration (the IC of cell50) it is for assessing one of common method of Drug inhibition tumor proliferation ability.This
Invention has selected the human normal cell line and tumour cell of different tissue sources totally 8 kinds of cell detection Warangalone's antitumor
Ability, the influence of Warangalone cell proliferations is determined using mtt assay, drug treating time is 72h, as a result such as the institute of table 1
Show：HeLa is human cervical carcinoma cell, and HepG2 is human liver cancer cell, and M321 and MCF-7 are human breast cancer cell, LO2 people's normal hepatocytes
Cell, chem-5 is normal Glial cells.The growth of tumour cell after being handled through Warangalone is all by different degrees of
Suppression, by analysis it can be seen that Warangalone to cervical carcinoma, breast cancer, several different tumour cells of liver cancer IC50
Scope is between 13.3-29.6 μ Μ, substantially less than normal liver cell LO2 (IC50=69.5+5.63 μ Μ) and Glial cells
Chem-5(76.9+5.64μΜ).Wherein HeLa IC50Value is minimum, is 13.3+1.36μΜ.As a result show that Warangalone is selected
The suppression tumour cell of selecting property, and be selective suppression human cervical carcinoma cell.
Table 1Warangalone is to the swollen source oncocyte of different tissues and the inhibitory action of the propagation of normal cell
Embodiment 2Warangalone is to HeLa cell inhibitory effect action effectives
Assessed respectively using mtt assay various concentrations Warangalone (0,5,10,15,20,25,30 μM) to HeLa cells
Act on cell growth status after 12h, 24h, 48h and 72h.As a result as shown in figure 1, growths of the Warangalone to HeLa cells
Inhibitory action is in dose dependent, the IC that effect 12h, 24h, 48h and 72h are acted on HeLa cell inhibitory effects50Value is respectively
37.82 ± 0.42 μM, 20.97 ± 0.55 μM, 17.38 ± 0.44 μM, 13.31 ± 0.26 μM, and Warangalone is thin to HeLa
Born of the same parents' effect 48h compares to be obvious apoptosis phenomenon caused by cell.
Changes of the embodiment 3Warangalone to HeLa cellular morphologies
The HeLa of logarithmic phase is laid in 6 orifice plates, after cell attachment add various concentrations medicine act on respectively 24h and
After 48h, the form of cell is observed under inverted microscope and is taken pictures.As shown in Fig. 2 compared with blank control group cell, with
The increase of Warangalone drug concentrations, HeLa cell is in addition to quantity is reduced with the increase of concentration, and shape is also with concentration
Increase and there occurs significant change.The change in shape of 10 μM of cells of low concentration is not substantially that cell quantity has been reduced；
Most cells form generation changes at 20 μM, and fusiformis and circle are gradually become by rhombus, and adherent ability declines；At 30 μM, carefully
Born of the same parents are mostly rounded, light transmittance increase, gradually come off from wall.As a result the suppression cell of Warangalone conspicuousnesses is shown
Propagation, and change cellular morphology, and in time-dose dependence.
Influences of the embodiment 4Warangalone to HeLa karyomorphisms
Due to the membrane passage increase of apoptosis, therefore it is easier to enter compared to normal cell Hoechst 3342.
Secondly the change binding ability of DNA and dyestuff of apoptotic cell dyeing structure is eager to excel compared with normal cell and is more easy to by Hoechst
3342 dyeing, therefore sapphirine is presented by the stained cells cores of Hoechst 3342 in the cell of apoptosis.Testing result such as Fig. 3 institutes
Show, the Warangalone of various concentrations, which is acted on, to carry out Hoechst 3342 to it after HeLa cells 24h and dye, aobvious with fluorescence
Micro mirror observes the change of HeLa karyomorphisms, as a result shows and gradually subtracts as cell quantity can be observed in the increase of drug concentration
Few, cell karyorrhexis, core are disintegrated and the phenomenon of chromatin pyknosis is all the more obvious, and in dose dependent.
Inhibitory action of the embodiment 5Warangalone to HeLa cell invasions and transfer ability
The invasion and attack of malignant cell and transfer ability it is more stronger than normal cell be one of its important feature, height transfer
Tumour cell there is stronger cell motility.Therefore the medicine of tumor cell invasion and transfer ability can be suppressed by finding
Treatment to tumour has great importance.In order to probe into whether Warangalone has to HeLa cell invasions and transfer ability
Inhibitory action, we assess Warangalone to HeLa cell migration energy by cell scratch experiment and Transwell experiments
The influence of power and invasive ability.In order to exclude be not as medicine act on cause cell-lethal and cause migration with invasive ability under
Warangalone activities are adjusted to 1 μM, 2 μM, 4 μM, using 1 μM of cis-platinum as positive control, at medicine by drop, this experiment
The reason time is 24h.Influences of the Warangalone to HeLa cell by cell invasive abilities is as shown in Fig. 4-A, as medicine is acted on
Concentration increase, the cell quantity through lower room above transwell cells is gradually decreased, and in dose dependent；1μM、2μ
Cell invasion inhibiting rate is respectively 88.33%, 49.48%, 35.59% after M, 4 μM and positive controls processing, and 86.76% such as
Shown in Fig. 4-B.
Scratch experiment result is moved compared with blank with the increase cell of medicine activity to scored area as shown in Figure 5
The ability of shifting gradually weakens, when medicine activity is 2 μM and 4 μM to the inhibitory action of the migration of cell compared with control group
With significant difference, and the inhibitory action and positive controls cis-platinum (1 μM) of medicine activity cell migration when being 1 μM
Quite；As a result show that Warangalone can significantly inhibit the invasion and attack and migration of HeLa cells.
Influences of the embodiment 6Warangalone to the HeLa cell cycles
The cell cycle of mammal can be divided into：G0/G1 phases (DNA pre-synthesis phases), S phases (DNA synthesizes the phase), G2/M phases
(DNA post-synthesis phases and division stage).And study and find that many antineoplastics are to suppress tumour cell by Cycle Arrest
Growth, in order to verify whether Warangalone is also relevant with the retardance of cell cycle to the inhibitory action of HeLa cells.We adopt
Influence with Flow cytometry Warangalone to the HeLa cell cycles.This experiment have detected different pharmaceutical concentration (10
μM, 20 μM, 30 μM) after processing HeLa cells 48h, the influence to its period profile.As a result as shown in Fig. 6-A, with control group phase
Than with the increase of drug concentration, apoptotic peak Sub-G1 is also sharply increased, and low concentration group is 17.23%, and middle concentration group is
36.32%, high concentration group is 58.18%, and statistical analysis is found compared with control group, is respectively provided with statistical significance (P<0.05)
See Fig. 6-B.It is not statistically significant and Warangalone influences little to G0/G1 and G2/M.To sum up result shows,
Mainly by apoptotic pathways, not cell-cycle arrest is acted on inhibitory action of the Warangalone to cervical cancer cell.
Influences of the flow cytometry Warangalone of embodiment 7 to HeLa Apoptosis
Fluorescein FITC marks Annexin V and PI to be combined and is commonly used for distinguishing the early apoptosis detection method withered and withered with evening.
This experiment passes through (10 μM, 20 μM, 30 μM) processing HeLa cells 48h of Flow cytometry various concentrations Warangalone
Afterwards to the influence of Apoptosis.Testing result such as Fig. 7-A, 10 μM, 20 μM and 30 μM of the Warangalone compared with control group
Handle after HeLa cells 48h, apoptosis rate is respectively 6.63%, 22.2%, 31.5%.Statistical analysis find as shown in Fig. 7-B, in
Concentration and high concentration group have significant difference compared with control group.As a result show that Warangalone can induce HeLa cells
Apoptosis, and as the increase of concentration is in dose dependent.
Embodiment 8Warangalone induction HeLa mitochondrial membrane potential in anoxic declines
The decline of mitochondrial membrane potential is usually associated with during apoptosis, under apoptotic stimulus, mitochondrial membrane potential
Dissipation easily activate mitochondrial apoptotic pathway initiate apoptosis cascade reaction.And JC-1 dyeing is detection mitochondrial membrane potential change
Common method.Therefore this experiment have detected various concentrations Warangalone (10 μM, 20 μ by JC-1 staining for flow cell arts
M, 30 μM) act on the influence of change after HeLa cells 24h and 48h to HeLa mitochondrial membrane potential in anoxic.Experimental result is such as
Shown in Fig. 8, control group, 10 μM of low dose group, 20 μM of middle dose group, 30 μM of corresponding greens of high dose group during medicine effect 24h
Fluorescence proportion is respectively 0.50%, 2.31%, 12.99%, 48.72%.Shared by the corresponding green fluorescences of medicine effect 48h
Ratio is respectively 0.96%, 3.80%, 25.17%, 79.71%.Compared with control group, with the increasing of Warangalone concentration
Plus, the ratio shared by green fluorescence also gradually increases, i.e. the dissipation increase of mitochondrial membrane potential.And drug-treated 48h is to line
The dissipation of mitochondrial membrane potential than 24h medicine substantially, illustrates to be in regular hour dependence.As a result show that Warangalone processing is thin
Mitochondrial film potential is destroyed after born of the same parents, and in the mitochondrial membrane potential for reducing HeLa cells of concentration-time depended,
Thus illustrate that the process mitochondria of Warangalone induction HeLa Apoptosis is also assisted in wherein.
Embodiment 9Warangalone promotes the intracellular ROS of HeLa generation
Active oxygen (ROS) plays very important effect in cellular process, be the reason for many diseases occur it
One.Active oxygen is the product of internal aerobic metabolism, mainly including O2 -、NO、H2O2Deng.Research shows that ROS up-regulation is flavonoids
One of the reason for compound inducing apoptosis of tumour cell, ROS can be a variety of apoptosis ways as signaling molecule mediating apoptosis
The common medium in footpath.The change of intracellular ROS levels whether can be caused to carry out mediated cell to probe into Warangalone to wither
Die, we detect the level of ROS in HeLa cells using DCFH-DA fluorescence probes.As a result as shown in Figure 9 with various concentrations
Warangalone handles HeLa cells, is detected from 5 time points, and ROS contents rise compared with control group, and treatment group 0 is arrived
ROS levels are gradually increasing during 60min, are then gradually tended towards stability afterwards.When ROS contents are maximum, i.e. 60min time points different agent
Measure after Warangalone processing HeLa cells, ROS levels increase and raised with medicine activity.As a result show
Warangalone is acted on after HeLa cells, can significantly improve intracellular ROS level.And excessive ROS accumulations can cause cell
Damage, the peroxidating of such as protein, the inactivation of internal enzyme, DNA oxidative damage even results in the apoptosis of cell.
Embodiment 10Warangalone induces HeLa Apoptosis by adjusting Bcl-2 family proteins
Mitochondrial membrane electricity after Warangalone processing HeLa cells is found according to the testing result of JC-1 mitochondrial membrane potentials
Position is in dose-dependently to reduce with Warangalone concentration, therefore speculates that Warangalone mainly passes through mitochondria pathway
To induce HeLa Apoptosis.And Bcl-2 families serve as very important angle in the mitochondria pathway regulation and control of Apoptosis
Color, the change of mitochondrial membrane potential is regulated and controled by the expression of Bcl-2 family proteins.Bcl-2 family proteins include two classes：One class is to promote
Another kind of apoptotic proteins, such as Bad, Bax, BID are anti-apoptotic proteins, such as Bcl-2, Bcl-xl.In Bcl-2 family proteins
Anti-apoptotic proteins are acted on and pro apoptotic protein effect can check and balance, once balance destruction cell will be mediated by mitochondria
Signal path carry out active cell apoptosis.In order to further elucidate the mechanism of Warangalone inducing cell apoptosis, we pass through
After Western bloting detection Warangalone effects 48h, each protein expression situation result of Bcl-2 families shows
After Warangalone function cells, pro apoptotic protein Bad, Bax up-regulated expression；Anti-apoptotic proteins Bcl-2, Bcl-XLTable
Up to also lowering, as shown in Figure 10-A.We also detect the release of cromoci simultaneously, as a result find the release of pigment C in kytoplasm
Amount increases in dose dependent, as shown in figure 10-b.Result above shows Warangalone by regulating and controlling Bcl-2 family proteins
Expression activate injury of mitochondria, promote the release of antiapoptotic factors cromoci, and then induce the apoptosis of HeLa cells.
Embodiment 11Warangalone is by activating caspase family protein induced expression HeLa Apoptosis
Caspase (cysteine-aspartic proteases, caspases) is that a class is deposited
It is protease in cytoplasm.In most cases, the final execution of natural death of cerebral cells will rely on swashing for caspases cascade reactions
It is living.Caspase-8 and caspase-9 are the initiators of Apoptosis, and they, which distinguish mediated death recipient cell apoptotic signal, leads to
Road and mitochondrial apoptosis signal path, and caspase-3 is the final executor of Apoptosis in caspase family proteins.In order to
Checking Warangalone whether have activated caspase-3, caspase-8 and caspase-9, we using Fluorometric assay its
After activity, the Warangalone processing HeLa cells Warangalone of various concentrations, caspase Activation such as Figure 11 institutes
Show, the activity and Warangalone concentration for as a result showing caspase-3, caspase-8 and caspase-9 are in dose dependent.
Concentration is caspase-3, caspase-8 after 10 μ Μ Warangalone processing cells, and caspase-9 activity is without significantly change
Change, when concentration for the treatment of is 20 μ Μ and 30 μ Μ, caspase-3 and caspase-9 level of activity is significantly carried compared with control group
Height, but caspase-8 only has conspicuousness raising in 30 μ Μ.Further demonstrate that Warangalone mainly passes through mitochondria
The endogenous pathway of mediation induces HeLa Apoptosis.
PARP full name polyadenylic acid diphosphonic acid phosphoribosynltransferases, are a kind of DNA albumen repair enzymes, be Apoptosis core into
Member's topmost cutting substrates of caspase-3, play an important role in apoptotic process.Cell at Warangalone
After HeLa cells 48h, there is obvious PARP cutting rods band (89kDa) in drug-treated group, and with Warangalone concentration
Increase PARP cutting degree also gradually increase, as shown in Figure 12-A.As a result show Warangalone induction of intracellular
PARP is cut, and then promotes Apoptosis.Mainly lured to further prove Warangalone by mitochondria pathway
Guided cell apoptosis, we further have detected caspase-3, caspase-8 and caspase-9 by Western bloting
Expression quantity, as a result show that caspase-3 and caspase-9 expression quantity are on a declining curve, and Caspase-8 change without significantly
Sex differernce；Image statistical analyses, using β-actin protein expressions gray values as standard, calculate Caspase-3 protein expressions with
The relative quantity of control group is as shown in Figure 12-B.As the increase of Warangalone concentration is in dose-dependently to reduce
Caspase-3, caspase-9 expression quantity, and because the expression quantity of caspase-8 after dosing changes without conspicuousness, explanation
Warangalone is mainly the endogenous apoptotic signal path mediated by mitochondria come inducing cell apoptosis.
Embodiment 12Warangalone induction HeLa cells p53 phosphorylation, have activated MAPK signal paths
The endogenous apoptosis that the external source apoptosis pathway mitochondria that apoptosis pathway mainly has death receptor to mediate is mediated
Approach, but any apoptosis pathway all regulated and controled by p53, and it is activated and DNA oxidative damage is closely related.By above
Western bloting experimental results find that Bcl-2 family proteins change after Warangalone effects, and Bcl-2 family
The expression of race's albumen is regulated and controled by p53.We have found that Warangalone is acted in the experiment detected according to above ROS levels again
In ROS being caused to produce after HeLa cells.Research shows ROS generation, can activate the phosphorylation of p53 albumen, and p53
Activation can further activate the signaling pathway protein in downstream, including mitochondria family protein and death receptor family etc..AKT
Have confirmed that and played an important role in Apoptosis and drug resistance with ERK, ERK is capable of the Proliferation, Differentiation of regulating cell and turned
Move etc., suppress the generation of Apoptosis by activating anti-apoptotic proteins and suppressing caspase activation, Akt similar to ERK leads to
Suppression pro apoptotic protein such as p53, Bad etc. expression is crossed to promote Apoptosis.Exist with ERK and Akt on the contrary, MAPK family proteins
Under environmental stimuli effect, by promoting JNK, p38 phosphorylation promotes Apoptosis.
Therefore we have detected p53, and MAPK the and AKT signal path phases that p53 is mediated by Western bloting
Close the activation situation of albumen.As a result as shown in figure 13, various concentrations Warangalone processing HeLa cells are on dose dependent
ERK phosphorylation level is inhibited, while p38 and p53 phosphorylation can be promoted, and total ERK and p38 expression quantity are basic
It is constant, but AKT and JNK expression quantity are not made significant difference.As a result show that Warangalone may be by activating p53 mediations
MAPK signal paths induce cervical cancer cell HeLa Apoptosis.
Claims (2)
1. climb application of the trifoliate jewelvine isoflavones in prevention and/or treatment uterine neck cancer drug is prepared, it is characterised in that the climbing
The structural formula of trifoliate jewelvine isoflavones is as follows：
。
2. application according to claim 1, it is characterised in that the medicine includes pharmaceutically acceptable salt or carrier.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
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| CN110283182A (en) * | 2019-04-22 | 2019-09-27 | 暨南大学 | A kind of preparation method of isoflavone compound |
| CN115819432A (en) * | 2022-11-16 | 2023-03-21 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
-
2017
- 2017-06-22 CN CN201710482745.XA patent/CN107233338A/en active Pending
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| CHOKCHAICHAMNANKIT D: "Prenylated Flavonoids from the Leaves of Derris malaccensis and their Cytotoxicity", 《NATURAL PRODUCT COMMUNICATIONS》 * |
| CHUNG SH等: "Prevention and treatment of cervical cancer in mice using estrogen receptor antagonists", 《PNAS》 * |
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Cited By (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110283182A (en) * | 2019-04-22 | 2019-09-27 | 暨南大学 | A kind of preparation method of isoflavone compound |
| CN115819432A (en) * | 2022-11-16 | 2023-03-21 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
| CN115819432B (en) * | 2022-11-16 | 2024-02-23 | 成都市华大基因医学研究院有限公司 | Compound and medicine for treating cervical cancer |
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