CN105687182A - Anti-tumor application of ventilago leiocarpa extract - Google Patents
Anti-tumor application of ventilago leiocarpa extract Download PDFInfo
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Abstract
The invention discloses application of a ventilago leiocarpa extract in preparing an anti-tumor drug. The pharmacodynamic experiment shows that the ventilago leiocarpa extract can remarkably inhibit human liver cancer HepG2 cell proliferation in vitro, is dose-dependent, and has an IC50 value as 124.77mu mol.L-1 acted on an HepG2 cell for 24h. The HE staining, acridine orange staining and flow cytometry result shows that the ventilago leiocarpa extract can induce cell apoptosis and can enable a cell cycle to retard at a G2/M period. The immunofluorescence method detection finds that the ventilago leiocarpa extract can cause the depolymerization of cytoskeletal protein F-actin, so that the ventilago leiocarpa extract has better anti-tumor effect, can be used for developing the anti-tumor drug, and has a wide application prospect.
Description
Technical field
The present invention relates to the application of medicine, particularly relate to the antitumor application of ventilagin。
Background technology
Ventilago leiocarpa, [Classification system] VentilagoleiocarpaBenth, is Rhamnaceae plant, and [another name] Radix seu Caulis Verntilaginis Leiocarpae, Radix seu Caulis Verntilaginis Leiocarpae, Ophiorriza succirubra, blue veins rattan, car pusher enter stone, draw cattle to enter stone, originates from domestic Taiwan, Fujian, Guangdong, Guangxi, Hunan, Yunnan；Also there are distribution in India, Burma, Vietnam；It is born under less than 1500 meters sparse woods of height above sea level or in shrubbery or under intermountain limes marginis or sparse woods。Anemia, the multiple disease such as rheumatic arthritis and lumbar muscle strain are treated in Guangxi radical cure among the people。Ventilago plant contains abundant quinones, thus causes the interest of vegetalization scholar。Answer hundred equalitys once to report this kind of plant root produced from Hainan Island and get rheum emodin, rheum emodin-6,8-dimethyl ether, 1-hydroxyl-6,7,8-trimethoxy-3-tectoquinones, ventiloquinone and lupeol。Seven crystallised components got by the ethanol extraction producing ventilago leiocarpa root from Guangxi, according to physicochemical property and spectroscopic data, be identified respectively as physcion, rheum emodin, 1,2,4,8-tetrahydroxy-3-tectoquinone, ventiloquinone-I and a new naphthoquinone compound, called after ventilagin (Ventilagolin, 5)。
Tumor (tumour) refers to that body is under various tumorigenesis factor effects, some cell of local organization loses the normal regulation to its growth on gene level, the neoplasm causing its clonal abnormality hypertrophy and formed, because this neoplasm is many in occupancy block-like protrusions, also referred to as vegetation (neoplasm)。It is generally believed that tumor cell is monoclonicity, namely all oncocytes in a tumor are all the offsprings of the cell of a sudden change。The form that the naked eyes of tumor see form naked eyes sight tumor is varied, and can reflect the good pernicious of tumor to a certain extent。Tumor is generally divided into optimum and pernicious two big classes by educational circles。
Benign tumor poor growth, in expansive growth, often there is complete peplos on surface, less General Symptoms except local symptom, tissue infiltration does not shift to whole body yet towards periphery, not easily recurs after excision, body harm is less, such as lipoma, hemangioma, adenoma, cyst etc.。
Malignant growth is rapid, growth tissue infiltration towards periphery often, surface is several without peplos, often has whole body to shift, the visible atypical karyokinesis of pathologic finding, except local symptom, General Symptoms is obvious, and cachexia occur more in end-stage patients, and after excision, relapse rate is high, body harm is big, such as osteocarcinoma, the esophageal carcinoma, hepatocarcinoma, pulmonary carcinoma, leukemia, osteosarcoma etc.。Deschampsia caespitosa katydid's disease rate of malignant tumor has the trend raised year by year, also accounts for former position, thus be a kind of disease of keypoint control in the cause of death of various diseases。
Benign tumor also can be changed into pernicious sometimes, is called benign tumor malignant change, as fibroma can be transformed into fibrosarcoma。Some disease is easily changed into malignant tumor, as atrophic gastritis can develop into gastric cancer；Junctional nevus can develop into malignant melanoma, and these diseases are called disease or precancerous lesion before cancer。
Malignant tumor is the commonly encountered diseases that a class serious harm human life is healthy, and the conventional means treating malignant tumor at present is operative treatment, chemotherapy, radiotherapy and biologic treatment etc.。But most of patients has been enter into late period time medical, is not suitable for excision, and the late result of chemicotherapy is also all poor。Seek active and effective prevention by way of and effective medicine seem very urgent and necessary。
There is presently no document and be disclosed the antitumor application of ventilagin。
Summary of the invention
It is an object of the invention to provide the application of the antitumor of ventilagin, ventilagin antitumor can in the application in preparing antitumor drug。
For reaching above-mentioned purpose, the technical solution used in the present invention is:
Ventilagin application in preparing antitumor drug。
Described antitumor drug is medicines resistant to liver cancer。
Described antitumor drug is the medicine that human hepatoma HepG2 cell can be suppressed to breed。
Described antitumor drug is for can induce the apoptotic medicine of HepG2。
Described antitumor drug is can by the cell cycle arrest medicine in the G2/M phase。
Described antitumor drug is the medicine that cytoskeletal protein F-actin depolymerization can be caused to rupture。
The pharmacodynamics test of the present invention shows, after ventilagin effect 24h, MTT result shows, ventilagin is at 50～200umol L-1In concentration range, the propagation of HepG2 cell there is is inhibitory action, and along with the increase of drug level, the inhibitory action of cell is strengthened gradually, presents dose dependent。Ventilagin acts on the IC of HepG2 cell 24h50Value is 124.77umol L-1。
The pharmacodynamics test of the present invention shows, cell is observed after HE dyes, and the normal HepG2 cell cultivated is fusiformis, and cell space is big, and endochylema enriches, common karyokinesis picture。After ventilagin effect, HepG2 cell number significantly reduces, cell shrinkage spindle, and endochylema reduces, it is seen that substantially vacuolation, the dense dye of karyopyknosis, it is seen that apoptotic body。
The pharmacodynamics test of the present invention shows, observes after Acridine Orange Staining, and the normal HepG2 cell film cultivated is completely smooth, and karyomorphism is full, in uniform green, dyes shallower。After ventilagin effect, HepG2 cell quantity reduces, and after birth shrinkage, nucleus volume diminishes relatively, chromatin concentration, and fluorescence is remarkably reinforced, it is seen that the apoptosis features such as apoptotic body。
The pharmacodynamics test of the present invention shows, AnnexinVFITC PI flow cytomery result shows, along with the increase of ventilagin concentration, apoptosis rate increases, group difference statistically significant (P < 0.01)。HepG2 cell is had apoptosis-induced effect by prompting ventilagin, and in dose dependent。
The pharmacodynamics test of the present invention shows, after ventilagin effect HepG2 cell, flow cytomery finds that each phase of cell cycle is variant, and main manifestations is that G2/M cell proportion increases, and G0/G1 phase cell proportion reduces, and group difference is statistically significant。Prompting ventilagin can by HepG2 cell block in the fissional G2/M phase, thus suppressing the division growth of cell。
The pharmacodynamics test of the present invention shows, Actingreen488 can be specific binding with intracellular filamentous actin F-actin, is green fluorescence with FITC coupling, is mainly distributed in cell membrane and Cytoplasm。Observing under laser confocal scanning microscope, blank group HepG2 cytochrome oxidase isozymes is good, in irregular shape, it is seen that a large amount of burr pseudopodium, in Cytoplasm, F-actin fibrin is strip filament shape, and structural integrity, queueing discipline, green fluorescence is stronger。After ventilagin effect, cell size, burr pseudopodium reduces, F-actin fibrin in kytoplasm significantly reduces, and filament ruptures, arrangement disorder, endochylema is substantially vacuolation change as seen, and damaged F-actin fibrous fracture end is heaped-up, and green fluorescence power is uneven。
Compared with prior art, the method have the advantages that
1, the ventilagin of the present invention is one of bioactive ingredients of ventilago leiocarpa, draws materials conveniently, pure natural。
2, by the pharmacodynamics test of the present invention, it was demonstrated that ventilagin can substantially suppress the propagation of human hepatoma HepG2 cell, in dose dependent, acts on the IC of HepG2 cell 24h50Value is 124.77umol L-1。HE dyeing, Acridine orange and flow cytometry results show, ventilagin can inducing cell apoptosis, can by cell cycle arrest in the G2/M phase。Immuno-fluorescence assay finds, ventilagin can cause cytoskeletal protein F-actin depolymerization to rupture, and therefore ventilagin has good antitumor action, can be used for developing anti-tumor medicaments, have a extensive future。
3, the present invention is using ventilagin as antitumor drug, can liver function protecting to greatest extent, recover liver function, reduce complication to greatest extent, health will not be produced any toxic and side effects, conventional means operative treatment than traditional treatment malignant tumor, chemotherapy is well a lot, operative treatment for be generally tumor early stage and mid-term, but most of patients has been enter into late period time medical, it is not suitable for excision, and for example chemotherapy of tumours is while killing tumor cell, also normal cell and immunocyte are together killed, the health of patient is caused great injury。
Accompanying drawing explanation
Fig. 1 variable concentrations ventilagin inhibitory action (n=4, ± S) to HepG2 cell；
The impact (HE × 100, blank group) on HepG2 cellular morphology of Fig. 2 ventilagin；
Fig. 3 ventilagin impact (HE × 100, ventilagin 100umolL on HepG2 cellular morphology-1)；
Fig. 4 ventilagin impact (HE × 100, ventilagin 120umolL on HepG2 cellular morphology-1)；
The impact (acridine orange × 100, blank group) on HepG2 cellular morphology of Fig. 5 ventilagin；
Fig. 6 ventilagin impact (acridine orange × 100, ventilagin 100umolL on HepG2 cellular morphology-1)；
Fig. 7 ventilagin impact (acridine orange × 100, ventilagin 120umolL on HepG2 cellular morphology-1)；
Fig. 8 ventilagin induction apoptotic effect of HepG2 (blank group)；
Fig. 9 ventilagin induction HepG2 apoptotic effect (ventilagin 80umolL-1)；
Figure 10 ventilagin induction HepG2 apoptotic effect (ventilagin 120umolL-1)；
Figure 11 ventilagin induction HepG2 apoptotic effect (ventilagin 180umolL-1)；
The effect (blank group) of Figure 12 ventilagin retardance HepG2 cell cycle；
Effect (the ventilagin 80umolL of Figure 13 ventilagin retardance HepG2 cell cycle-1)；
Effect (the ventilagin 120umolL of Figure 14 ventilagin retardance HepG2 cell cycle-1)；
Effect (the ventilagin 180umolL of Figure 15 ventilagin retardance HepG2 cell cycle-1)；
The impact (blank group) on HepG2 cytoskeletal protein F-actin of Figure 16 ventilagin；
Figure 17 ventilagin impact (ventilagin 120umolL on HepG2 cytoskeletal protein F-actin-1)；
Figure 18 ventilagin impact (ventilagin 180umolL-on HepG2 cytoskeletal protein F-actin1)。
Detailed description of the invention
Embodiment 1
Ventilagin provided by the invention, by Guangxi traditional Chinese medicine the separated acquisition of academy's chemistry, aubergine acicular crystal, is dissolved into 10umol mL with DMSO-1Storing solution, filtration sterilization, dilute by DMEM culture medium during experiment。
Below in conjunction with concrete pharmacodynamic experiment, provided by the invention ventilagin antineoplastic effect is expanded on further。
Material
1.1 cell strains
HepG2 cell lines, is purchased from the refined medical college cell bank in Hunan。
Medicine and reagent
Ventilagin, by Guangxi traditional Chinese medicine the separated acquisition of academy's chemistry, aubergine acicular crystal, is dissolved into 10umol mL with DMSO-1Storing solution, filtration sterilization, dilute by DMEM culture medium during experiment；DMEM high glucose medium, doctor moral company；Hyclone, dimethyl sulfoxide (DMSO), Giobco company；Methyl thiazoly tetrazolium assay (MTT), biotopped company；HE staining kit, Acridine orange test kit, green skies biotechnology research institute；AnnexinVFITC PI cell apoptosis detection kit, life company；Cell cycle detection kit, Lian Ke company；4% paraformaldehyde, TritonX-100, Chengdu Ke Long chemical reagent factory；ActinGreen488Reddyprobesreagent dye liquor, DAPI dye liquor, life company；Anti-fluorescent quenching mountant, green skies biotechnology research institute。
Instrument
CO2 gas incubator, Thermo, the U.S.；The long microplate reader of all-wave, Thermo, the U.S.；EVOSFLAuto fluorescence microscope, Life, the U.S.；Flow cytometer, BD, the U.S.；High speed room temperature centrifuge, Eppendorf, Germany；Laser confocal scanning microscope, NikonA1, Japan。
Method
1.2.1HepG2 the cultivation of cell
Cell is in 37 DEG C, 5%CO2In incubator, with the DMEM high glucose medium conventional single layer Secondary Culture in culture bottle containing 10% hyclone, the cell of trophophase of taking the logarithm is tested。
Method detection cell proliferation inhibition rate
Cell dissociation counts, every hole 105Individual cell is inoculated in 96 orifice plates, adherent growth 24h。Each group adds the ventilagin of variable concentrations: 200,150,100,50umol L-1, parallel 4 holes of each concentration, blank group adds isopyknic DMEM culture medium, and solvent control group adds the DMSO solution of respective concentration, acts on 24h。Every hole adds 20ulMTT(5g L-1) solution, incubator is hatched 4h, abandon supernatant, every hole adds 100ulDMSO, shakes dissolving crystallized gently, microplate reader 490nm place detection absorbance OD value, inhibitory rate of cell growth (IR), cell survival rate is obtained by following equation, adopt cell survival rate that drug dose logarithm is mapped, through curve matching, obtain half-inhibition concentration (IC by graphing method50)。
Cell survival rate=experimental group OD value/matched group OD value × 100%
Proliferation inhibition rate=1-(experimental group OD value/matched group OD value) × 100%
1.2.3HE, Acridine orange observation of cell form
Overnight, distilled water rinses, and 75% soak with ethanol 6h volatilizes standby in coverslip bubble acid。The cell dissociation counting of exponential phase, every hole 5 × 105Individual cell is inoculated in 6 orifice plates of the coverslip after being placed with process, adherent growth 24h。Add the ventilagin effect 24h of variable concentrations。
HE dyes: abandoning supernatant, 95% ethanol fixes 20min, PBS 2 times。Taking out coverslip, put down gently on microscope slide, haematoxylin dyeing 5min, dye liquor, eosin stains 2min are washed in bath off, and dye liquor, glycerol mounting are washed in bath off, and microscope is observed。
Acridine orange: abandon supernatant, 20min fixed by 95% ethanol, takes out coverslip, puts down gently on microscope slide, 1% acetic acid effect 30s, and 0.02% Acridine orange 1min adds CaCl2Effect 2min, PBS rinsing, removes residual dye liquor, glycerol mounting, fluorescence microscope。
Flow cytometry (FCM) detects apoptosis rate
The cell dissociation counting of exponential phase, every hole 106Individual cell is inoculated in 6 orifice plates, adherent growth 24h。Add the ventilagin effect 24h of variable concentrations。Collect supernatant and cell, 1000rpm min-1Centrifugal 5min, removes culture medium, washs with PBS, is resuspended in 100ulloadingbuffer by cell, and making cell concentration is 106Individual/mL。Adding 5ulAnnexinV-FITC and 1ulPI dye liquor in cell suspension, mix gently, lucifuge hatches 15min, add 400ulloadingbuffer mixing, sieve, the cell suspension prepared is proceeded in 12mm × 75mm test tube (FALCON), flow cytomery apoptosis rate。The fluorescence compensation group that apoptosis induction stimulates is set simultaneously: 1, only add 5ulAnnexinV-FITC；2,1ulPI is only added；3, it is not added with any dyestuff, only adds the loadingbuffer of 500ul。
Flow cytometry (FCM) detects cell cycle
The cell dissociation counting of exponential phase, every hole 106Individual cell is inoculated in 6 orifice plates, adherent growth 24h。Add the ventilagin effect 24h of variable concentrations。Collect cell, 1300rpm min-1Centrifugal 5min, abandons supernatant, adds the resuspended washed cell of 1mLPBS, 1300rpm min-1Centrifugal 5min, abandons supernatant, repeated washing 1 time, abandons supernatant, be slowly added to 75% ethanol of pre-cooling, fixes overnight for 4 DEG C。1300rpm min-1Centrifugal 15min discards fixative, adds 1mLPBS and washs 1 time, 1300rpm min-1Centrifugal 20min, abandons supernatant, stays 100ulPBS re-suspended cell, adds 10ulRNasA enzyme (10mg ml-1), 37 DEG C of water-bath 30min, add 300ulPI dyeing, 4 DEG C of dye core 30min, sieve, flow cytomery cell cycle。
Immuno-fluorescence assay cytoskeletal protein
The cell dissociation counting of exponential phase, by 106Individual cell is inoculated in copolymerization Jiao's special culture dish, adherent growth 24h。Add the ventilagin effect 24h of variable concentrations。Culture dish is taken out from incubator, 4% paraformaldehyde fixes 20min, PBS, and 0.2%TritonX-100 changes 15min thoroughly, PBS, confining liquid closes 30min, PBS, hatches 30min for ActinGreen488Reddyprobesreagent20-25 DEG C, PBS remnants dye liquor, DAPI lucifuge hatches 5min, PBS, anti-fluorescent quenching mountant mounting。Laser confocal scanning microscope adopts perfect focusing system dynamic bidirectional scan pattern, and selective exitation wavelength 488nm launches wavelength 530nm, laser power 9.0mW, takes the photograph figure when Photomultiplier tube voltage 110V。
Result
2.1 ventilagin are to HepG2 cell inhibitory effect effect
After medicine effect 24h, MTT result shows, ventilagin is at 50～200umol L-1In concentration range, the propagation of HepG2 cell there is is inhibitory action, and along with the increase of drug level, the inhibitory action of cell is strengthened gradually, presents dose dependent, see accompanying drawing 1。Ventilagin acts on the IC of HepG2 cell 24h50Value is 124.77umol L-1。
The ventilagin impact on HepG2 morphocytology
Cell is observed after HE dyes, and the normal HepG2 cell cultivated is fusiformis, and cell space is big, and endochylema enriches, common karyokinesis picture。After ventilagin effect, HepG2 cell number significantly reduces, cell shrinkage spindle, and endochylema reduces, it is seen that substantially vacuolation, the dense dye of karyopyknosis, it is seen that apoptotic body。See accompanying drawing 2-accompanying drawing 4。
Observing after Acridine Orange Staining, the normal HepG2 cell film cultivated is completely smooth, and karyomorphism is full, in uniform green, dyes shallower。After ventilagin effect, HepG2 cell quantity reduces, and after birth shrinkage, nucleus volume diminishes relatively, chromatin concentration, and fluorescence is remarkably reinforced, it is seen that the apoptosis features such as apoptotic body。See accompanying drawing 5-accompanying drawing 7。
The ventilagin impact on HepG2 apoptosis rate
AnnexinVFITC PI flow cytomery result shows, along with the increase of ventilagin concentration, apoptosis rate increases, and group difference statistically significant (P < 0.01), in Table 1, accompanying drawing 8-accompanying drawing 11。HepG2 cell is had apoptosis-induced effect by prompting ventilagin, and in dose dependent。
The ventilagin impact on HepG2 cell cycle
After ventilagin effect HepG2 cell, flow cytomery finds that each phase of cell cycle is variant, and main manifestations is G2/ M cell proportion increases, G0/G1Phase cell proportion reduces, and group difference is statistically significant, in Table 2, accompanying drawing 12-accompanying drawing 15。Prompting ventilagin can by HepG2 cell block in fissional G2/ M the phase, thus suppressing the division growth of cell。
The ventilagin impact on HepG2 cytoskeletal protein F-actin
Actingreen488 can be specific binding with intracellular filamentous actin F-actin, is green fluorescence with FITC coupling, is mainly distributed in cell membrane and Cytoplasm。Observing under laser confocal scanning microscope, blank group HepG2 cytochrome oxidase isozymes is good, in irregular shape, it is seen that a large amount of burr pseudopodium, in Cytoplasm, F-actin fibrin is strip filament shape, and structural integrity, queueing discipline, green fluorescence is stronger。After ventilagin effect, cell size, burr pseudopodium reduces, F-actin fibrin in kytoplasm significantly reduces, and filament ruptures, arrangement disorder, endochylema is substantially vacuolation change as seen, and damaged F-actin fibrous fracture end is heaped-up, and green fluorescence power is uneven。See accompanying drawing 16-accompanying drawing 18。
Result
Ventilagin can substantially suppress the propagation of human hepatoma HepG2 cell, in dose dependent, acts on the IC of HepG2 cell 24h50Value is 124.77umol L-1。HE dyeing, Acridine orange and flow cytometry results show, ventilagin can inducing cell apoptosis, can by cell cycle arrest in the G2/M phase。Immuno-fluorescence assay finds, ventilagin can cause cytoskeletal protein F-actin depolymerization to rupture。
Conclusion
The external propagation that can effectively suppress HepG2 cell of ventilagin, its mechanism is likely to and cell cycle arrest, inducing cell apoptosis, and cytoskeletal protein F-actin fracture is relevant。
By above-mentioned pharmacodynamics test, it is achieved that technical scheme:
Ventilagin application in preparing antitumor drug。
Described antitumor drug is medicines resistant to liver cancer。
Described antitumor drug is the medicine that human hepatoma HepG2 cell can be suppressed to breed。
Described antitumor drug is for can induce the apoptotic medicine of HepG2。
Described antitumor drug is can by the cell cycle arrest medicine in the G2/M phase。
Described antitumor drug is the medicine that cytoskeletal protein F-actin depolymerization can be caused to rupture。
Claims (6)
1. ventilagin application in preparing antitumor drug。
2. application according to claim 1, it is characterised in that: described antitumor drug is medicines resistant to liver cancer。
3. application according to claim 2, it is characterised in that: described antitumor drug is the medicine that human hepatoma HepG2 cell can be suppressed to breed。
4. application according to claim 2, it is characterised in that: described antitumor drug is for can induce the apoptotic medicine of HepG2。
5. application according to claim 2, it is characterised in that: described antitumor drug is can by the cell cycle arrest medicine in the G2/M phase。
6. the application according to claim or 2, it is characterised in that: described antitumor drug is the medicine that cytoskeletal protein F-actin depolymerization can be caused to rupture。
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| CN113456625A (en) * | 2021-07-29 | 2021-10-01 | 广西壮族自治区中医药研究院 | Application of pterocarpin in inhibiting Pim-1 expression |
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Non-Patent Citations (2)
| Title |
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| DO NASCIMENTO等: "Bioactive extracts and chemical constituents of two endophytic strains of Fusarium oxysporum", 《REVISTA BRASILEIRA DE FARMACOGNOSIA BRAZILIAN JOURNAL OF PHARMACOGNOSY》 * |
| 陆阳: "《醌类化学》", 30 April 2009, 化学工业出版社 * |
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| Publication number | Priority date | Publication date | Assignee | Title |
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| CN113456625A (en) * | 2021-07-29 | 2021-10-01 | 广西壮族自治区中医药研究院 | Application of pterocarpin in inhibiting Pim-1 expression |
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