CN107929308A - Application of the panax japonicus polysaccharides in prevention and/or treatment liver-cancer medicine is prepared - Google Patents
Application of the panax japonicus polysaccharides in prevention and/or treatment liver-cancer medicine is prepared Download PDFInfo
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Abstract
The invention belongs to the medical usage technical field of plant polyose, specifically discloses a kind of application of panax japonicus polysaccharides in prevention and/or treatment liver-cancer medicine is prepared.The application has found PSPJ first（30‑100 mg/kg）There is significant inhibition to the tumor growth of the tumour cell of Murine Hepatoma22 tumor-bearing mice（Tumour inhibiting rate is respectively 41.7% and 54.3%）.Also, PSPJ is to the general physical condition, routine blood indexes, Liver and kidney function of Murine Hepatoma22 tumor-bearing mice without obvious toxic action.The application also found that PSPJ has the acute liver damage of LPS/D GalN inducing mouses clearly prevention and protective effect; its mechanism of action is probably PSPJ by suppressing the generation of response to oxidative stress and inflammatory reaction; so as to prevent and prevent hepatic injury; improve the function of damaged liver, the possibility for finally preventing hepatic injury from being converted to liver cancer.
Description
Technical field
The present invention relates to the medical usage technical field of plant polyose, and in particular to a kind of panax japonicus polysaccharides are preparing prevention
And/or the application in treatment liver-cancer medicine.
Background technology
Liver cancer is a kind of malignant tumour for seriously endangering human health, its incidence is high and lethality remains high.Liver cancer
Pathogenic factor is extremely complex, wherein, the missing of chronic persistent inflammation and tumor suppressor gene is an important factor for causing liver cancer to occur.
At present, most tumor suppressor gene regulation and control hepatoma cell proliferations, the mechanism of apoptosis have been studied clear.In view of some tumor suppressor genes exist
It can also be expressed in immunocyte, have the scorching suppression cancer dual-use function of suppression concurrently in immunocyte and tumour cell, and then exempt from by targeting
Common signaling molecule in epidemic disease cell and tumour cell, plays the generation for efficiently blocking scorching canceration (particularly inflammation associated hepatocellular carcinoma)
Development is the main Research Thinking of the application.Therefore, the application mainly studies panax japonicus polysaccharides and is made by anti-inflammatory and immune activation
For suppressing hepatocellular carcinoma, for panax japonicus polysaccharides as immunologic adjuvant treatment malignant disease clinical practice provides theory according to
According to.
In the prior art there is not yet relevant report, the application will fill up this blank.
The content of the invention
For the deficiencies in the prior art, it is an object of the invention to provide a kind of panax japonicus polysaccharides to prepare prevention
And/or the application in treatment liver-cancer medicine.
Compared with prior art, the present invention has the following advantages and effects：
1st, this method prepares that panax japonicus polysaccharides (PSPJ) simple process is easy, and controllability is strong.
2nd, the panax japonicus polysaccharides purity that this method obtains is high, and yield is higher.
3rd, the application has found that PSPJ has dose dependent prevention to the LPS/D-GalN acute livers induced first
With protective effect.Mechanism of action is probably the generation for suppressing response to oxidative stress and inflammatory reaction, prevents and prevents hepatic injury,
Improve the function of damaged liver, it is final to prevent conversion of the inflammation to liver cancer.
4th, the application has found internal lifes of the PSPJ (30-100mg/kg) to the tumour cell of Murine Hepatoma22 tumor-bearing mice first
The long general body with significant inhibition (tumour inhibiting rate is respectively 41.7% and 54.3%) while PSPJ to H22 tumor-bearing mices
Matter situation, routine blood indexes, Liver and kidney function are without obvious toxic action.
Brief description of the drawings
Fig. 1 is Sephadex G-75 pillar layer separation panax japonicus Thick many candies elution curves in embodiment 1.
Fig. 2 is the panax japonicus polysaccharides HPLC figures after pillar layer separation in embodiment 1.
Chromatographic condition：Chromatographic column is Shodex OHpak SB-804 HQ (8 × 300mm), shows poor photodetector, 0.1M
NaCl is mobile phase, flow velocity 0.5mL/min, 35 DEG C of column temperature, 20 μ L of sample size.
Fig. 3 is the survivorship curve figure that panax japonicus polysaccharides influence acute hepatic injury mice.
Fig. 4 panax japonicus polysaccharides are to mouse liver injury morphology and changes in histopathology.
Embodiment
Applicant in conjunction with specific embodiments will be described in further detail technical scheme below.Ying Li
Solution, herein below should not be construed as in any way the limitation for claims of the present invention being claimed scope.
Embodiment 1
The preparation of panax japonicus polysaccharides：
Raw material panax japonicus medicinal material is the dry of araliaceae ginseng plant panax japonicus (Panax japonicus C.A.Mey.)
Dry rhizome, plants panax japonicus for family, originates from Enshitujianationalitymiaonationality Autonomous Prefecture Xuanen County Chun Muying townshiies mud dam.
Step is as follows：
Dry panax japonicus medicinal powder is taken, adding 95% ethanol, (V/V, the percentage of ethanol described in this specification are dense
Degree refers both to concentration of volume percent, does not repeat hereinafter), flow back 3h at 60 DEG C, degreasing；
80% ethanol is added, flow back 2h at 60 DEG C, takes off monose and oligosaccharide；
The dregs of a decoction are placed in baking oven after drying, are extracted 3 times by the use of purified water as solvent refluxing, each 2h, merging filtrate is simultaneously
It is placed in Rotary Evaporators and is concentrated into liquid extract state, add ethanol, it is 80% to adjust concentration of alcohol, and 4 DEG C overnight, next day mistake
Filter, precipitation drying, up to panax japonicus crude product；
Gained panax japonicus crude product is taken, adds (60 DEG C) of appropriate warm water to dissolve,, will after the 48h that dialyses in flowing water after removing protein
Dialyzate vacuum freezedrying, up to panax japonicus Thick many candies.
By panax japonicus Thick many candies after DEAE-Sepharose FF column purifications 3 times；Again through Sephadex G-75 post separations
Purifying, obtains a main peak, will be dry after peak position eluent dialysis desalination, obtains panax japonicus polysaccharides, abbreviation PSPJ, related data
It is shown in Table 1.1.
Table 1.1
After testing, gained panax japonicus polysaccharides are mainly by glucose, galacturonic acid, galactolipin, glucuronic acid, sandlwood
Sugar, arabinose, xylose etc. form, its mass fraction is as shown in table 1.2.
Each monosaccharide component mass fraction table in 1.2 panax japonicus polysaccharides of table
Panax japonicus Thick many candies are after DEAE-Sepharose FF and Sephadex G-75 pillar layer separations, and elution curve is such as
Shown in Fig. 1.Further, confirm that panax japonicus polysaccharides after purification are homogeneity polysaccharide using HPLC chromatogram technology, see Fig. 2.
Embodiment 2
The anti-H22 liver cancer cells activity of panax japonicus polysaccharides and general toxicity research prepared by embodiment 1
2.1 experiment material
2.1.1 animal and cell line
Kunming mouse：Half male and half female, 18~22g of weight, is provided by Disease Prevention Control Center, Hubei Prov, credit number
For：SCXK (Hubei Province)：2008-0003.
H22 cell lines are given by the old trip's wing teacher of pharmaceutical college of South-Center University For Nationalities, are stored in -80 DEG C of refrigerator.Recovery
When centrifuge, the DMSO in frozen stock solution is removed, with normal saline dilution into 1*106A/mL, mouse abdomen is inoculated in by every 0.2mL
Intracavitary, is passed on after seven days, takes third generation H22 ascites tumor mouse ascites, and 1 is pressed with physiological saline:10 dilutions, every 0.2mL inoculation
It is subcutaneous in mouse right fore armpit, establish H22 solid tumor models.
2.1.2 experiment reagent
Panax japonicus polysaccharides：Embodiment 1 is prepared；
Sodium chloride injection：Binghu Shuanghe Pharmaceutical Co., Ltd., Wuhan, lot number：20150927.
Heparin sodium：BIOSHARP bio tech ltd, lot number 201609；
Ethylenediamine tetra-acetic acid (EDTA):Sinopharm Chemical Reagent Co., Ltd., lot number：F20100108；
5 FU 5 fluorouracil (5-FU):Shanghai crystalline substance pure reagent Co., Ltd, lot number：20141108.
2.2 experimental method
2.2.1 the foundation of solid tumor models and medication
Kunming mice 60 is taken, establishes H22 solid tumor models.Weigh after after 2 three days, random packet, every group of 12 (male and female
It is fifty-fifty).If normal group (Non-tumor), model group (Saline), positive controls (5-FU 10mg/kg) and panax japonicus polysaccharides
Administration group (30,100mg/kg).Normal group and model group are same as above to physiological saline, administering mode.Fasting can't help after the last administration
More than when water 12 is small, mouse is put to death using cervical dislocation method, oxter solid tumor is taken and weighs and record.Other histoorgans are fast
Speed taking-up saves backup after weighing.Inhibiting rate is calculated by formula below：Tumor control rate (%)=(blank control group is averaged knurl
Weight-administration group is averaged knurl weight)/blank control group is averaged knurl weight × 100.Shoot formation is calculated according to following formula：Organ refers to
=10 × organ weight of number (mg)/mouse weight (g)
2.2.2 the measure of blood parameters
The mouse blood that the method for blood collects is taken using frame bottom veniplex, a part is through EDTA anti-freezings, for detecting four kinds
Routine blood indexes, leucocyte (WBC), red blood cell (RBC), hemoglobin (HGB), blood platelet (PLT).Another part resists through heparin
After solidifying, 10min is centrifuged with the speed of 3000r/min, with the following kidney function indicator of Virus monitory：Transaminase (ALT, AST), urine
Plain nitrogen (BUN), uric acid (UA) and creatinine (CRE).
2.2.3 data analysis
As a result represented using mean+SD (Mean ± SD).All statistical analyses Orgin-7.5 softwares
It is t check analyses, * P<0.05 represents there is significant difference；**P<0.01 represents there is pole significant difference.
2.3 results and analysis
2.3.1 panax japonicus polysaccharides evaluate the inhibition of H22 hepatocellular carcinomas
In order to evaluate inhibition of the panax japonicus polysaccharides to H22 hepatocellular carcinomas, mice bearing H_ 22 solid tumor models are established,
It is administered with same dosage, as shown in table 2.1, the average tumor weight of blank group group is 1.27g.In PSPJ (30 and 100mg/
Kg) in group, average tumor weight is reduced to 0.74g and 0.58g respectively.It is flat in PSPJ administration groups compared with negative control group
The significant sex differernce of equal tumor weight.Tumor control rate (61.4%) after 5-FU is treated, but this group of tumor-bearing mice is averaged
Weight also drastically declines and has the mouse dead at the end of the study.On the contrary, the tumour inhibiting rate of PSPJ (100mg/kg) is
54.3%, the weight of tumor-bearing mice is had little to no effect, and administration group mouse does not occur death condition.
Inhibitory action (Mean ± SE, n=12) of 2.1 panax japonicus polysaccharides of table to H22 tumor-bearing mice tumour growths
Compared with blank group:#p<0.01；btumor inhibitory rate.
2.3.2 panax japonicus polysaccharides are to H22 tumor-bearing mice toxicity assessments
In order to assess toxic actions of the PSPJ to normal liver cell, the work of the serum parameters, i.e. ALT, AST of liver function is measured
Property.The serum levels of the obvious increase ALT and AST of 5-FU treatments, but PSPJ has no influence on this (table 2.2).In order to investigate PSPJ
To the toxic action of host's kidney, we have evaluated their serum renal function marker, including BUN, UA and CRE.Such as table
Shown in 2.3, positive drug group serum BUN and CRE rise, PSPJ administration groups are kept approximately constant.Meanwhile we also detect PSPJ pairs
The influence of the concentration of blood WBC, RBC, HGB and PLT.Compared with blank group, 5-FU groups reduce the WBC contents in blood, and
PSPJ does not have much impact it, and the amount of RBC, HGB and PLT remain unchanged (table 2.4) in all experimental groups.
Influence (Mean ± SE, n=12) of 2.2 panax japonicus polysaccharides of table to tumor-bearing mice liver function
Compared with blank group:#p<0.01.
Influence (Mean ± SE, n=12) of 2.3 panax japonicus polysaccharides of table to tumor-bearing mice renal function
Compared with blank group:#p<0.01
Influence (Mean ± SE, n=12) of 2.4 panax japonicus polysaccharides of table to tumor-bearing mice blood routine
Compared with blank group:#p<0.01.
2.4 discuss
The present embodiment is by establishing H22 bearing mouse models, to mouse weight change, survival number of days, tumor weight, tumor suppression
The indexs such as rate, blood routine, hepatic and renal function are observed.The results show that panax japonicus polysaccharides have the hepatocellular carcinoma of H22 tumor-bearing mices
There are a degree of inhibition and no toxic action.Changed by mouse weight before and after recording experiment, administration panax japonicus is more
After sugar, there is not exception in the weight of experiment mice, and before experiment terminates, mouse does not have dead appearance.In experimentation,
Make discovery from observation, diet, activity, hair, the excrement of panax japonicus administration group mouse are normal, drug poisoning do not occur and show
As, and the mouse of 5-FU groups becomes thin, and erects hair, or even phenomena such as death.It is more by calculating tumour inhibiting rate display administration panax japonicus
Tumour inhibiting rate after sugar is respectively 41.7% and 54.3%, shows preferable tumor killing effect.
Glutamic-pyruvic transaminase (ALT) and glutamic-oxalacetic transaminease (AST) are the reflection common indexs of liver function.Liver is human body maximum
Removing toxic substances organ, both level contents height has with liver function and directly contacts.After panax japonicus polysaccharides are administered, the liver of experiment mice
There is not obvious exception in dirty function, illustrates panax japonicus polysaccharides without drug induccd toxicity.Urea nitrogen (BUN), uric acid (UA) and creatinine
(CRE) it is clinical most common three renal function Testing index.Kidney is the excretory organs of human body maximum, and panax japonicus polysaccharides are administered
Afterwards, its effluent does not influence renal function exception.By detecting physiochemical indice, panax japonicus polysaccharides are to leucocyte, red blood cell, blood
Platelet is improved trend, and compared with positive drug, every physiochemical indice all dramatically increases.These results of study demonstrate bamboo jointly
Section gracilis polysaccharide has the efficient ability for suppressing tumour growth of low toxicity in vivo.
Embodiment 3
The protective effect of panax japonicus polysaccharides prepared by embodiment 1 to LPS/D-GalN inducing mouse acute liver damages：
Using LPS/D-GalN inducing mouses acute liver damage as model, research panax japonicus polysaccharides are to acute liver damage
Prevention and protective effect simultaneously are attempted to inquire into its mechanism.
3.1 experimental animals and reagent
3.1.1 experimental animal
SPF grades of male mouse of kunming 48,18~22g of weight, it is dynamic purchased from Hubei Province Animal Experimental Study center, experiment
Thing production licence number：SCXK (Hubei Province) 2015-0018.
3.1.2 reagent
Panax japonicus polysaccharides：Embodiment 1 is prepared；Lipopolysaccharides (LPS) is purchased from Biosharp；Amine-galactose (D-GalN)
Purchased from Tokyo Chemical Industry；Alanine aminotransferase (ALT), aspartate aminotransferase (AST), go back
Prototype glutathione (GSH), superoxide dismutase (SOD) and malonaldehyde (MDA) assay kit are purchased from Nanjing and build up
Biological study institute；Tumor necrosis factor α (TNF-α), interleukin-1 beta (IL-1 β), interleukin-6 (IL-6) are containing measurement
Determine kit and be purchased from Shanghai Yuan Ye biotechnologies company.
3.2 method
3.2.1 packet administration and animal model
48 kunming mices are randomly divided into 4 groups, i.e. Normal group, model group, PSPJ administration groups, and gastric infusion is (normal
Control group and model group give isometric physiological saline, and administration group gives the PSPJ of 50,150mg/kg respectively), 1 time a day,
Successive administration 7 days.After last dose 2h, remaining each group mouse peritoneal injection LPS (8 μ g/kg) and D- in addition to Normal group
GalN (800mg/kg) prepares acute hepatic injury model.
3.2.2 the collection and processing of sample
Observed in 24h and record the death condition of mouse, and plucked eyeball when experiment mice will be dead and take blood, separate blood
Clearly.Mouse is dissected immediately after taking blood, and the hepatic tissue fritter for taking mouse right lobe of liver same area size identical is placed in 10% neutral first
It is fixed in aldehyde, observation pathology of hepar change is dyed for HE, -80 DEG C of preservations of remaining liver are used for biochemical analysis.
3.2.3 index of correlation detects
The death condition of each group mouse different time points in 24h is recorded, and draws survivorship curve.Liver is taken, is taken pictures simultaneously
Weigh, calculate liver index.According to kit specification, the level of ALT, AST, GSH, SOD and MDA in mice serum are detected；
TNF-α, IL-1 β and IL-6 levels are measured with ELISA method in mouse liver even slurry.
3.2.4 data analysis
Experimental data is expressed as mean ± standard deviation (Mean ± SE), and application Sigma-plot10.0 statistical softwares carry out
Analysis.Examined using double tail t and carry out two groups of sample average comparative analysis, one-way analysis of variance distinguishes whether multigroup have statistics
Meaning, P<0.05 shows difference with statistical significance.
3.3 results and analysis
3.3.1 influence of the panax japonicus polysaccharides to acute hepatic injury mice survival rate
The acute liver of LPS/D-GalN inductions can cause model mice (6h) mortality in a short time, lead to
Prevention and guarantor of the medicine to hepatic injury can preferably be evaluated by crossing life span and survival rate of the observation administration mouse after modeling
Shield acts on.Experimental result is shown：Model group mouse starts death in modeling 4h or so, and the time that peak mortality occurs is left for 5h
The right side, 24h survival rates are 16.7%.In administration group, the peak mortality time of PSPJ low dose group mouse is 8h or so, and 24h gives birth to
Deposit rate 50%；PSPJ high dose group dead mouse rush hours are 4.5 times of model group close to 10h, 24h survival rates, are compared
PSPJ low dose groups improve 25% (Fig. 3).This shows that PSPJ has prevention to the LPS/D-GalN acute livers induced
With protective effect, and there is preferable dose dependent.Then we have carried out tracing study to the time-to-live for the mouse that survives again,
The results show：The model group mouse limit time-to-live was at 2 days, and the limit time-to-live of PSPJ high dose groups can even reach
7 days.
3.3.2 panax japonicus polysaccharides are to acute hepatic injury mice liver morphology and pathological effect
Liver appearance and pathology form are to evaluate hepatic injury and medicine to the most directly perceived of damage prevention and protective effect
Index.Normal group mouse liver appearance color is light, and edge is lubricious, and matter is tough；In terms of liver histopathology form, cell size
Homogeneous, marshalling, structural integrity, it is central that nucleus is located at liver cell.Model group liver appearance color is dark red, has obvious swollen
Swollen, extravasated blood；Hepatic tissue pathology damage is serious, is full of small vacuole in degeneration of liver cells, endochylema, and have obvious liver bleeding and inflammation
Disease cellular infiltration.After PSPJ is administered, obvious improvement is presented in the appearance and color of mouse liver, and pathologic finding shows that PSPJ gives
Medicine group mouse liver cell gap reduces, and high dose group is congested and cell infiltration situation significantly improves, and it is normal to be bordering on recovery.Explanation
PSPJ can dose-dependently alleviate the liver appearance of LPS/D-GalN inductions and change (experimental result such as figure of micromorphology
Shown in 4).
3.3.3 influence of the panax japonicus polysaccharides to hepatic injury mouse ALT, AST and liver index level
Mouse liver index reflects liver damage degree indirectly, and the ALT and AST in mice serum can directly react mouse
Liver function.After LPS/D-GalN is stimulated, the level of ALT, AST increase 4.1 times and 3.1 respectively in model group mice serum
Times, mouse liver index also have conspicuousness rise (##P<0.01), illustrate that LPS/D-GalN result in hepatic injury, show as liver
The oedema and dysfunction of liver of tissue.Compared with model group, the level of ALT, AST and liver refer in PSPJ administration group mice serums
Number has different degrees of decline, and all indexs of wherein high dose group decrease beyond 40% (the experimental result such as institute of table 3.1
Show).Illustrate that PSPJ can dose-dependently improve the dysfunction of liver of LPS/D-GalN induced liver injury mouse and edema due to dysfunction of the liver swells.
Influence (Mean ± SE, n=12) of 3.1 panax japonicus polysaccharides of table to hepatic injury mouse liver function indexes and liver index
Compared with normal group#P<0.05,##P<0.01；Compared with model group*P<0.05,**P<0.01, similarly hereinafter.
3.3.4 influence of the panax japonicus polysaccharides to hepatic injury mouse MDA, SOD and GSH level
Antioxidative Factors SOD, GSH and oxidative stress marker MDA reflection body oxidative stress status.Work as LPS/D-
After GalN inducing mouse hepatic injuries, SOD and GSH activity in its hepatic tissue are reduced, the increase of MDA contents.In model group, liver group
Knit the level of middle GSH and SOD does not reduce 3.2 times and 1.0 times compared with normal components, and MDA levels increase 0.97 times, and has aobvious
Work sex differernce (##P<0.01), illustrate that LPS/D-GalN inducing mouse hepatic injuries are related with oxidative stress.Compared with model group,
The horizontal rises of GSH and SOD in PSPJ administration group murine liver tissues, MDA is horizontal to be reduced, GSH and MDA changes wherein in high dose group
Significantly (* * P<0.01) (experimental result is as shown in table 3.2).Illustrate that PSPJ can improve LPS/D-GalN inducing mouse hepatic injuries
Oxidative stress status.
Influence (Mean ± SE, n=12) of 3.2 panax japonicus polysaccharides of table to hepatic injury mouse MDA, SOD and GSH level
Compared with normal group#P<0.05,##P<0.01；Compared with model group*P<0.05,**P<0.01, similarly hereinafter.
3.3.5 influence of the panax japonicus polysaccharides to hepatic injury murine liver tissue inflammatory mediator TNF-α, IL-1 β and IL-6
The degree of acute liver has significantly with internal inflammatory mediator TNF-α, the concentration level of IL-1 β and IL-6
Positive correlation.Compared with normal group, TNF-α, IL-1 β and IL-6 concentration in model group murine liver tissue significantly rise (##P<
0.01), front and rear 10 times or so of difference.Illustrate experiment mice after LPS/D-GalN is stimulated, induce serious hepar damnification, promote
Into a large amount of releases of inflammatory factor, while also illustrate this experiment modeling success.Compared with model group, after PSPJ is treated, by
TNF-α, the concentration of IL-1 β and IL-6 reduce 0.44 times, 0.62 times and 0.31 times respectively in damage hepatic tissue, and with preferable
Dose-effect relationship (result is as shown in table 3.3).Illustrate that PSPJ can be suppressed by the release for the inflammatory factor for preventing murine liver tissue
Its inflammatory reaction and reach prevention and protective effect to LPS/D-GalN inducing mouse hepatic injuries.
Influence (Mean ± SE, n=of 3.3 panax japonicus polysaccharides of table to hepatic injury murine liver tissue TNF-α, IL-1 β and IL-6
12)
Compared with normal group#P<0.05,##P<0.01；Compared with model group*P<0.05,**P<0.01, similarly hereinafter.
3.4 discuss
Originally test result indicates that, PSPJ can extend survival rate and the time-to-live of experiment mice, improve the appearance of liver
And tissue morphology；Compared to model group, after PSPJ is administered, in mice serum AST, ALT and the equal conspicuousness of liver index decline (**P
<0.01), SOD and GSH is horizontal in liver tissue homogenate rises, the equal conspicuousness decline of MDA, TNF-α, the content of IL-1 β and IL-6 (**
P<0.01)。
Intraperitoneal injection LPS and D-GalN is the more easily method for building acute liver model.LPS is leather
Endotoxic main component secreted by gram-negative bacteria, LPS is by stimulating the immunocyte including macrophage to discharge
Inflammatory factor, so that apoptosis and necrosis can occur for liver cell.D-GalN can be pressed down by consuming the uridine triphosphate in liver
Large biological molecule of the system using RNA and protein as representative synthesizes, and causes inflammation reaction and the necrosis of liver cell diffusivity.
Under the synergistic effect of LPS and D-GalN, the liver cell mortality in a short time of experimental animal, liver physiology function seriously by
Damage.In this experiment, survival rate of the model group mouse in 24h is only that 16.7%, PSPJ group mouse 24h survival rates substantially carry
Height, the liver cell extent of damage significantly reduce, and Serum ALT and AST contents are substantially less than model group.Above experimental fact shows PSPJ
There is protection liver cell, to anti-liver injury.
The hepatic injury of resulted from chemical medicine generally changes with body oxidative stress status to be closely related.This can further cause
SOD and GSH contents reduce in liver, and MDA contents rise.Similarly, it has been found that in model group murine liver tissue, SOD and
GSH is horizontal to be reduced, the increase of MDA contents.These experimental results prompt liver oxidative stress to be damaged in LPS/D-GalN combined inductions liver
Important function is played during wound.For PSPJ high dose groups compared with model group, the activity of SOD, GSH have been respectively increased 4.02 times
With 1.58 times, MDA reduces 1.65 times, and difference has statistical significance.Show that PSPJ can improve the oxygen of mouse damaged liver
Change stress situation.
TNF-α, IL-1 β and IL-6 are the inflammatory factors secreted by hepatic macrophages.The inflammation such as TNF-α, IL-1 β, IL-6
On the one hand inflammation factor acts on surface of hepatocytes acceptor, cause necrosis of liver cells, and NF- κ B signals lead in another aspect active cell
Road, further increases its burst size to positive feedback, aggravates hepatocellular injury.It was found that the joint in LPS/D-GalN is made
Under, TNF-α, the content of IL-1 β and IL-6 are significantly raised in hepatic tissue, and this phenomenon can effectively be suppressed by PSPJ, prompt
Suppress liver inflammatory reaction and play key player in the hepatocyte protection activity of PSPJ.
In conclusion the result of study preliminary proof of the present embodiment Acute Hepatics of the PSPJ to LPS/D-GalN inducing mouses
Damage has clearly prevention and protective effect, its mechanism of action is probably the hair for suppressing response to oxidative stress and inflammatory reaction
It is raw, so as to prevent and prevent hepatic injury, improve the function of damaged liver, it is final to prevent conversion of the liver inflammation to liver cancer.
Claims (1)
1. application of the panax japonicus polysaccharides in prevention and/or treatment liver-cancer medicine is prepared.
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