CN111387142A - Method for constructing mouse atherosclerosis model by using L PS and tyloxapol - Google Patents
Method for constructing mouse atherosclerosis model by using L PS and tyloxapol Download PDFInfo
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- CN111387142A CN111387142A CN202010360359.5A CN202010360359A CN111387142A CN 111387142 A CN111387142 A CN 111387142A CN 202010360359 A CN202010360359 A CN 202010360359A CN 111387142 A CN111387142 A CN 111387142A
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- MDYZKJNTKZIUSK-UHFFFAOYSA-N tyloxapol Chemical compound O=C.C1CO1.CC(C)(C)CC(C)(C)C1=CC=C(O)C=C1 MDYZKJNTKZIUSK-UHFFFAOYSA-N 0.000 title claims abstract description 45
- 201000001320 Atherosclerosis Diseases 0.000 title claims abstract description 34
- 238000000034 method Methods 0.000 title claims abstract description 25
- 229960004224 tyloxapol Drugs 0.000 title claims abstract description 25
- 229920001664 tyloxapol Polymers 0.000 title claims abstract description 25
- 241000699666 Mus <mouse, genus> Species 0.000 claims description 30
- 241000699670 Mus sp. Species 0.000 claims description 13
- 238000010172 mouse model Methods 0.000 claims description 11
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- 239000007928 intraperitoneal injection Substances 0.000 claims description 4
- 238000002474 experimental method Methods 0.000 abstract description 12
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- 208000037260 Atherosclerotic Plaque Diseases 0.000 abstract 1
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- NPGIHFRTRXVWOY-UHFFFAOYSA-N Oil red O Chemical compound Cc1ccc(C)c(c1)N=Nc1cc(C)c(cc1C)N=Nc1c(O)ccc2ccccc12 NPGIHFRTRXVWOY-UHFFFAOYSA-N 0.000 description 3
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- QGZKDVFQNNGYKY-UHFFFAOYSA-N Ammonia Chemical compound N QGZKDVFQNNGYKY-UHFFFAOYSA-N 0.000 description 2
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- 108010059886 Apolipoprotein A-I Proteins 0.000 description 1
- 102000005666 Apolipoprotein A-I Human genes 0.000 description 1
- 108010087614 Apolipoprotein A-II Proteins 0.000 description 1
- 102000009081 Apolipoprotein A-II Human genes 0.000 description 1
- 101710095339 Apolipoprotein E Proteins 0.000 description 1
- 102100029470 Apolipoprotein E Human genes 0.000 description 1
- 206010003210 Arteriosclerosis Diseases 0.000 description 1
- 241000894006 Bacteria Species 0.000 description 1
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- WSFSSNUMVMOOMR-UHFFFAOYSA-N Formaldehyde Chemical compound O=C WSFSSNUMVMOOMR-UHFFFAOYSA-N 0.000 description 1
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- 208000031226 Hyperlipidaemia Diseases 0.000 description 1
- 206010061218 Inflammation Diseases 0.000 description 1
- 102000000853 LDL receptors Human genes 0.000 description 1
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- 241000699660 Mus musculus Species 0.000 description 1
- 241000283973 Oryctolagus cuniculus Species 0.000 description 1
- 102000014190 Phosphatidylcholine-sterol O-acyltransferase Human genes 0.000 description 1
- 108010011964 Phosphatidylcholine-sterol O-acyltransferase Proteins 0.000 description 1
- 241000605862 Porphyromonas gingivalis Species 0.000 description 1
- FAPWRFPIFSIZLT-UHFFFAOYSA-M Sodium chloride Chemical compound [Na+].[Cl-] FAPWRFPIFSIZLT-UHFFFAOYSA-M 0.000 description 1
- 241000282887 Suidae Species 0.000 description 1
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- YQGOJNYOYNNSMM-UHFFFAOYSA-N eosin Chemical compound [Na+].OC(=O)C1=CC=CC=C1C1=C2C=C(Br)C(=O)C(Br)=C2OC2=C(Br)C(O)=C(Br)C=C21 YQGOJNYOYNNSMM-UHFFFAOYSA-N 0.000 description 1
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- 230000000968 intestinal effect Effects 0.000 description 1
- 150000002632 lipids Chemical class 0.000 description 1
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- 150000003904 phospholipids Chemical class 0.000 description 1
- 108090000623 proteins and genes Proteins 0.000 description 1
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- 238000011830 transgenic mouse model Methods 0.000 description 1
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Images
Classifications
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- A—HUMAN NECESSITIES
- A01—AGRICULTURE; FORESTRY; ANIMAL HUSBANDRY; HUNTING; TRAPPING; FISHING
- A01K—ANIMAL HUSBANDRY; AVICULTURE; APICULTURE; PISCICULTURE; FISHING; REARING OR BREEDING ANIMALS, NOT OTHERWISE PROVIDED FOR; NEW BREEDS OF ANIMALS
- A01K67/00—Rearing or breeding animals, not otherwise provided for; New or modified breeds of animals
- A01K67/02—Breeding vertebrates
-
- A—HUMAN NECESSITIES
- A01—AGRICULTURE; FORESTRY; ANIMAL HUSBANDRY; HUNTING; TRAPPING; FISHING
- A01K—ANIMAL HUSBANDRY; AVICULTURE; APICULTURE; PISCICULTURE; FISHING; REARING OR BREEDING ANIMALS, NOT OTHERWISE PROVIDED FOR; NEW BREEDS OF ANIMALS
- A01K2207/00—Modified animals
- A01K2207/20—Animals treated with compounds which are neither proteins nor nucleic acids
-
- A—HUMAN NECESSITIES
- A01—AGRICULTURE; FORESTRY; ANIMAL HUSBANDRY; HUNTING; TRAPPING; FISHING
- A01K—ANIMAL HUSBANDRY; AVICULTURE; APICULTURE; PISCICULTURE; FISHING; REARING OR BREEDING ANIMALS, NOT OTHERWISE PROVIDED FOR; NEW BREEDS OF ANIMALS
- A01K2227/00—Animals characterised by species
- A01K2227/10—Mammal
- A01K2227/105—Murine
-
- A—HUMAN NECESSITIES
- A01—AGRICULTURE; FORESTRY; ANIMAL HUSBANDRY; HUNTING; TRAPPING; FISHING
- A01K—ANIMAL HUSBANDRY; AVICULTURE; APICULTURE; PISCICULTURE; FISHING; REARING OR BREEDING ANIMALS, NOT OTHERWISE PROVIDED FOR; NEW BREEDS OF ANIMALS
- A01K2267/00—Animals characterised by purpose
- A01K2267/03—Animal model, e.g. for test or diseases
- A01K2267/035—Animal model for multifactorial diseases
- A01K2267/0375—Animal model for cardiovascular diseases
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- Life Sciences & Earth Sciences (AREA)
- Environmental Sciences (AREA)
- Animal Behavior & Ethology (AREA)
- Zoology (AREA)
- Animal Husbandry (AREA)
- Biodiversity & Conservation Biology (AREA)
- Investigating Or Analysing Biological Materials (AREA)
- Measuring Or Testing Involving Enzymes Or Micro-Organisms (AREA)
Abstract
The invention discloses a method for constructing a mouse atherosclerosis model by using L PS and tyloxapol, which firstly utilizes L PS and tyloxapol to induce the mouse atherosclerosis model for a long time and experiments prove that the contents of Triglyceride (TG), Total Cholesterol (TC) and low-density lipoprotein (L D L) in the serum of a mouse of the model are obviously increased, and atherosclerotic plaques are formed at the aortic valve of the mouse.
Description
Technical Field
The invention relates to the technical field of animal experiment models, in particular to a method for constructing a mouse atherosclerosis model by using L PS and tyloxapol, which belongs to the technical field of biology.
Background
Atherosclerosis is a chronic disease and is the underlying cause of most cardiovascular disease occurrences. Cardiovascular disease caused by atherosclerosis has a high mortality rate worldwide. Among them, atherosclerotic cardiovascular diseases are characterized pathologically mainly by dysfunction of arterial endothelial cells. In the past, the pathogenesis of atherosclerosis has been considered to be vessel wall lipid accumulation. However, it has been found that the pathogenesis of atherosclerosis is complex, with immune cells and inflammation as well as hyperlipidemia playing a key role in the development of atherosclerosis. Therefore, the obtained atherosclerosis animal model has good molding stability, high speed and low cost, and has great significance for researching the generation and development mechanism of atherosclerosis and screening drugs for treating atherosclerosis.
An ideal animal model of atherosclerosis should resemble human anatomy and pathophysiology to make it possible to use in medical and pharmaceutical studies to obtain results that can be extrapolated to human medicine. Moreover, it must be readily available, be able to be maintained at reasonable cost, be easy to handle, and have the same pathological conditions as humans. In general, animal models of atherosclerosis are the accelerated formation of plaques resulting from a cholesterol-rich diet and the development of other risk factors that trigger atherosclerosis. In the selection of the atherosclerosis model animals, mice and rabbits are widely used, followed by pigs and non-human primates. Each model has its advantages and limitations. The mouse has the advantages of fast reproduction, easy operation, capability of monitoring the occurrence of atherosclerosis in a reasonable time and the like. Therefore, the method has scientific and reasonable property for constructing the atherosclerosis model based on the mouse.
At present, methods for inducing a mouse atherosclerosis model are mainly divided into: high fat feeding induced mouse model;high cholesterol fed induced mouse model; apolipoprotein E (Apo E)-/-) Knockout mouse model, low density lipoprotein receptor (L D L-R)-/-) Knocking out the model; apo E-/-And L D L-R-/-A mouse model; in addition, there are many genes that are knocked out to favor the development of atherosclerosis in mice, such as Apo A-1, Apo A-II, Apo A-IV, and transgenic mice such as lecithin cholesterol acyltransferase and phospholipid transporter. However, the method for inducing atherosclerosis of mice has a plurality of defects, such as anorexia of the mice and the stability of molding are not facilitated by feeding methods such as high fat feeding; in addition, feeding methods such as high-fat feeding also have the problems of long film forming period and high experiment cost; the knockout mouse model is expensive in experimental cost, and in order to achieve a better effect, the mouse is fed with high-fat food, which undoubtedly further increases the experimental cost. Therefore, the deep research on atherosclerosis by finding a molding method with low experimental cost and short molding period is irresistible.
The research in recent years shows that some bacteria such as intestinal flora and porphyromonas gingivalis can accelerate the generation of atherosclerosis, which is related to the generation of a large amount of L PS, L PS generates excessive to cause strong inflammatory response of organisms, and continuous inflammatory response is an important factor for the generation of atherosclerosis.
Disclosure of Invention
Technical problem to be solved
Aiming at the defects of the prior art, the invention provides a method for constructing a mouse atherosclerosis model by using L PS and tyloxapol, the method can reduce the experiment cost, the modeling success rate is high, and the obtained model mouse can conveniently research the pathogenesis of atherosclerosis and screen drugs for treating atherosclerosis.
(II) technical scheme
In order to achieve the aim, the invention provides a technical scheme of a method for constructing a mouse atherosclerosis model by using L PS and tyloxapol.
Preferably, the mouse is a male C57B L/6 mouse.
Preferably, 50 μ g of L PS is used to inject the drug into the mice by intraperitoneal injection.
Preferably, the induction time of L PS is once a week for 8 weeks.
Preferably, tyloxapol is injected into the body of the mouse by means of intraperitoneal injection with 500 mg/kg.
Preferably, the induction time of tyloxapol is once every other day for 8 weeks.
Preferably, L PS and tyloxapol are induced simultaneously in the mouse model.
Preferably, a common daily ration is adopted to construct a mouse model, after the construction of the mouse model is completed, the contents of TC, TG and L D L in the serum of the mouse are measured, and the aortic valve plaque formation condition of the mouse is observed by using HE staining and oil red O staining.
(III) advantageous effects
Compared with the prior art, the method has the following beneficial effects:
the invention discloses L PS and tyloxapol can successfully construct a mouse atherosclerosis model for the first time, the invention can successfully induce the mouse atherosclerosis model within 8 weeks in a short period, which greatly shortens the modeling time and successfully solves the problem of long modeling time, the invention does not need high-fat feeding, which greatly reduces the experiment cost and improves the feasibility of the experiment, the invention has simple experiment technology and convenient operation, and is beneficial to the increase of the model forming rate.
Drawings
FIG. 1 is a flow chart of the operation of the mouse model induced with L PS and tyloxapol;
FIG. 2 is a graph showing the results of the content of TC, TG, &lTtT transition = L "&gTt L &lTt/T &gTt D L in the serum after mice were induced with L PS and tyloxapol for 8 weeks;
FIG. 3 is a graph showing the results of HE staining of aortic valve 8 weeks after mice were induced with L PS and tyloxapol;
FIG. 4 is a graph showing the results of aortic oil red O staining 8 weeks after mice were induced with L PS and tyloxapol;
indicates that as compared to the blank group,*p<0.05，**p<0.01, the acronym L PS bacterial endotoxin, TC total cholesterol, TG triglyceride, L D L low density lipoprotein.
Detailed Description
The invention will be further described with reference to specific embodiments and drawings, the advantages and features of which will become apparent as the description proceeds. These examples are illustrative only and do not limit the scope of the present invention in any way. It will be understood by those skilled in the art that various changes in form and details may be made therein without departing from the spirit and scope of the invention, and that such changes and modifications may be made without departing from the spirit and scope of the invention.
The detailed operation method of this example is as follows:
material
SPF male C57B L/6 mice, 20-22g, were provided by Liaoning Biotechnology Ltd, and the laboratory animals production license numbers SCXK2010-0001, L PS and tyloxapol were purchased from Sigma, and TC, TG, L D L measurement kits were purchased from Nanjing to build bioengineering institute.
Example 1L procedure for the PS and tyloxapol-induced mouse model
The mice are divided into four groups, namely a blank group (normal saline), an L PS group (50 mu g), a tyloxapol group (500mg/kg), a L PS group (50 mu g) + tyloxapol group (500mg/kg), a L PS group and tyloxapol are administrated by intraperitoneal injection, the administration period of the L PS group is once a week, the administration period of the tyloxapol group is once every other day, and the administration periods of the L PS group and the tyloxapol group are both administrated for 8 weeks, wherein the operation flow of inducing the mouse model by the L PS group (50 mu g) + the tyloxapol group (500mg/kg) is shown in figure 1.
Figure 1 shows a molding cycle of 8 weeks, wherein L PS was injected intraperitoneally on the first day of the week, and tyloxapol was injected every other day.
EXAMPLE 2 determination of the content of TC, TG, L D L in mouse serum
The experimental method comprises the following steps:
(1) after example 1, blood was collected by an eyeball-blood collection method, and after standing at room temperature for 2 hours, serum was allowed to precipitate. The collected blood was centrifuged at 3000rpm for 5min and the upper serum was aspirated.
(2) According to the instructions of TC, TG and L D L, the TC, TG and L D L kits are respectively used for measuring the content of TC, TG and L D L in the serum of the mice, and the values are read by a microplate reader.
(3) The experimental results are shown in figure 2.
The results of FIG. 2 show that L PS + tyloxapol significantly increased the serum TC, TG and L D L0 levels in mice, as shown in FIG. 2A, the TG content in tyloxapol group and L1 PS + tyloxapol group was significantly increased (p <0.01) and the TG content in L2 PS + tyloxapol group was highest as compared to the blank group, as shown in FIG. 2B, the TC content in tyloxapol group and L PS + tyloxapol group was significantly increased (p <0.01) and the TC content in L PS + tyloxapol group was highest as compared to the blank group, as shown in FIG. 2C, the TC content in tyloxapol group and L PS + tyloxapol group L D L was significantly increased (p <0.01) and the TC content in L PS + tyloxapol group L D L was highest as compared to the blank group.
Example 3 mouse aortic valve HE staining experiment
The experimental method comprises the following steps:
(1) the aortic root of the mouse was fixed in 4% formaldehyde solution for 24 h.
(2) Taking out the aorta root of the mouse, soaking in 70% alcohol for 1h, 80% alcohol for 1h, 90% alcohol for 1h, 95% alcohol for 1h, 100% alcohol for 1h, and then 100% alcohol for 1h to complete tissue dehydration.
(3) And taking out the aortic root of the mouse, and soaking in xylene I and xylene II for 15min respectively to complete tissue transparency.
(4) And taking out the aortic root of the mouse, and soaking in the wax I for 30min, the wax II for 30min and the wax III for 30min respectively to finish the tissue waxing.
(5) The aortic root of the mouse was removed and the tissue embedded in an embedding cassette on an embedding apparatus.
(6) Cutting into pieces with a slicer, slicing, and spreading in 42 deg.C water bath. The attached sections were placed in an oven at 65 ℃ overnight.
(7) Taking out the slices, and respectively putting the slices into dimethylbenzene I for 10min and dimethylbenzene II for 10min for dewaxing.
(8) Taking out, slicing, soaking in 100% ethanol for 5min, soaking in 95% ethanol for 5min, soaking in 90% ethanol for 5min, soaking in 80% ethanol for 5min, soaking in 70% ethanol for 5min, and dehydrating.
(9) Taking out the slices, rinsing in tap water, and staining with hematoxylin for 5 min.
(10) Taking out, slicing, washing with tap water, standing for 5min, and soaking in 80% ethanol for 5 min.
(11) Eosin staining for 2 min.
(12) Taking out the dyed slices, sequentially soaking in 95% alcohol for 5min, 100% alcohol for 5min, then 100% alcohol for 10min, xylene I for 10min, and xylene II for 10min.
(13) The slices were taken out and mounted with mounting medium.
(14) The lesion site was observed by an optical microscope at 40-fold and 100-fold magnification.
(15) The experimental results are shown in figure 3.
FIG. 3HE staining results show that both tyloxapol group and L PS + tyloxapol group had foam cell production, but L PS + tyloxapol group had a greater range of atherosclerotic lesions.
Example 4 mouse aortic valve oil Red O staining experiment
The experimental method comprises the following steps:
(1) the obtained mouse aorta root is embedded and fixed in OCT embedding medium.
(2) The embedded tissue was sectioned with a frozen microtome.
(3) The slices were washed in tap water for 10min.
(4) The sections were soaked in 60% isopropanol for 2 s.
(5) Sections were stained with 0.5% oil red for 15 min.
(6) The slices were washed with 60% isopropyl alcohol and then washed with tap water.
(7) The sections were washed with tap water after 30s of hematoxylin counterstaining.
(8) The sections were washed with ammonia, reconstituted blue, tap water.
(9) The sheets were mounted with mounting medium, left to stand at room temperature after drying and observed as soon as possible.
(10) The lipid droplets were observed by an optical microscope at 40-fold and 100-fold magnification.
(11) The experimental results are shown in figure 4.
FIG. 4 shows that lipid accumulation in artery walls of both tyloxapol group and L PS + tyloxapol group is observed in oil red O staining, but lipid accumulation in artery intima is more serious in L PS + tyloxapol group.
Multiple comparisons and statistical significance were performed between different groups using one-way anova. Statistical analysis was performed using GraphPadPrism 7.
Claims (8)
1. A method for constructing a mouse atherosclerosis model by using L PS and tyloxapol is characterized in that L PS and tyloxapol are used in combination to construct the mouse atherosclerosis model.
2. The method of claim 1, wherein the mouse is a male C57B L/6 mouse.
3. The method of claim 1, wherein the mice are injected intraperitoneally with 50 μ g of L PS.
4. The method of claim 1, wherein the induction time of L PS is once per week for 8 weeks.
5. The method of claim 1, wherein tyloxapol is administered to the mouse by intraperitoneal injection at a dose of 500 mg/kg.
6. The method of claim 1, wherein the induction of tyloxapol is performed once every other day for 8 weeks.
7. The method of claim 1, wherein L PS and tyloxapol are simultaneously induced in the mouse model.
8. The method of claim 1, wherein the mouse model is constructed using normal ration.
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Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN112675156A (en) * | 2021-01-20 | 2021-04-20 | 吉林大学 | Application of erythritol in preparation of medicine for treating non-alcoholic fatty liver disease |
Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2007002493A2 (en) * | 2005-06-22 | 2007-01-04 | The Regents Of The University Of Michigan | Compositions and methods for modulating the acute phase response |
-
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Patent Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| WO2007002493A2 (en) * | 2005-06-22 | 2007-01-04 | The Regents Of The University Of Michigan | Compositions and methods for modulating the acute phase response |
Non-Patent Citations (4)
| Title |
|---|
| 刘五州等: "家兔高脂血症和动脉粥样硬化模型研究进展", 《甘肃中医药大学学报》 * |
| 徐晓杰: "《现代临床病理学》", 31 May 2018, 湖北科学技术出版社 * |
| 朱竟赫: "高脂血症实验动物模型研究概述", 《实验动物科学》 * |
| 黄爱良等: "动脉粥样硬化动物模型构建的方法与现状", 《中国组织工程研究》 * |
Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN112675156A (en) * | 2021-01-20 | 2021-04-20 | 吉林大学 | Application of erythritol in preparation of medicine for treating non-alcoholic fatty liver disease |
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