CN102499175A - Method for building mouse model with multiple-generation obesity and fatty liver pathologic change - Google Patents
Method for building mouse model with multiple-generation obesity and fatty liver pathologic change Download PDFInfo
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Abstract
The invention discloses a method for building a mouse model with multiple-generation obesity and fatty liver pathologic change. The method comprises the steps of: respectively feeding mice with normal food (NC) and high-fat food (HF) to obtain F0-generation mice, namely an NCF0 group and an HFF0 group; feeding female mice with different foods until sexual maturity, breeding with male mice fed with normal food to obtain F1-generation mice, namely an NCF1 group and an HFF1 group; after ablactation, respectively and continuously feeding the two groups of mice with normal food and high-fat food, respectively feeding female mice with normal food and high-fat food until sexual maturity, breeding with male mice fed with normal food to obtain F2-generation mice, namely an NCF2 group and an HFF2 group; and after ablactation, respectively and continuously feeding the NCF2 group and HFF2 group of mice with normal food and high-fat food. The specific modeling route is shown in Figure 1. The result shows that the obesity degree, insulin resistance degree and fatty liver pathologic change degree of the mice fed with high-fat food are progressively increased generation by generation.
Description
Technical field
The present invention relates to a kind of foundation of mouse model, specifically set up many methods for high lipid food nursing acceleration obesity and fatty live lesions mouse model, the mouse model of foundation can be used to study high lipid food to liver and fat striding for influencing.
Background technology
Overweightly and fat become the public health problem that countries in the world are extremely paid close attention to.It is overweight or fat that 2/3rds adult is arranged in the U.S., and Europe and other developed countries have that to surpass half the adult be overweight or fat.Chinese once were the thin partially colonies of build.Along with The development in society and economy, people's the physiological activity or the work of bearing a heavy burden significantly reduce, and the overweight and fat number of China has catches up with the Hesperian impetus rapidly.State-owned 1.84 hundred million people belonged to overweight crowd during national nutrition in 2002 and health survey showed, had 0.31 hundred million people to belong to obese people.In these ten years, obese people increased twice from 1992 to 2002.The fat risk that can increase multiple disease generation is like hypertension, diabetes B, fatty liver, breast cancer etc.
NASH (NAFLD non-alcoholic fatty liver disease) shows as the accumulation of triglycerides too much in liver, and its pathological change shows as simple steatosis, fat hepatitis, cirrhosis and hepatitis with the progress of the course of disease.Along with China's rapid economy development, the raising day by day of living standards of the people, the incidence of disease of NASH is obvious ascendant trend, has become the healthy chronic disease of a kind of harm humans.Research shows that the incidence of disease of adult's NASH has reached 25% in western countries, and the incidence of disease of China some areas NAFLD also reaches 15%, and the incidence of disease of NASH can be up to arriving 80%-90% among obesity and the type-II diabetes patient.
Fat and NAFLD mainly occurs in the mid-aged population, yet the teen-age in recent years incidence of disease significantly increases.Obesity and type-II diabetes that adult's obesity and NAFLD high incidence can cause with the picked-up of the minimizing of people's activity and out-of-proportion high lipid food are explained, and the reason of the increase of the teen-age obesity and the NAFLD incidence of disease is not very clear.Nineteen ninety-five; David doctor Barker of Britain MRC environmental epidemiology research institute has proposed owing to the malnutritive fetal growth that produces limits the generation of later disease and the physiology and the structure of human body are had long-term influence with this hypothesis of theory (The fetal origins hypothesis) that the colleague has proposed the embryo source property of human diseases.For decades people find that constantly new evidence support Barker is theoretical.AD (the FOAD of fetus origin; Fetal Origins ofAdult Disease) be one type with development of fetus and the early stage relevant common disease of factor of children, for example obesity, diabetes, coronary vasodilator property cardiopathy, hypertension, chronic renal disease etc.Research shows, the baby of mother's fat or pregnancy duration diabetes adolescence more early tend to obesity and type-II diabetes; The filial generation of the rodent that mother is fat has higher risk or more is easy to generate obesity and NAFLD.
Liver is control sugar and a lipometabolic major organs in the human body.Research shows, from the beginning the storage increase of fat and lipid are synthesized and can be causeed fat and NAFLD in the liver of the mouse of mouse that high lipid food is fed and gene delection.The abnormal expression of liver X receptor causes the rising of acetyl-CoA carboxylase and synthetase of fatty acid level, thereby causes fat and fatty liver.
Animal model is with artificial method; Make animal under certain paathogenic factor (physics, chemistry, biology) effect; Cause animal tissue, organ or whole body necessarily to damage; Function, the metabolism of some similar human diseases, the variation or the various diseases of morphosis aspect occur, study generation, the rule of development of human diseases, for prevention, the treatment (comprising that novel drugs is on probation) of research human diseases provides theoretical foundation through this means.Over nearly 40 years, scholars adopt several different methods to set up different fatty liver models, yet these models all are not suitable for the generation influence of striding of fat and fatty liver and study.
Summary of the invention
The objective of the invention is to be directed against above-mentioned deficiency, a kind of method of setting up many for high lipid food nursing acceleration obesity and fatty live lesions is provided, be used to study high lipid food striding liver for influence.
For realizing above-mentioned purpose, the present invention sets up many methods for high lipid food nursing acceleration obesity and fatty live lesions mouse model and comprises the steps:
1, a kind of method of setting up many for obesity and fatty live lesions mouse model, it comprises the steps:
1) female mouse of C57BL/6 and the male mouse normal diet fed are used normally (NC) and high fat (as containing 34.9% lard) food (HF) nursing respectively in 4-6 week when age is big, to obtain the 1st generation mouse (F0), be NC F0 and HF F0 group.Wherein female mouse bred utilizing different foods to feed the male mouse of feeding to sexual maturity (general month) and normal diet 1 generation, to obtain the 2nd generation mouse (F1).The filial generation that NC F0 organizes female mouse is NC F1 group.The filial generation that HF F0 organizes female mouse is HF F1 group.
2) the mouse wean with NC F1 group and HF F1 group continues to feed normal and high lipid food respectively.HF F1 and NC F1 organize female mouse and normal breed with the male mouse of high lipid food to sexual maturity (month, 8 ages in week are big) with the normal diet nursing feeding respectively, to obtain the 3rd generation mouse (F2).The filial generation of the female mouse of NC F1 group is NC F2 group, and the filial generation of the female mouse of HF F1 group then is HF F2 group.
3) continue to feed normal and high lipid food respectively after the mouse wean of NC F2 group and HF F2 group.
4) each, is collected its blood and liver samples and carries out each item physical signs, the detection of fatty liver pathology index and molecular biology aspect when different foods fed for 12 week for male mouse.
In addition, can repeating step 2)-3), obtain manyly for mouse model, for example repeating step 2) and 1～3 time.
The feeding time of above-mentioned male mouse can be regulated according to the experiment needs, for example continues to feed 2～8 months, and preferably feeding is to be used for experiment in 3 months.
The time that the male mouse that above-mentioned female mouse and normal diet are fed breeds generally is to end to its sexual maturity, in wean back 1 month usually.
Above-mentioned high lipid food is on the basis of normal feed, to add fat, the food that fat content is improved, and for example fat accounts for the total caloric mouse feed more than 50% of food, and preferred fat accounts for the mouse feed of food total caloric 60%.The fat that is added includes but not limited to lard.
Above-mentioned mouse can be to be C57BL/6, BALB/c, C3H, DBA/2, FVB/N mouse, preferred C57BL/6 mouse.
Through said method, the present invention has set up many mouse models for high lipid food nursing acceleration obesity and fatty live lesions, has filled up domestic and international blank.Experimentizing through this mouse model has proved that phase under the nursing of high lipid food is in the same time; The all fat male second filial mouse of grandmother and mother is than the male second filial mouse of grandmother and the non-obesity-related of mother; The obesity disease time early, the more serious and fatty degeneration of liver heighten degree of insulin resistance; These variations are because high lipid food causes that in liver, go down to posterity sexual abnormality accumulation of liver X receptor is caused.
Description of drawings
Fig. 1: the many of high lipid food nursing set up route map for obesity mice.
(the male mouse of square expression, the female mouse of circular expression.NC is that normal diet is fed, and HF is that high lipid food is fed.F0, F1, F2 represent to feed algebraically.NC F0 and HF F0 are respectively F0 generation normal and that high lipid food is fed, and NC F1 and HF F1 are respectively F1 generation normal and that high lipid food is fed, the F2 generation that NC F2 and HF F2 are respectively normal and high lipid food is fed)
Fig. 2: high lipid food influenced the generation of striding of mouse sugar tolerance (glucose tolerance).(
compares with the mouse that normal diet is fed; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared)
Fig. 3: high lipid food influenced the generation of striding of insulin (insulin) susceptibility.(
compares with the mouse that normal diet is fed; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared)
Fig. 4: high lipid food influenced the generation of striding of insulin in the blood (insulin), leptin (leptin) and triglycerides.(A:
compares with the mouse that normal diet is fed; B: in
and high lipid food are fed F0 generation, compared; C: in § p＜0.05 and high lipid food are fed F1 generation, compared)
Fig. 5: high lipid food is striden generation influence (
is compared with the mouse that normal diet is fed obesity mice is adipohepatic; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared)
Fig. 6: in the generation of striding that high lipid food is expressed liver X receptor in the liver, influence.(
compares with the mouse that normal diet is fed; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared)
Fig. 7: in the generation of striding that high lipid food is expressed liver X receptor in the liver, influence.(
compares with the mouse that normal diet is fed; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared)
Embodiment
Following examples are used to further specify the present invention, but should not be construed as limitation of the present invention.Under the situation that does not deviate from essence of the present invention and spirit, various modifications or retouching to the present invention carries out all belong to scope of the present invention.
Embodiment 1
This example is an example with the C57BL/6 mouse, explains that the present invention sets up many methods of feeding the mouse model that quickens fat and fatty live lesions for high lipid food.
Experiment material: the C57BL/6 mouse is available from (Wuhan University zoopery center); Mouse feed is available from (the auspicious imperial feed in Wuhan City); High lipid food is for adding fat to the mouse feed that accounts for food total caloric 60%.
Experimental technique:
This is tested employed C57BL/6 mouse and breeds for Wuhan University's Experimental Animal Center.The big C57BL/6 offspring (female mouse and male mouse) in age in 4-6 week who normal diet is fed female mouse uses normal (NC) and high lipid food (HF) to feed respectively, is NC F0 (normal 1 generation) and HF F0 and organizes (high fat 1 generation).Wherein female mouse breeds with male mouse that normal diet is fed after different foods are fed one month, obtains 2 generation mouse (F1).The filial generation that NC F0 organizes female mouse is NC F1 group, and generation mice wean back continues to feed (normal 2 generations) with normal diet.The filial generation that HF F0 organizes female mouse is HF F1 group, and the generation mice wean continues to feed (high fat 2 generations) with high lipid food.HF F1 and NC F1 organize female mouse and when different foods feed that 8 weeks, ages were big, breed with the male mouse of normal diet nursing, obtain 3 generation mouse (F2).The filial generation that NC F1 organizes female mouse is NC F2 group, and generation mice wean back continues to feed (normal 3 generations) with normal diet.The filial generation that HFF1 organizes female mouse then is a HF F2 group, and the generation mice wean continues to feed (high fat 3 generations) with high lipid food.Concrete model is set up route and is seen Fig. 1.
Mouse is raised and management is undertaken by conventional method, and each week is all write down the consumption of food.
Result: show that through identifying the mouse of adopting high lipid food to feed all presents fat state, for follow-up study is laid a good foundation.
Embodiment 2: high lipid food influenced the generation of striding of C57BL/6 mouse
The male mouse of all experimental group after different foods are fed 3 months, is estimated their each item physical signs and fatty liver pathology index.In the generation of striding of obese degree, insulin resistance and hepatic disease, influence in this model to study.The index system that the present invention adopted:
The detection of the various physiological properties of experiment mice (comprising body weight, blood sugar, liver weight and liver weight/body weight); Adopt the HE decoration method by the adipohepatic degree of each experimental group of certain criterion evaluation; Adopt the Western blotting reaction with the activation level of liver X receptor gene in liver.
1, high lipid food influenced the generation of striding of C57BL/6 mouse each item physical signs
High lipid food and normal diet were fed after 3 months, measured the body weight and the height of each experimental mice, and tail vein measuring blood sugar of blood extracting level.Take by weighing near the fat weight of the dirty weight of liver, epididymis, kidney weight and the cardiac weight of every group of mouse.The result sees table 1.
Table 1: high lipid food is striden generation influence experiment knot to C57BL/6 mouse each item physical signs
Annotate:
compare with the mouse that normal diet is fed; In
and high lipid food are fed F0 generation, compared; In § p＜0.05 and high lipid food are fed F1 generation, compared.
In experimental result shows that high lipid food feeds F0 generation, compared with the normal diet enteral feeding group, and the body weight that shows significance raises, and fat weight and kidney weight raise near the body-mass index, epididymis.Fat weight, kidney weight and cardiac weight and high lipid food are fed F0 generation and have been compared further rising near the epididymis in F1 generation that high lipid food is fed, and the weight of liver is compared with the normal diet enteral feeding group to begin to have more significantly to be increased.Yet F0 generation of feeding than high lipid food in high lipid food is fed F2 generation and F1 are for comparing, and the weight of body weight, body-mass index and liver sharply increases.F2 is because the growth rate increase of F2 causes for the rapid increase of body weight, rather than the food intake increase causes.Simultaneously, the non-fasting blood-glucose in high lipid food F2 generation of feeding and F1 generation is compared the rising that highly significant is all arranged with fasting blood-glucose with the normal diet enteral feeding group.Show that high lipid food strides generation influence, the particularly weight of liver to some physical signs of mouse.
2, high lipid food influenced the generation of striding of mouse sugar tolerance (glucose tolerance)
Glucose tolerance experiment (GTT glucose tolerance test) is a kind of method that detects the mouse blood sugar regulating power.After each experimental mice spent the night on an empty stomach, lumbar injection glucose (1.5g/kg BW) was in measuring blood during respectively at 0,20,40,60 and 120 minute behind the injectable dextrose monohydrate.The result sees Fig. 2
As shown in Figure 2, in F0 generation that F0 generation that high lipid food is fed and normal diet are fed, compared and begins to occur the sugar tolerance, and F1 generation that F2 generation that high lipid food is fed and high lipid food are fed is compared and serious sugar tolerance occurs.Through the experiment of 2 hours glucose tolerances, the blood sugar recovery in F0 generation that high lipid food is fed is to normal level, and the blood sugar in high lipid food is fed F2 generation still is in a high level with the F2 that normal diet is fed for comparing.
3, high lipid food influenced the generation of striding of the plain susceptibility of mouse islets
Insulin resistance experiment (ITT insulin tolerance test) is to detect a kind of method of mouse to insulin sensitivity.With each experiment mice 6 hours on an empty stomach, lumbar injection insulin (0.5U/kg BW), in measuring blood during respectively at 0,20,40,60 and 120 minute behind the insulin injection.The result sees Fig. 3
As shown in Figure 3, in F0 generation that F0 generation that high lipid food is fed and normal diet are fed, compared insulin sensitivity and reduces, and the F2 representative that high lipid food is fed is revealed more serious insulin sensitivity and descended.
4, high lipid food influenced the generation of striding of insulin in the mouse blood (insulin), leptin (leptin) and triglycerides (triglyceride)
With leaving standstill a period of time behind the blood collecting, get the content analysis that serum carries out insulin, leptin and triglycerides after centrifugal.Utilize insulin ELISA Kit and leptin ELISA Kit to detect the two content, with the content of triglycerides Assay Kit detection triglycerides.The result sees Fig. 4.
As shown in Figure 4, in F0 generation of feeding with normal diet enteral feeding group and high lipid food, compared, and the F2 that high lipid food is fed significantly raises for the insulin content in the blood.In addition, F0 generation that high lipid food is fed and F1 are high for the content of the leptin (leptin) in the normal diet enteral feeding group blood, and the F2 that high lipid food is fed is higher for the content of the leptin in the blood (leptin) for the F0 generation and the F1 that feed than high lipid food.Triglycerides (triglyceride) content than the obvious height of normal diet enteral feeding group much in the F1 generation that high lipid food is fed and the F2 blood in generation.
5, high lipid food is striden for influence obesity mice is adipohepatic
Liver is to be a main organ with the metabolic function in the health, and is playing the part of deoxidation in the health the inside, stores glycogen, secreted protein synthetic or the like.When the metabolism in the liver got muddled, too much triglycerides accumulated in liver, will cause the liver fat sex change, and then developed into fatty hepatitis, and cirrhosis and liver cancer take place at last.
With the liver of each experimental mice with 10% neutral formalin fixing after, carry out the routine paraffin wax embedding.Liver section carries out H&E dyeing.Semi-quantitative analysis under the visual field of 400 times of multiplication factors, behind the Olympus BX60 microphotograph that is equipped with CCD, is carried out according to the standard of former research report in 5-7 zone of the liver section picked at random of each mouse.The fatty degeneration of liver proportion is divided into 4 marks: it is 0 that the hepatic parenchymal cells steatosis is lower than 5%, and 5%-30% is 1, and 33%-66% is 2, and being higher than 66% is 3.The fatty degeneration of liver position is divided into 4 marks: only at Zone 3 steatosis being arranged is 0, and at Zone 1 steatosis being arranged is 1, and not subregional steatosis is arranged is 2, and at whole lobuli hepatis steatosis being arranged all is 3.Irritability bubble appearance sex change (ballooning) is divided into 3 marks: not having the sex change of bubble appearance is 0, and a small amount of bubble appearance sex change is 1, and the sex change of great amount of bubbles appearance is 2.The result sees Fig. 5.
Shown in Fig. 5 result, liver shows the so more and more serious morphological feature of bubble appearance steatosis in the F2 generation from the gentle steatosis in F0 generation that high lipid food is fed and F1 generation to the high lipid food nursing.It is more serious that F0 generation that high lipid food is fed and F1 generation and normal diet enteral feeding group are compared fatty degeneration of liver; Do not show as in that Zone 1 is even subregional steatosis arranged; And in high lipid food is fed F2 generation and high lipid food are fed F0 generation, is more serious for comparing fatty degeneration of liver with F1; Showing as whole lobuli hepatis all has steatosis, a large amount of bubble appearance steatosises.
6, high lipid food influenced the generation of striding of liver X receptor α and β
Research shows that LXR has important effect in lipogenesis, glycometabolism and various cell signallings path, especially in glycometabolism.LXR β wide expression is in various organs, and LXR α only is expressed in the vigorous tissue of lipid-metabolism, like liver, intestines, kidney, spleen.The two all combines with retinoids acceptor RXR α to form heterodimer and brings into play function.
Shred after liver downcut, place RIPA buffer solution (green the skies company) ultrasonication.Total protein concentration is with BCA protein quantification standard measure.Behind the albumen process SDS-PAGE electrophoresis of equivalent, be transferred to (U.S. Bio-rad company) on the cellulose membrane.Cellulose membrane through the sealing of 5% skim milk after, hatch with the antibody of anti-PPAR α.Rinsing adds corresponding two anti-hatching again through the cellulose membrane of antibody incubation.After reacting with ECL reagent, the protein band of antibody recognition can be through showing on the X-ray sheet after the overexposure.(U.S. Bio-rad company) carries out quantitative analysis to protein band with Quantity One 1-D analysis software.After the gray scale of a certain protein band calculated, the mean value and the standard deviation of getting a certain expressing quantity of each experimental group, and be standard (being made as 1) with the mean value of normal diet enteral feeding group.The result sees Fig. 6 and Fig. 7.
Like Fig. 6 and shown in Figure 7, compare with the normal diet enteral feeding group, the F0 generation (4.8 times) that high lipid food is fed, F1 generation (7.4 times) and F2 for the increase of (13.2 times) significance the expression of LXR α.Like Fig. 6 and shown in Figure 7, compare with the normal diet enteral feeding group, and the multiple that LXR β expression increases is respectively F1 generation (1.5 times) and F2 generation (8 times)
In sum, the present invention proved under the nursing of same high lipid food, and more the obesity time of occurrence is Zao than the mouse of control group for all fat male filial generation of grandmother and mother, the even more serious and fatty degeneration of liver heighten degree of insulin resistance.Be to be used to study high lipid food from now on to the molecule mechanism of striding the generation influence of liver and the important new model of screening of medicaments target spot.
Claims (7)
- A foundation many generations fat and fatty live lesions methods, it comprises the steps:1) female mouse and the male mouse normal diet fed were fed with normal and high lipid food respectively when 4-6 week, age was big, to obtain F0 for mouse, were NC F0 and HF F0 group; Wherein female mouse breeds utilizing different foods to feed the male mouse of feeding with normal diet to the sexual maturity F0 generation, to obtain F1 for mouse; The filial generation that NC F0 organizes female mouse is NC F1 group, and the filial generation that HF F0 organizes female mouse is HF F1 group;2) the mouse wean with NC F1 group and HF F1 group continues to feed normal and high lipid food respectively, and HF F1 and NC F1 organize female mouse feeding respectively normally and breeding with the male mouse of normal diet nursing after high lipid food to the sexual maturity, to obtain F2 for mouse; The filial generation of the female mouse of NC F1 group is NC F2 group, and the filial generation of the female mouse of HF F1 group then is HF F2 group;3) continue to feed normal and high lipid food respectively after the mouse wean of NC F2 group and HF F2 group.
- 2. method according to claim 1 is characterized in that, the different food feeding times of said male mouse are 3 months.
- 3. method according to claim 1 is characterized in that, the different food feeding times of said female mouse are 1 month.
- 4. according to each described method of claim 1 ~ 3, it is characterized in that said high lipid food accounts for the mouse feed of food total caloric 60% for fat.
- 5. according to each described method of claim 1 ~ 3, it is characterized in that said mouse is the C57BL/6 mouse.
- 6. according to each described method of claim 1 ~ 3, it is characterized in that, also comprise repeating step 2) 1 ~ 3 time.
- 7. according to each described method of claim 1 ~ 3; It is characterized in that also comprising that step 4) male mouse of each generation is after different foods are fed 3 months; Collect its blood and liver samples and carry out each item physical signs, the detection of fatty liver pathology index and molecular biology aspect.
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Cited By (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN103782955A (en) * | 2013-12-25 | 2014-05-14 | 湖南师范大学 | Method for building SD rat alimentary obesity model |
| CN114208776A (en) * | 2022-01-27 | 2022-03-22 | 安徽医科大学 | Construction method of male sterility mouse model |
| CN114600832A (en) * | 2022-04-01 | 2022-06-10 | 西南医科大学 | Mouse heart failure model and preparation method thereof |
-
2011
- 2011-10-18 CN CN2011103164419A patent/CN102499175A/en active Pending
Non-Patent Citations (5)
| Title |
|---|
| CATHERINE GALLOU-KABAN等: "Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods", 《AMERICAN JOURNAL OF PHYSIOLOGY - ENDOCRINOLOGY AND METABOLISM》 * |
| GREGORY A. DUNN: "Maternal High-Fat Diet Effects on Third-Generation Female Body Size via the Paternal Lineage", 《ENDOCRINOLOGY》 * |
| 关光玉等: "酒精性脂肪肝小鼠模型的建立", 《宁夏医学杂志》 * |
| 崔立坤: "长期高脂饲料喂养致小鼠肥胖模型的建立", 《J JINING MED UNIV》 * |
| 汤锦花等: "营养性肥胖大鼠模型的建立及评价", 《同济大学学报》 * |
Cited By (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN103782955A (en) * | 2013-12-25 | 2014-05-14 | 湖南师范大学 | Method for building SD rat alimentary obesity model |
| CN114208776A (en) * | 2022-01-27 | 2022-03-22 | 安徽医科大学 | Construction method of male sterility mouse model |
| CN114208776B (en) * | 2022-01-27 | 2022-11-25 | 安徽医科大学 | Construction method of male sterility mouse model |
| CN114600832A (en) * | 2022-04-01 | 2022-06-10 | 西南医科大学 | Mouse heart failure model and preparation method thereof |
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Application publication date: 20120620 |