34 results about "Wild type mice" patented technology

Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. Also disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse which is unable to absorb maternal IgG in the prenatal or neonatal stage of development Methods of using the transgenic knockout mouse, and cells derived therefrom, are also disclosed.

The invention discloses a novel application of an inhibitor for protein HSD17B13 or coding genes thereof. The novel application provided by the invention particularly means the application of the inhibitor for the protein HSD17B13 or the coding genes thereof in preparation of products for preventing and / or treating fatty liver. Proved by experiments, through immunizing a C57 wild-type mouse by using a recombinant adenovirus carrying an HSD17B13 gene, the condition that the liver of the mouse is subjected to obvious fatty change can be observed, oil red of a slice of the liver is stained and shows the accumulation of a lot of fat, and the content of triglyceride and cholesterol in liver tissues is increased remarkably, so that the HSD17B13 possibly participates in the formation process of fatty liver. The novel application has an important significance in prevention and / or treatment of fatty liver.

The invention discloses a novel application of an inhibitor for protein HSD17B13 or coding genes thereof. The novel application provided by the invention particularly means the application of the inhibitor for the protein HSD17B13 or the coding genes thereof in preparation of products for preventing and / or treating fatty liver. Proved by experiments, through immunizing a C57 wild-type mouse by using a recombinant adenovirus carrying an HSD17B13 gene, the condition that the liver of the mouse is subjected to obvious fatty change can be observed, oil red of a slice of the liver is stained and shows the accumulation of a lot of fat, and the content of triglyceride and cholesterol in liver tissues is increased remarkably, so that the HSD17B13 possibly participates in the formation process of fatty liver. The novel application has an important significance in prevention and / or treatment of fatty liver.

The invention provides a construction method of an SDK2 gene mutation mice model. The mice model comprises the following steps of designing and constructing sgRNA capable of specifically identifying an SDK2 gene on the basis of a CRISPR / Cas9 system, injecting the sgRNA and a targeting vector constructed on the basis of the sgRNA into a mice fertilized egg; and after embryo transplantation, screening out F0-generation mice with SDK2 gene mutation from the output mice, and hybridizing the F0-generation mice with wild type mice to obtain an F1-generation mice model with SDK2 gene mutation. The mice model constructed by the method can be stably passaged, the action mechanism of the SDK2 gene in mice hereditary cataract can be conveniently researched in practical application, and under the condition that human patient research materials are not easy to obtain and are restricted by medical ethics, the SDK2 gene can be stably cloned. The mice model provided by the invention can become an important tool in the research of hereditary cataract, and a research model capable of realizing stable heredity is provided in the research of pathogenesis, treatment methods, drug screening, cataract surgery and the like.

The invention discloses functions and application of responsive to centrifugal force and shear stress gene 1 (RECS1) to treatment of restenosis after vascular injury. An RECS1 knockout mouse and a wild type mouse are taken as experimental subjects, and detection on mouse internal membrane regeneration, vessel wall cell proliferation level and smooth muscle cell phenotype transformation is carried out by a vascular injury model. Detection results prove that by virtue of RECS1 knockout, internal membrane regeneration and cell proliferation can be obviously inhibited, and smooth muscle cells are inhibited to be transformed into synthetic phenotype from contractile phenotype. Therefore, the functions of the RECS1 to the restenosis after vascular injury are mainly embodied in that internal membrane regeneration, cell proliferation and smooth muscle cell phenotype transformation are promoted by the RECS1. Aiming at the functions of the RECS1, the RECS1 can be used as a drug target for screening medicines for preventing, relieving and / or treating the disease of restenosis after vascular injury; an inhibitor of the RECS1 can be used for preparing medicines and arterial stents for preventing, relieving and / or treating the restenosis after vascular injury.

The invention discloses functions and application of SHPS1 in treatment of post-vascular injury restenosis, belonging to the field of functions and applications of genes. SHPS1 gene knockout mice and wild type mice are taken as experimental subjects, and due to a vascular injury model, the mouse neointima formation, vascular wall cell proliferation level and smooth muscle cell phenotype transform are detected. The result proves that SHPS1 gene knockout can obviously promote neointima neogenesis and cell proliferation and promote transformation of smooth muscle cells from a shrinkage manner to a synthetic manner. Thus the functions of SHPS1 in post-vascular injury restenosis are realized, which mainly shows that SHPS1 has the functions of inhibiting neointima formation and cell proliferation and inhibiting smooth muscle cell phenotype transformation. Aiming at the functions of the SHPS1, the SHPS1 can be used for preparing medicines and arterial stents for preventing, relieving and / or treating the post-vascular injury restenosis.

The invention discloses a method for constructing a spontaneous hyperuricemia mouse model. The method for constructing the spontaneous hyperuricemia mouse model provided by the invention comprises the following step: knocking out urate oxidase genes of a target mouse by utilizing transcription activator-like effector nuclease to obtain a homozygote mouse from which the urate oxidase genes are knocked out, namely the spontaneous hyperuricemia mouse model. Experiments prove that the serum uric acid level of the spontaneous hyperuricemia mouse model obtained by the method disclosed by the invention is 3-4 times that of a wild type mouse and achieves the hyperuricemia level, and the pathogenesis of spontaneous hyperuricemia is better simulated. In addition, as the serum uric acid level of the mouse model obtained by the method disclosed by the invention is lower than the ultrahigh-level serum uric acid value reported in the previous literature, the lethal hyperuricemia does not exist, and the survival time of the mouse is long, so that long-term experiment of the mouse is facilitated.

The invention provides a construction method of a mouse lung cancer model. The method includes the steps of: S1, taking C57BL / 6J wild-type mice of 6-8 weeks old, performing adaptation for 1-2 weeks, then putting the mice into a main cabinet of an inhalation exposure cabinet for benzopyrene exposure with the condition parameters of: 5d / week, 5-8h / day, a benzopyrene exposure concentration of 9-12microg / m<3>, and stopping feeding of the mice and allowing free drinking during the exposure; and S2, performing exposure for 23-28 weeks, thus obtaining the mouse lung cancer model. The invention belongs to the field of biotechnology. The method provided by the invention causes no artificial damage to the original structure of the lung, also does not cause infection or other interferences, conformsto the actual environmental exposure way of the human body, can better reflect the actual occurrence of lung cancer in the human body, and is beneficial to the development of lung cancer-related therapeutic drugs.

The invention discloses a function of tumor progress site 2 in treatment of fatty liver and type 2 diabetes as well as an application thereof. According to the invention, TPL2 gene knockout mice and wild type mice are taken as the experiment objects, through a high-fat diet-induced obesity mice model, the result shows that compared with the wild type C 57 mice, body weight of the TPL2 gene knockout mice is mitigated, the fasting blood glucose level is lower than that of a control group WT mice, and the hepatic dysfunction is obviously mitigated. Through intraperitoneal glucose tolerance experiment, the endurance of the TPL2 gene knockout mice on glucose is obviously enhanced. the mice liver tissue cholesterol content change result instructs that TPL2-KO mice fatty liver pathology of a HFD group (High fat diet) is obviously mitigated, and the lipid accumulation is obviously reduced. TPL2 can be taken as a drug target for treating fatty liver and / or type 2 diabetes, and its inhibitor can be used for preparing a drug to treating fatty liver and / or type 2 diabetes.

The invention provides a construction method of a mouse model with conditional mTERT overexpression and an application thereof. The construction method comprises the following steps: constructing a targeting vector through a seamless cloning technology, wherein the targeting vector comprises a 3.3 kb 5'homologous arm, a CAG promoter, loxp-stop-loxp, TERT-3XFlag-IRES-EGFP-WPRE-polyA and a 3.3 kb 3'homologous arm; cas9 mRNA, gRNA and the targeting vector are microinjected into fertilized eggs of wild type mice to obtain F0-generation mice, homologous recombination positive F0-generation mice are identified, F1-generation mice are obtained through breeding after backcross, and the F1-generation mice are conditional mTERT overexpressed mouse models. The mouse constructed by the construction method provided by the invention can mate with different Cre tool mice to realize specific overexpression in various tissues, organs and cell types of the whole body. The mouse can be used for modeling various transgenic models for researching embryo and nerve development, senescence, wound repair, tumor occurrence, development and treatment, and the mating of the mouse and a CreERT tool mouse can control the time of TERT overexpression through tamoxifen.

The invention discloses a CAMSAP1 protein and the application of a gene thereof as an epileptic drug target. The 13th exon of CAMSAP1 is selected as a target site, and a wild mouse is knocked out through a homologous recombination method to acquire a knocked-out mouse. Experiments prove that compared with wild type mice, the knocked-out mouse is small in size and light in weight, and the death rate is increased. The CAMSAP1 protein is knocked out to change the polarity of neurons. The knocked-down CAMSAP1 protein can influence the transformation of neurons from multipolar cells to bipolar cells, resulting in abnormal migration of neurons along radial glial cells (the migration of neurons is influenced), and abnormal layered arrangement of neurons in cerebral cortex. The knocked-out CAMSAP1protein can cause epilepsy. Therefore, the CAMSAP1 protein can maintain normal growth of neurons and prevent and / or treat epilepsy. The CAMSAP1 protein and the application, which are provided by theinvention, have an important application value.

The invention relates to a construction method of a congenital cataract disease animal model, which comprises the steps of firstly, designing a gRNA target site sequence for a second exon region of a mouse GJA8 gene, amplifying a homologous arm and a cKO region, and respectively connecting the homologous arm and the cKO region to a vector; injecting positive clones into blastula by electroporation ES cells of the constructed plasmids, transferring the blastula into a mouse body, and obtaining a first builder mouse after a birth mouse is mature; mating with a wild type mouse to obtain a heterozygote mouse F1 generation with gene mutation; finally, mating the F1 generation of heterozygote mice with the same genotype to obtain F2 generation of gene mutation homozygote mice. According to the construction method of the congenital cataract disease animal model provided by the invention, typical characteristics of congenital cataract, such as crystalline lens degeneration opacity and crystalline lens epithelial apoptosis, can be obtained, the animal model can be used for researching congenital cataract diseases and screening medicines for treating the congenital cataract diseases, and application prospect is promising.

The invention discloses application of PSMB8 and a PSMB8 inhibitor to preparation of medicine for treating fatty liver and related diseases. Primary hepatocytes of C57BL / 6 wild type mice and PSMB8 knock-down C57BL / 6 mice are separated; the functions of PSMB8 gene are studied by a palmitate and oleic acid stimulation induced liver cell lipid accumulation model. The result proves that when the PSMB8expression is lowered, the PA+OA stimulation induced primary hepatocyte lipid accumulation is obviously reduced, i.e., the PSMB8 gene can promote the development and progression of fatty liver and related diseases; in an HFHC (high fat and high cholesterol) induced WT mouse fatty liver disease model, PR-957 can obviously inhibit HFHC induced weight increase, white grease increase and liver lipidaccumulation; the development and progression of the fatty liver and related diseases are inhibited. Therefore the PSMB8 provides a target for developing medicine for preventing, relieving and / or treating the fatty liver and related diseases.

The invention discloses an application of USP10 in hepatic ischemia reperfusion injury. A USP10 gene knockout mouse and a C57BL / 6 wild type mouse are selected as experimental subjects, mouse hepatic ischemia reperfusion injury models are constructed respectively, the function of USP10 in hepatic ischemia reperfusion injury is researched, the new function of the USP10 gene in hepatic ischemia reperfusion injury is found, and the application of the USP10 gene in hepatic ischemia reperfusion injury is developed. The over-expression of the USP10 can relieve the hepatic ischemia reperfusion injury by inhibiting inflammation and cell apoptosis, so that the USP10 can be applied to the preparation of the medicine for preventing / treating the hepatic ischemia reperfusion injury, and a new medicine target is provided for the hepatic ischemia reperfusion injury.

The invention belongs to the technical field of experimental models, relates to a medicament for intervening in an inflammation related chemically induced pancreatic cancer animal model, and in particularly relates to application of caerulin in preparing a sensitizing preparation for synergizing dimethylbenzanthracene (DMBA) to induce a pancreatic cancer animal model. According to the application, an effective sensitizing preparation is provided to a medicament DMBA for inducing a C57 wild type mouse pancreatic cancer model, and the prepared animal model is an ideal tool for further studying pancreatic precancerous lesions and pancreatic cancer; by virtue of the synergetic effect of caerulin, the experiment cycle can be shortened, the experiment efficiency can be improved, and the experiment cost can be saved; occurrence and development of multiple steps in the process of intervening in the pancreatic cancer animal model and changes of histology are extremely similar to the developing process of pancreatic cancer of human beings, so that normal pancreas ductal epithelium, atypical hyperplasia of pancreas ductal epithelium, carcinoma in situ of pancreas ductal epithelium and invasive pancreatic cancer in the pancreatic cancer developing process can reappear.

The invention relates to the technical field of animal model construction, in particular to a construction method and application of a glycogen accumulation disease Ib type gene point mutation mouse model. A homozygous mouse model with SLC37A4 gene point mutation is obtained by a method of hybridizing a heterozygous mouse with the SLC37A4 gene point mutation with other strains of wild type mice, and is used for truly simulating clinical diseases of patients with glycogen accumulation disease Ib caused by SLC37A4 gene defects due to the SLC37A4 gene point mutation. The point mutation mouse model obtained by adopting the construction method can be applied to research on pathogenesis of the glycogen accumulation disease Ib and development of drugs for treating the glycogen accumulation disease Ib.

The invention provides a construction method of a mouse lung cancer model. The method includes the steps of: S1, taking C57BL / 6J wild-type mice of 6-8 weeks old, performing adaptation for 1-2 weeks, then putting the mice into a main cabinet of an inhalation exposure cabinet for benzopyrene exposure with the condition parameters of: 5d / week, 5-8h / day, a benzopyrene exposure concentration of 9-12microg / m<3>, and stopping feeding of the mice and allowing free drinking during the exposure; and S2, performing exposure for 23-28 weeks, thus obtaining the mouse lung cancer model. The invention belongs to the field of biotechnology. The method provided by the invention causes no artificial damage to the original structure of the lung, also does not cause infection or other interferences, conformsto the actual environmental exposure way of the human body, can better reflect the actual occurrence of lung cancer in the human body, and is beneficial to the development of lung cancer-related therapeutic drugs.

The invention relates to the technical field of cancer animal model establishment, in particular to a primary mouse liver cancer model based on liver oval cell malignancy and an establishment method and an application thereof. The establishment method comprises the following steps: transforming liver oval cells by using a proto-oncogene to obtain liver cancer stem cells; performing in-situ transplantation on the liver cancer stem cells to the liver of a receptor mouse to obtain a primary mouse liver cancer model; wherein the acceptor mouse is a wild type mouse subjected to X-ray irradiation treatment. According to the scheme, aiming at the limitation of the existing primary liver cancer animal model, a novel primary model for simulating the whole occurrence and development natural process of the primary liver cancer is established, so that the effect and mechanism of a specific gene in the occurrence and development of the primary liver cancer can be accurately researched, and whether the gene can be used as an effective treatment target or not is verified. By utilizing the model in the scheme, potential new targets and new drugs for treating the primary liver cancer can be screened, and conditions are created for researching and developing novel drugs or treatment methods for treating the primary liver cancer.

The invention provides a plaque corneal dystrophy animal model, a construction method of a gene therapy vector and a delivery system, and relates to the technical field of model construction. According to the animal model, animal Chst5 genes are knocked out from corneal endothelium in an anterior chamber injection mode or through Chst5R50H point mutation, and compared with an existing animal model, the eye symptom similarity is higher. The invention also provides a gene therapy vector which is realized by injecting the adeno-associated virus vector into the anterior chamber to carry the wild type mouse Chst5 gene. In the embodiment of the invention, the treatment of plaque corneal dystrophy can be realized by injecting the gene therapy vector into the anterior chamber of the mouse model.

The invention relates to the technical field of medicines, and provides a new application of a beta-arrestin-1 protein. The new application is the application of the beta-arrestin-1 in preparing a medicine or a health care product for preventing or treating myocardial infarction. Experiments prove that the myocardial infarction area of a mouse is outstandingly increased after the beta-arrestin-1 is knockout, the myocardial infarction area is outstandingly decreased after the beta-arrestin-1 is extremely expressed; in addition, left ventricular ejection fraction and left ventricular fractional shortening are obviously lower than those of a wild type mice group after the beta-arrestin-1 is knockout, and the left ventricular ejection fraction and the left ventricular fractional shortening are outstandingly enhanced after the beta-arrestin-1 is extremely expressed. Thus, the beta-arrestin-1 plays a protective role in the prognosis of the myocardial infarction.

The invention discloses application of TRPV1 in screening or preparing medicines for preventing, relieving and / or treating liver diseases, and belongs to the field of functions and application of genes. According to the application, TRPV1 gene overexpressed and knocked-out C57 / BL mouses are taken as experimental subjects, and through research on an acute liver injury model, a hepatic fibrosis model, a non-alcoholic fatty liver model and an alcoholic fatty liver model, results show that compared with a control group mouse, the TRPV1 gene overexpressed mouse is obviously inhibited in liver injury and obviously improved in liver function; and compared with a wild type mouse, the liver pathological injury of the TRPV1 gene knockout mouse is obviously aggravated, and the liver function is obviously deteriorated. Aiming at the functions of the TRPV1, the expression of the TRPV1 gene can be promoted through a specific agonist or an overexpression system of the TRPV1 so as to interfere with liver diseases such as liver inflammation, liver fibrosis and the like.

The invention discloses application of HAP1 in screening neuroinflammation treatment drugs, and belongs to the technical field of biological medicines. According to the invention, an HAP1 wild type mouse is selected as a control group, an HAP1 heterozygote mouse is selected as an experimental group, neuropathologic acute pain is constructed, and postoperative inflammatory responses of the two groups of mice are respectively detected. Results show that by reducing the expression of the HAP1, the inflammatory response can be obviously reduced, the activation level of glial cells is reduced, and the release of inflammatory factors is inhibited; and finally, the effect of controlling neuroinflammation is achieved. The discovery can provide a new molecular target for pain research.

The invention discloses a method for obtaining mouse haploid stem cells. The method comprises the following steps of: 1, injecting p53 knocked-out mouse haploid embryonic stem cells into a wild type mouse blastocyst by a microinjection method to obtain a reconstructed embryo; step 2, transplanting the reconstructed embryo back to an oviduct of a 0.5-day false pregnant female mouse or a uterus of a2.5-day false pregnant female mouse, performing dissecting when the embryo develops to E6.5 days, and separating an epiblast area; and step 3, culturing the epiblast region in a culture medium to finally form the mouse haploid epiblast stem cells. According to the invention, through a p53-KO method, spontaneous doubling of haploid stem cells in an in-vivo differentiation process is effectively inhibited, and a mouse haploid epiblast stem cell line derived from implanted epiblast tissue is successfully established in vitro by a chimeric technology.

The invention discloses a pemphigus vulgaris animal model construction method, which comprises the following steps: carrying out primary immunization / booster immunization on a wild type mouse by using a vaccination technology and taking desmoplasmin 3 as a vaccine antigen, starting to appear phenotypes within 28-35 days, including blisters, epidermis exfoliation and skin ulceration on the rear feet and the tail of the mouse with the overall phenotype; a serum autoantibody; the pemphigus vulgaris immunotherapy kit has the advantages that pemphigus vulgaris changes such as epidermis spinous layer debonding and antibody deposition in histological examination are simulated, part of mice have disease phenotypes such as local skin unhairing, fester and canthus conjunctivitis, clinical symptoms of pemphigus vulgaris are simulated, and an important tool is provided for pemphigus vulgaris immunotherapy.

The invention discloses a function of transcription induction spermiogenesis gene 40(Tisp40) in treatment of angiostenosis after damage and an application thereof. The application is characterized in that Tisp40 gene knockout mice and wild type mice are taken as experiment objects, through a vascular injury model, detection of mice neointima formation, vessel wall cell proliferation level and smooth muscle cell phenotype transition can be carried out. The result shows that Tisp40 gene knockout can obviously inhibit neointima formation and cell proliferation, and can inhibit transition of contractile smooth muscle cell to synthetic smooth muscle cell. The function of Tisp40 gene in angiostenosis after damage mainly embodies as promotion of neointima formation, cell proliferation and smooth muscle cell phenotype transition. By aiming at the function of Tisp40, Tisp40 can be used as a medicine target for screening the medicines for preventing, alleviating and / or treating angiostenosis after damage. A inhibitor of Tisp40 can be used for preparing the medicine and arterial stent for preventing, alleviating and / or treating angiostenosis after damage.

The invention relates to the field of inner ear stem cells, in particular to a method for regulating proliferation and differentiation of inner ear stem cells through Rassf2 and application of Rassf2 in hair cell regeneration. The regulation and control method comprises the following steps: 1, detecting expression conditions of Shh or Hippo and Rassf2 in cochlea in a wild type mouse; 2, studying the effect of Shh or Hippo and Rassf2 on proliferation and differentiation of the inner ear stem cells which are separated in a flow mode in an in-vitro experiment; 3, researching the effects of Shh or Hippo and Rassf2 on a living hair cell neomycin injury model. By using the Lgr5-EGFP-CreERT2 tool mouse, the separation of the inner ear stem cells (Lgr5 positive cells) is accurate and a large amount of the inner ear stem cells (Lgr5 positive cells) can be realized, and a relatively good research premise can be achieved: the Lgr5 positive inner ear stem cells of the mouse are sorted. Besides, after the separated inner ear stem cells are subjected to balling and differentiation experiments by researching Shh, Hippo and Rassf2 in an in-vitro experiment, the specific action mechanism of Shh, Hippo and Rassf2 in regulation and control of proliferation and differentiation of the inner ear stem cells and hair cell regeneration can be deeply explored.

The invention relates to the field of biological medicines, in particular to a method for marking adjacent astrocytes, which is used for solving the problems of low efficiency, high technical difficulty and difficulty in popularization and application of dual fluorescence marking in the prior art, and can further realize multiple fluorescence marking. The method mainly comprises the steps of plasmid construction, virus packaging, virus injection and image acquisition, in the plasmid construction step, different fluorescent proteins are inoculated into skeleton plasmids, then plasmids containing target genes and pHelper plasmids of AAV5 are co-transfected into a human embryo kidney cell line (AAV-293) to complete virus packaging, during virus injection, P0 or P1 wild type mice are adopted, after the virus is expressed for 2-4 weeks, operations such as perfusion sampling and the like are carried out, so that a multi-brain region is reached, and the marking of adjacent astrocytes is efficiently completed.

The invention discloses application of PSMB8 and a PSMB8 inhibitor to preparation of medicine for treating fatty liver and related diseases. Primary hepatocytes of C57BL / 6 wild type mice and PSMB8 knock-down C57BL / 6 mice are separated; the functions of PSMB8 gene are studied by a palmitate and oleic acid stimulation induced liver cell lipid accumulation model. The result proves that when the PSMB8expression is lowered, the PA+OA stimulation induced primary hepatocyte lipid accumulation is obviously reduced, i.e., the PSMB8 gene can promote the development and progression of fatty liver and related diseases; in an HFHC (high fat and high cholesterol) induced WT mouse fatty liver disease model, PR-957 can obviously inhibit HFHC induced weight increase, white grease increase and liver lipidaccumulation; the development and progression of the fatty liver and related diseases are inhibited. Therefore the PSMB8 provides a target for developing medicine for preventing, relieving and / or treating the fatty liver and related diseases.

Doxorubicin (Dox), a potent anti-cancer drug, can cause cardiac dysfunction and failure. Endogenous Fibroblast Growth Factor-2 (FGF2), a protein implicated in cardioprotection, regulates cardiac vulnerability to Dox. In wild type mice and in humans, cardiac FGF2 is composed of a mixture of mostly high (Hi-) but also low (Lo) molecular weight isoforms and is produced mainly by non-myocytes. We compared wild type mice, FGF2(WT), to mice genetically engineered as to express: no FGF2, FGF2(−); only Hi-FGF2, FGF2(Hi); only Lo-FGF2, FGF2(Lo). Sole expression of endogenous L0-FGF2 in vivo, or by fibroblasts in vitro, protects cardiomyocytes from Dox. In a wild type environment, neutralization of endogenous Hi-FGF2 presents a potential prophylactic treatment against Dox-induced cardiotoxicity.

The invention relates to novel application of puer tea, in particular to application of the puer tea for eliminating formaldehyde biological damage. In the invention, a deep experimental research is carried out, and a wild type mouse embryo fibroblast (MEF) is utilized to test the killing action of the formaldehyde to normal cells and the protection action of the puer tea to the normal cells; the cells are massively dead after being treated with 100-300 micron mol / L formaldehyde; however, only a few cells under the protection of puer tea extract which is added in advance are dead after being treatment with formaldehyde with the same concentration. Meanwhile, an Annexin V-FITC cell apoptosis detection kit is used for detecting apoptosis of cells treated with formaldehyde and the protection action of the puer tea. Clearly proved by test data, the puer tea can efficiently prevent death of the normal cells, caused by the formaldehyde, and discloses the control effect of the puer tea to the formaldehyde biological damage.