兔眼葡萄膜炎时肿瘤坏死因子的改变

采用玻璃体内注射内毒素脂多糖的方法制作兔葡萄膜炎模型，检测了房水内细胞浓度、蛋白浓度、房水及血清中肿瘤坏死因子含量的改变。结果显示葡萄膜炎模型兔房水中细胞数、蛋白浓度分别为（９．４６７±１．５６８）×１０９／Ｌ、（２５．５３１±４．６３５）ｇ／Ｌ，显著高于对照组的（０．００２±０．００２）×１０９／Ｌ（Ｐ＜０．０１）；房水中肿瘤坏死因子浓度为（４．６４３±０．５９１）ｎｇ／Ｌ，显著高于血清中的（０．０１２±０．００４）ｎｇ／Ｌ（Ｐ＜０．０１）；而对照组房水及血清均未测到。提示兔眼葡萄炎模型符合人类葡萄炎的病理特征，眼组织内产生的肿瘤坏死因子－α参与了葡萄膜炎的病理过程。

Establishment of VX2 breast carcinoma model in rabbit by injecting tumor mass suspension

Objective: To establish a stable model of VX2 breast carcinoma in rabbit and select the optimal way. Methods: Thirty female New Zealand rabbits were randomly divided into 3 groups with 10 in each. Tumor cell suspensions or tumor mass suspensions were injected into breast tissues of rabbits of group A and B, respectively. Tumor blocks were surgically implanted in rabbit breasts of group C. Tumor formation rate, tumor growth rate, and tumor-bearing survival time was compared, and the histological feature of tumor was observed. Results: Models were established conveniently and successfully in rabbits received injection of tumor mass suspensions. Tumor proliferated rapidly with the biological feature of squamous cell carcinoma. Conclusion: VX2 breast carcinoma model in rabbit was established successfully. Intramammary injection of tumor mass suspension is the best method.

Trans-arterial gene therapy for hepatocellular carcinoma in a rabbit model

AIM： To study the effect of adenovirus （Ad）-p53 gene therapy on hepatocellular carcinoma （HCC） in a rabbit model.METHODS： VX2 tumor was grown in the liver of 24rabbits. Animals were divided into four groups： group A receiving trans-arterial gene therapy （Ad-p53） only,group B receiving combined Ad-p53 therapy and transarterial embolization （lipiodol）, group C receiving transarterial chemoembolization （lipiodol ＋ mitomycin C）,control group （D） receiving sodium chloride. Tumor volume （V1） was measured by using MRI （d 13）.Interventional procedure was applied （d 14）.Tumor volume （V2） was assessed by MRT （d 21） and the mean ratio （V2/V1） was calculated. After the second MRI,specimens of the liver were abstained and examined immunohistochemically using mutant-type p53 antibody.The positive expression was scored.RESULTS： Compared with control group （（^-x） = 3.14± 0.64）, therapeutic groups all showed a significant decrease in the tumor growth ratio （P 〈 0.05）. A slight difference was found between group A （（^-x） =2.35 ±0.59） and group B （（^-x） = 1.75 ± 0.28） （P = 0.048）. Nostatistically significant difference was observed between group B and group C （（^-x） = 2.00 ± 0.44）. The positive expression rate of mutant-type p53 was the lowest in group B and significantly different between group A and group C （P 〈 0.05）.Compared to the control subjects, groups A and C both showed a decrease in the expression of mutant-type p53, but there was no significant difference between them.CONCLUSION： Trans-arterial Ad-p53 gene therapy can reduce tumor growth of HCC in rabbit model.

Establishment of a chronic left ventricular aneurysm model in rabbit

Objectives To establish a cost-effective and reproducible procedure for induction of chronic left ventricular aneurysm （LVA） in rabbits. Methods Acute myocardial infarction （AMI） was induced in 35 rabbits via concomitant ligation of the left anterior descending （LAD） coronary artery and the circumflex （Cx） branch at the middle portion. Development of AMI was co n-firmed by ST segment elevation and akinesis of the occluded area. Echocardiography, pathological evaluation, and agar i n-tra-chamber casting were utilized to validate the formation of LVA four weeks after the surgery. Left ventricular end systolic pressure （LVESP） and diastolic pressure （LVEDP） were measured before, immediately after and four weeks after ligation. D i-mensions of the ventricular chamber, thickness of the interventricular septum （IVS） and the left ventricular posterior wall （LVPW） left ventricular end diastolic volume （LVEDV） and systolic volume （LVESV）, and ejection fraction （EF） were recorded by echo-cardiography. Results Thirty one （88.6%） rabbits survived myocardial infarction and 26 of them developed aneurysm （83.9%）. The mean area of aneurysm was 33.4% ＆#177; 2.4% of the left ventricle. LVEF markedly decreased after LVA formation, whereas LVEDV, LVESV and the thickness of IVS as well as the dimension of ventricular chamber from apex to mitral valve annulus significantly increased. LVESP immediately dropped after ligation and recovered to a small extent after LVA formation. LVEDP progressively increased after ligation till LVA formation. Areas in the left ventricle （LV） that underwent fibrosis included the apex, anterior wall and lateral wall but not IVS. Agar intra-chamber cast showed that the bulging of LV wall was prominent in the area of aneurysm. Conclusions Ligation of LAD and Cx at the middle portion could induce develo pment of LVA at a mean area ratio of 33.4%＆#177;2.4%which involves the apex, anterior wall and lateral wall of the LV.

An Inactivated Vaccine from a Field Strain of Bovine Herpesvirus-1(BoHV-1) has High Antigenic Mass and Induces Strong Efficacy in a Rabbit Model

Bovine Herpesvirus-1 （BoHV-1） is a DNA virus belonging to the family Herpesviridae, subfamily Alfaherpesvirinae; it is a worldwide pathogen, causing serious economic losses in livestock. In Colombia there have been multiple isolates of BoHV-1 that have been subjected to molecular characterization, classifying most of the country isolates as BoHV-I.1. In the present study we developed and evaluated an ethyleneimine binary inactivated isolate from the native BoHV-1 strain （C6rdoba-2） in a rabbit model of vaccination and infection. The vaccine was evaluated in two phases, one of immunogenicity with vaccination and a booster after 21 days, and an evaluation phase of protection against challenge with a highly virulent reference strain. The results demonstrate optimum serum-conversion, with protective neutralizing antibody titers 28 days post vaccination and optimal protection against challenge with the reference strain with decreased clinical signs of infection, protection against the onset of fever and decrease of virus excretion post challenge. In conclusion, our results show the enormous potential that an immunogenic inactivated vaccine has produced from the native BoHV-I.1 strain, which produces a high antigen mass to the vaccine to induce optimal immunity and protection, and it is a strong candidate for evaluation and possible future use in different cattle populations.

Effect of ALA-PDT on the expressions of MMP-9, MMP-13 and TIMP-1 of hypertrophic scar model in rabbit ears

Objective: To investigate the effect of 5-aminolevulinic(ALA)-photodynamic therapy(PDT) on the expressions of MMP-9, MMP-13 and TIMP-1 of hypertrophic scar model in rabbit ears, and analyze the possible therapeutic mechanisms of ALA-PDT treatment to hypertrophic scars of rabbit ears. Methods: The experimental animals were randomly divided into normal control, negative control, high concentration of ALA-PDT, low concentration of ALA-PDT and PDT groups. The latter three groups received ALA-PDT treatment or PDT treatment once a week for 3 weeks. The specimens of the rabbits were collected respectively 1, 2 and 3 months after treatment to be used for RT-PCR and Western-blot test. Results: 1, 2 and 3 months after PDT treatment, the expressions of MMP-9 and MMP-13(including mRNA and protein) in hypertrophic scar tissues of three treatment groups were significantly higher than those of the negative control group(P<0.01), and the expression of TIMP-1 mRNA and protein of three treatment groups were significantly lower than that of the negative control group(P<0.01). There were also significant differences between high-concentration ALA-PDT treatment group and the low one(P<0.05). Conclusion: ALA-PDT is effective in treating hypertrophic scars of rabbit ears, and its possible therapeutic mechanisms are that ALA-PDT treatment generates oxidation activation effect to activate the activity of MMPs and induces the photoaging of fibroblasts of hypertrophic scar tissues of rabbit ears to inhibit the activity of TIMPs, which causes the up-regulation of MMPs and the down-regulation of TIMPs. Because of this, the degradation of collagen and ECM is accelerated and the formation of scars is suppressed.

Local administration of liposomal adriamycin inhibited proliferation of metastatic cells in axillary lymph nodes in rabbit breast cancer model

Objective： To assess the inhibitory effects of liposomal adriamycin （LADR） locally injected into mammary glands of VX2 tumor-bearing rabbits on proliferation of lymph nodal metastatic cells. Methods： Twenty-one VX2 tumor-bearing rabbits were randomly and equally divided into 3 groups. Rabbits were randomized to receive sham treatment （Group I）, subcutaneous LADR around tumor （Group Ⅱ） and intravenous free adriamycin （Group Ⅲ）, respectively. Breast tumor and axillary lymph nodes were harvested after 3 repeated treatment. Nodal sizes of both pre-and post-treatment were measured. Proliferating cell nuclear antigen （PCNA） mRNA in both tumor and lymph nodes were determined by RT-PCR. Results： The mean size of axillary lymph nodes in Group I, Ⅱ and Ⅲ increased by 3.70%, 1.55% and 2.89%, respectively, with significant difference between Group Ⅲ and I （P=-0.004） and between Group Ⅱ and Ⅲ（P=-0.002）. Relative expression values of PCNA mRNA in breast tumors of Group I, Ⅱ and Ⅲ were 0.486, 0.513 and 0.396, respectively. For Group Ⅲ, PCNA mRNA was significantly less expressed than that in Group I （P=-0.023） and Ⅱ（P=0.005）. Relative expression values of PCNA mRNA in axillary lymph nodes of Group I, Ⅱ and Ⅲ were 0.541, 0.329 and 0.450, respectively. Compared with Group I, Group Ⅲ showed a markedly decreased expression of PCNA （P=-0.021）. The least level ofPCNA mRNA was found in Group Ⅱ, with a significant difference from that in Group Ⅲ（P=-0.004）. Conclusion： Local injection of LADR was an effective therapeutic regimen for lymphatic metastases from breast cancer, regardless of its little effect on primary tumor.

The effect of body weight on the induction of mild hypothermia in a rabbit model of asphyxia cardiac arrest

Objective To investigate the effect of body weight on the induction of mild hypothermia in a rabbit model of asphyxia cardiac arrest. Methods Twenty-four rabbits were randomized into two groups： the ice bag group and the intravenous 4℃ saline group. Cardiac arrest was induced and after 3 minutes of cardiac arrest, cardiopulmonary resuscitation was begun. Simultaneously, mild hypothermia was induced by putting an ice bag over the abdomen or infusion of 4℃ saline via an ear vein. A 2℃ decrease of rectal temperature was considered as the completion of hypothermia induction. Induction times were recorded, compared, and analyzed with respect to body weight. Results All rabbits had restoration of spontaneous circulation （ROSC） and ROSC lasted during the experiment. Induction time in the ice bag group was significantly shorter than that in the intravenous 4℃ saline group （22.8 ± 4.7 min VS 42.5 ± 4.0 min, P〈 0.001）. Induction time significantly correlated with body weight in the ice bag group （Pearson Correlation： r = 0.725, P = 0.029）, but not in the intravenous 4℃ saline group （Pearson Correlation： P = 0.418）. Conclusions In a rabbit model, induction of mild hypothermia with an ice bag is faster than with intravenous 4~C saline; induction time positively correlates with body weight when an ice bag is used, but not when intravenous 4℃ saline used. The effect of body weight should be considered when choosing an appropriate method to achieve early induction of mild hypothermia

Development and characterization of urethral stricture model in rabbits

Objective： To establish an experimental model of urethral stricture in rabbits. Methods： A total of 21 adult male New Zealand rabbits were included into group. After intravenous anesthesia, urethroscopy was performed with a pediatric resectoscope （F13）. Fifteen animals were randomly selected as the study group. A lcm-long circumferential electrocoagulation of the bulbar urethra was performed to these animals until ulceration of the mucosa. The remaining 6 animals underwent video urethroscopy without electrocoagulation, serving as controls. On the 30th day, retrograde urethrogram and urethroscopy were performed to evaluate urethral stricture formation, histological examinations （HE and Sirius Red staining） were done to assess urethral pathological change. Results： Two rabbits in study group died and no death occurred in controls. Based on urethrogram and urethroscopy, no rabbits in control group developed urethral stricture, while significant stricture formation was observed in every case of the study group. Histological examination showed a normal urethra in control cases, while at stricture site of the study group extensive fibrosis of muscle and submucous tis High collagen expression in fibrosis tissue was assayed sue by was observed with a large number of fibroblasts infiltration Sirius Red staining. Conclusion： A lcm-long endoscopic electrocoagulation can successfully induce urethral stricture formation in rabbit models. This method offers an ideal animal model for the fundamental and clinical study of urethral stricture

Effects of nerve growth factor on delayed afterdepolarization and triggered activity in the infarcted ventricle of rabbit model

The noninfarcted myocardium underwent significant electrophysiological remodelling as part of the healed myocardial infarction remodelling. This study aimed at investigating the effects of nervous growth factor （NGF） on delayed afterdepolarizations （DADs） and triggered activity （TA） of the noninfarcted myocardium in the myocardial infarcted rabbit model. Rabbits with the left anterior descending coronary artery occlusion were prepared and recovered for 8 weeks （HMI group, n=9）. Other rabbits with myocardial infarction were infused NGF to the left stellate ganglion （HMI＋NGF group, 400 U/day for 8 weeks, n=8）. Myocytes were isolated from regions of the noninfarcted left ventricular free wall. Action potentials and ion currents were recorded with whole-cell patch clamp. The results showed that more DADs and TA events of HMI＋NGF myocytes than that of HMI and Ctrl group. Iti and ICa-L of NGF＋HMI myocytes were increased significantly compared with HMI and Ctrl cells, which contributed to DADs-related triggered arrhythmia. Comparing with HM1 and Ctrl myocytes, significant prolongations of APD50 and APD90 in HMI＋NGF myocytes were found. The results indicated the electrophysiological change of HMI myocytes with NGF infusion. It suggested that more events of DADs and TA in HMI myocytes with NGF treatment. The underlying mechanism may be involved in the increase of Iti and ICa-L.

Endostatin inhibits hypertrophic scarring in a rabbit ear model

Objective： The present study was designed to use an in vivo rabbit ear scar model to investigate the efficacy of systemic administration of endostatin in inhibiting scar formation. Methods： Eight male New Zealand white rabbits were randomly assigned to two groups. Scar model was established by making six full skin defect wounds in each ear. For the intervention group, intraperitoneal injection of endostatin was performed each day after the wound healed （about 15 d post wounding）. For the control group, equal volume of saline was injected. Thickness of scars in each group was measured by sliding caliper and the scar microcirculatory perfusion was assessed by laser Doppler flowmetry on Days 15, 21, 28, and 35 post wounding. Rabbits were euthanatized and their scars were harvested for histological and proteomic analyses on Day 35 post wounding. Results： Macroscopically, scars of the control group were thicker than those of the intervention group. Significant differences between the two groups were observed on Days 21 and 35 （p〈0.05）. Scar thickness, measured by scar elevation index （SEI） at Day 35 post wounding, was significantly reduced in the intervention group （1.09±0.19） compared with the controls （1.36±0.28）. Microvessel density （MVD） observed in the intervention group （1.73±0.94） was significantly lower than that of the control group （5.63±1.78） on Day 35. The distribution of collagen fibers in scars treated with endostatin was relatively regular, while collagen fibers in untreated controls were thicker and showed disordered alignment. Western blot analysis showed that the expressions of type I collagen and Bcl-2 were depressed by injection of endostatin. Conclusions： Our results from the rabbit ear hypertrophic scar model indicate that systemic application of endostatin could inhibit local hypertrophic scar formation, possibly through reducing scar vascularization and angiogenesis. Our results indicated that endostatin may promote the apoptosis of endothelial cells and block their release of platelet-dedved growth factor （PDGF） and fibroblast growth factor （FGF）, thereby controlling collagen production by fibroblasts. Blood vessel-targeted treatment may be a promising strategy for scar therapy.

Creation of a rabbit model for intrauterine adhesions using electrothermal injury

The pathogenesis and therapeutic treatment of intrauterine adhesions （IUAs） remain unsolved, highlighting the need for stable and effective experimental animal models. In this study, uterine electrocoagulaUon of twenty-one female New Zealand White rabbits was carried out to establish an IUA model. As rabbits have two completely separate uterine horns, each rabbit had its own internal control： one uterine horn was given an electrothermal injury （Group A, n=21）, and the contralateral uterine horn received no treatment and served as the control （Group B, n=21）. The en- dometrial morphology, number of endometrial glands, area of endometrial fibrosis, and number of implanted fetuses were compared between the two groups. In Group A, the numbers of endometrial glands on Days 7 and 14 and the number of implanted fetuses were significantly lower than those in Group B（P〈0.05, P〈0.05, and P〈0.01, respectively）, while the ratio of the area with endometrial stromal fibrosis to the total endometrial area was significantly increased （P〈0.01）. These results suggest that this method of electrothermal injury is effective for the establishment of a rabbit lUA model between 7 and 14 d after surgery.

Simultaneous quantification of hepatic MRI-PDFF and R2* in a rabbit model with nonalcoholic fatty liver disease

Quantification of hepatic fat and iron content is important for early detection and monitoring of nonalcoholic fatty liver disease(NAFLD) patients. This study evaluated quantification efficiency of hepatic proton density fat fraction(PDFF) by MRI using NAFLD rabbits. R2* was also measured to investigate whether it correlates with fat levels in NAFLD. NAFLD rabbit model was successfully established by high fat and cholesterol diet. Rabbits underwent MRI examination for fat and iron analyses,compared with liver histological findings. MR examinations were performed on a 3.0 T MR system using multi-echo 3 D gradient recalled echo(GRE) sequence. MRI-PDFF showed significant differences between different steatosis grades with medians of3.72%(normal), 5.43%(mild), 9.11%(moderate) and 11.17%(severe), whereas this was not observed in R2*. Close correlation between MRI-PDFF and histological steatosis was observed(r=0.78, P=0.000). Hepatic iron deposit was not found in any rabbits. There was no correlation between R2* and either liver MRI-PDFF or histological steatosis. MR measuring MRI-PDFF and R2* simultaneously provides promising quantification of steatosis and iron. Rabbit NAFLD model confirmed accuracy of MRI-PDFF for liver fat quantification. R2* measurement and relationship between fat and iron of NAFLD liver need further experimental investigation.

Use of N,O-carboxymethyl chitosan to prevent postsurgical adhesions in a rabbit double uterine horn model： a randomized controlled design

In previous studies, N,O-carboxymethyl chitosan has been shown to decrease the incidence and intensity of abdominal adhesions. In the present study, adhesions were induced in 220 rabbits using a double uterine horn model. Rabbits were randomized to receive an operation only or an operation+medical chitosan intraperitoneally. Twenty-two rabbits from each group were euthanized at one of five different times(Day 3, 7, 14, 28, or 42), and adhesion formation was given gross and histopathological scores. Reductions were observed in adhesion extent(P=0.0337) and tenacity(P=0.0271) as well as inflammation(P<0.0001) on Day 3 when medical chitosan was applied. Prior to Day 14, fibrosis was less obvious in the medical chitosan group(P<0.0005). The tenacity scores were significantly lower in the medical chitosan group following Day 14(P<0.05), while the type scores were lower in the medical chitosan group following Day 28(P<0.03). Thus, medical chitosan decreased both the gross and the histopathological scores of the induced adhesions.

A rabbit model of graded primary mechanical injury to brainstem

Objective： To introduce a new animal model of graded mechanical primary brainstem injury （BSI）. Methods： Altogether 45 rabbits were subjected to BSI by type II biological impact machine designed by the Third Military Medical University. The animals were divided into 4 experimental groups （n=10） and 1 control group （n=5） ac- cording to different magnitudes of impact pressure imposed on the occipital nodule： Group 1,500-520 kPa; Group 2, 520- 540 kPa; Group 3,540-560 kPa; Group 4, 560-580 kPa and Group 5, 0 kPa with 20 kPa increase in each grade. The im- pact depth was a constant 0.5 cm. After injury, the clinical symptoms and signs as well as pathological changes were observed. Results： Rabbits in Group 1 revealed mild physiologi- cal reaction of BSI. They had localized cerebral contusion with punctate hemorrhage and subarachnoid hemorrhage （SAH） was limited to the peripheral tissues at the impact area. In Group 2, obvious physiological reaction was observed. Local pathological lesions reached the superfi- cial layer of brainstem tissues; focal hemorrhage and girdle- shaped SAH in basilar pon were observed under microscope. In Group 3, BSI was more severe with a long respiratory depression. Pathological lesions reached the inner portionof brainstem with massive hemorrhage and the whole brainstem was wrapped by subarachnoid hematoma. In Group 4, most rabbits died due to severe BSI. Pathological lesions deepened to the central brainstem with wide patho- logical change, rapture of the medulla oblongata central canal. Group 5 was the control group, with normal brainstem structure and no lesion observed. Conclusion： This model successfully simulates differ- ent levels ofbrainstem mechanical injury and clearly shows the subsequent pathological changes following injury. It takes two external parameters （impact pressure and depth） and has a similar injury mechanism to clinical accelerating BSI. Moreover it is reproducible and stable, thus being be- neficial for exploring pathophysiological mechanism, diag- nosis and forensic identification of various degrees of BSI.

Establishment of a blunt impact-induced brain injury model in rabbits

Objective： To establish an animal model to replicate the blunt impact brain injury in forensic medicine. Methods： Twenty-four New Zealand white rabbits were randomly divided into control group （n=4）, minor injury group （n：10） and severe injury group （n=10）. Based on the BIM- II Horizontal Bio-impact Machine, self-designed iron bar was used to produce blunt brain injury. Two rabbits from each injury group were randomly selected to monitor the change ofintracranial pressure （ICP） during the impact- ing process by pressure microsensors. Six hours after injury, all the rabbits were dissected to observe the injury mor- phology and underwent routine pathological examination. Results： Varying degrees of nervous system positive signs were observed in all the injured rabbits. Within 6 hours, the mortality rate was 1/10 in the minor injury group and 6/10 in the severe injury group. Morphological changes con-sisted of different levels of scalp hematoma, skull fracture, epidural hematoma, subdural hematoma, subarachnoid hemo- rrhage and brain injury. At the moment of hitting, the ICP was greater in severe injury group than in mild injury group; and within the same group, the impact side showed positive pressure while the opposite side showed negative pressure. Conclusions： Under the rigidly-controlled experimental condition, this animal model has a good reproducibility and stable results. Meanwhile, it is able to simulate the morphology of iron strike-induced injury, thus can be used to study the mechanism of blunt head injury in forensic medicine.

Using the Implantable Electrical Stimulator for Peripheral Nerve Rehabilitation:A Study in an Animal Model

The present study presents a peripheral nerve injury animal model for evaluation of an implantable electrical stimulator we designed.The evaluation was confirmed by ethological,electrophysiological and histologic study.Twenty New Zealand rabbits were used.The left sciatic nerve was crushed with a micro-vessel clamp in all rabbits,and the stimulators were implanted in ten rabbits.The other ten rabbits were in a control group.As compared with the implantation group,3 and 6 weeks after operation,the histology showed the typical pathologic atrophy by hematoxylin-eosin(HE) ,the motor nerve conduction velocity(MCV) was found significantly slowed and the axon of crushed nerve at distal portion exhibited breakdown in the control group.These results reveal that the implantable electrical stimulator was effective and was suitable for implantation in an animal model.

Differentially expressed proteins on postoperative 3 days healing in rabbit Achilles tendon rupture model after early kinesitherapy

Objectives： Surgical repair of Achilles tendon （AT） rupture should immediately be followed by active tendon mobilization. The optimal time as to when the mobilization should begin is important yet controversial. Early kinesitherapy leads to reduced rehabilitation period. However, an insight into the detailed mechanism of this process has not been gained. Proteomic technique can be used to separate and purify the proteins by differential expression profile which is related to the function of different proteins, but research in the area of proteomic analysis of AT 3 days after repair has not been studied so far. Methods： Forty-seven New Zealand white rabbits were randomized into 3 groups. Group A （immobilization group, n=l 6） received postoperative cast immobilization; Group B （early motion group, n= 16） received early active motion treatments immediately following the repair of AT rupture from tenotomy. Another 15 rabbits served as control group （Group C）. The AT samples were prepared 3 days following the microsurgery. The proteins were separated employing two- dimensional polyacrylamide gel electrophoresis （2D-PAGE）. PDQuest software version 8.0 was used to identify differentially expressed proteins, followed by peptide mass fingerprint （PMF） and tandem mass spectrum analysis, using the National Center for Biotechnology Information （NCBI） protein database retrieval and then for bioinformatics analysis. Results： Amean of 446.33,436.33 and 462.67 protein spots on Achilles tendon samples of 13 rabbits in Group A, 14 rabbits in Group B and 13 rabbits in Group C were suc- cessfully detected in the 2D-PAGE. There were 40, 36 and 79 unique proteins in Groups A, B and C respectively. Some differentially expressed proteins were enzyme with the gel, matrix-assisted laser-desorption/ionization time-of-flight mass spectrometry （MALDI-TOF MS）. We successfully identified 9 and 11 different proteins in Groups A and B, such as GAPDH, phosphoglycerate kinase 1, pro-alpha-1 type 1 collagen, peroxiredoxin 1, alpha-l-antiproteinase E a-1 and MAD2L1 binding protein, etc. And some with the molecular chaperone, oxidative stress, energy metabolism, signal transduetion, coupled with the tendon cell expression and protein synthesis, proliferate, differentiate and are closely related to the AT healing. The GAPDH protein was further validated through Western blotting. It was indicated that some differentially expressed proteins were involved in various metabolism pathways and may play an important role in initial healing of AT rupture. Conclusion： Differentially expressed proteins in rabbit healing AT model may contribute to 3 days healing of AT rupture through a new mechanobiological mechanism due to the application of postoperative early kinesitherapy.