Relationship between the Expression of RASSF1A Protein and Promoter Hypermethylation of RASSF1A Gene in Bladder Tumor

To investigate the relationship between the expression of RASSF1A protein and promoter hypermethylation of RASSF1A gene, RASSF1A protein expression was measured by Western blotting in 10 specimens of normal bladder tissues and 23 specimens of bladder transitional cell carcinoma （BTCC）. The promoter methylation in BTCC and normal bladder tissues was detected by methylation-specific PCR （MSP）. The results showed that the expression level of RASSF1A protein was significantly lower in BTCC tissues than that in normal bladder tissues. However, it was not correlated with its clinical stages and pathological grades. The frequency of promoter methylation of RASSF1A gene was higher in BTCC tissues than that in normal bladder tissues. In 14 patients with the aberrant promoter methylation, 13 showed loss or low expression of RASSF 1A protein. It is concluded that RASSF1A gene promoter methylation may contribute to the low level or loss of RASSF1A protein expression, the inactivation of RASSF1A gene and the genesis of BTCC. But, it may bear no correlation with its clinical stages and pathological grades.     

Preventive Effects of Rhodosin and Melatonin from Damage Induced by β-Amyloid1-40 in Senile Rats

Objective: To study the protective and therapeutic effects of Rhodosin and Melatonin on Alzheimers disease(AD) rats. Methods: D-galactose was intraperitoneally injected in rats for 6 weeks and β-Amyloid1-40(Aβ1-40) was injected into bilateral hippocampus to make AD models. Rhodosin and Melatonin were intraperitoneally injected in rats for 4 weeks to determine the protective and therapeutic effects on rats with AD. Y-maze test, and passive avoidance task were used to determine the ability of learning and memory. The content of lipofuscin in the central cortex, the viscous coefficient of mitochondrial membrane, the activity of superoxide dismutase and the content of malondialdehyde in both sides of hippocampus were determined. And the apoptosis of hippocampus neurons was determined with transmission electron microscopy(TEM). Results: Melatonin as an antioxidant significantly improved learning and memory deficits in the rats with AD and reduced the increase in SOD, MDA, the viscous coefficient and lipofuscin to their normal levels, and it also showed the protective effects of apoptosis. Rhodosin showed the similar effects. Conclusion: Rhodosin and Melatonin had preventive and therapeutic effects on rats with AD probably by affecting the free radical levels in rats.     

AduoLa Fuzhenglin Down-regulates Microwave-induced Expression of β_1-adrenergic Receptor and Muscarinic Type 2 Acetylcholine Receptor in Myocardial Cells of Rats

<正>This paper is aimed to study the effect of ADL on expression ofβ1-AR and M2-AchR in myocardial cells of rats exposed to microwave radiation.Immunohistochemistry,Western blot and image analysis were used to detect the expression ofβ1-AR and M2-AchR in myocardial cells at 7 and 14 d     

Endoplasmic Reticulum Stress Induced by Tunicamycin and Antagonistic Effect of Tiantai No.1(天泰1号) on Mesenchymal Stem Cells

<正>Objective:Changes of the internal and external cellular environments can induce calcium homeostasis disorder and unfolded protein aggregation in the endoplasmic reticulum(ER).This ER function disorder is called endoplasmic reticulum stress(ERS).Severe long-term ERS can trigger the ER apoptosis signaling pathway,resulting in cell apoptosis and organism injury.Recent researches revealed that ERS-induced cell death was involved in the neurocyte retrogradation in the progress of neuron degenerative diseases,such as Alzheimer's disease(AD),Parkinson's disease and so on.Therefore,the protection effect of the traditional Chinese drug——Tiantai No.1(天泰1号) on the ERS injury of AD was investigated at the molecular gene level in this study with a view to explore the gene pharmacodynamic actions and mechanisms of this drug.Methods: Primarily cultured marrow mesenchymal stem cells(MSCs) of rats were treated by tunicamycin(TM) in order to induce ERS.RT-PCR,fluorescence immunocytochemistry and Western blot techniques were used to determine the mRNA and protein expression levels of the protective stress protein-ER molecular chaperones GRP78 and GRP94(which would assist cells to resist cellular stress injury),and to determine the mRNA and protein expression levels of apoptosis promoting molecule Caspase-12 on the membrane of the ER,respectively. Results:Protein expression levels of GRP78 and GRP94 were significantly increased in the TM-induced MSCs, and the mRNA level of Caspase-12 was also remarkably increased in the TM-induced MSCs(P0.05).All these proved that the ERS model was successfully established by TM in MSC.Meanwhile,the mRNA and protein levels of GRP78 and GRP94 were all significantly increased compared with the model group(P0.05 or P0.01) after MSCs were treated with Tiantai No.1 while the mRNA and protein expression levels of Caspase-12 were significantly decreased compared with the model group(P0.05 or P0.01).This effect showed a dose dependent manner.Conclusion:Tiantai No.1 might attenuate the cell apoptosis induced by ERS injury,and thus protect the neurons against AD.     

Effects of Chloroquine on GFAP, PCNA and Cyclin D1 in Hippocampus and Cerebral Cortex of Rats with Seizures Induced by Pentylenetetrazole

The effects of chloroquine on glial fibrillary acidic protein （GFAP）, proliferation cell nuclear antigen （PCNA） and Cyclin D1 in hippocampus and cerebral cortex of rats with seizures induced by pentylenetetrazole （PTZ） were observed in the present study. Forty-eight male adult Sprague-Dawley （SD） rats were randomly divided into control group, chloroquine intervening group, and PTZ group. The behavior and electroencephalogram （EEG） were observed and recorded. GFAP and PCNA were examined with immunohistochemistry. The content of Cyclin D1 in hippocampus and cerebral cortex was inspected with Western blot. The results showed no seizure activity in the control group, severe seizure activity in the PTZ group （Ⅳ - Ⅴ degree）, and slight seizure activity （ Ⅰ -- Ⅲ degree） in the chloroquine intervening group （P〈0.05）. EEG recordings showed no epileptic spikes in the control group, high amplitude with fast frequency in the PTZ group, low amplitude and slow frequency in the chloroquine intervening group. The expression of GFAP and the positive index of PCNA in the PTZ group were higher than those of control group （P 〈0.05 and P〈0.01, respectively）. No differences in GFAP expression and PCNA index were observed between chloroquine intervening and control groups （P〉0.05）. The content of Cyclin D1 in hippocampus and cerebral cortex was significantly higher in the PTZ group than in control and chloroquine intervening groups （P〈 0.05）. Therefore, it is considered that chloroquine, by inhibiting the functions and proliferation of glial cells in the hippocampus and cerebral cortex, can alleviate the seizure activities. These results suggest that chloroquine may be an ideal anticonvulsant in preventing and treating epilepsy.     

Immunoregulative Mechanism of the Leydig Cell in the Infection by Expression1 of IL-1,IL-6,TGF-β, Fas and FasL mRNA

Objective To investigate the immune regulative mechanism of Leydig cells in the local infection of rat＇s testis. Methods Ureaplasma Urealyticum（UU） was injected into rat＇s bladder, which mimicked an ascending infectious way, and at the same time culture medium was injected into rat＇s bladder as the control. The rats were sacrificed at week 1, 2 and 3 after injection respectively. Then pathological changes in testis were analyzed by histological examination. At the same time Leydig cells were separated from rat＇s testis. The comparasion of levels of IL-1,IL-6, TGF-β, Fas and FasL mRNA expression among the three groups was made by RT-PCR. Results As compared with control group, the levels of IL-1, IL-6, TGF-fl mRNA expression for UU supernatant and living UU groups increased; and levels of Fas and FasL mRNA expression decreased and increased respectively after UU infection. Conclusion During anti-infective immunity, rat＇s Leydig cells may regulate immune function of the testis by changing the levels of IL-1, IL-6, TGF-β, Fas and FasL mRNA expression and may contribute to maintain immune privilege of the testis.     

Antagonistic Effects of Tranilast on Proliferation and Collagen Synthesis Induced by TGF-β2 in Cultured Human Trabecular Meshwork Cells

Primaryopen angleglaucoma (POAG)isalead ingcauseofblindness ,whichinvolvesopticneuropa thyaccompaniedbycharacteristicvisualfielddefectsandisoftenassociatedwithelevatedintraocularpres sureduetodisturbanceofaqueoushumoroutflowthroughthetrabecularmeshwork …     

The Effect of Vitamin A on Secretion of IFN-γ and IL-4 in A549 Cells Induced by Mycoplasma Pneumoniae

In order to investigate the effect of vitamin A (VA) on the secretion of IFN-γ and IL-4 in Mycoplasma Pneumoniae (MP)-induced A549 cells, A549 cells were co-cultured with MP for different time lengths and then the levels of IFN-γ and IL-4 in the cell culture supernatants were detected before and after treatment with different concentrations of VA by using the enzyme-linked immu-nosorbent assay ( ELISA). The results showed that the level of IFN-γ and IL-4 in the supernatants of MP-induced A549 cells was much higher than that in non-induced cells (P<0.01). After application of VA, IL-4 level was not increased until the concentration of VA was up to 0.5×10-5 mol/L (P<0.01). However, with concentration of VA increased up to 1×10-4 mol/L, IL-4 was significantly suppressed (P<0.01). It was concluded that MP could induce the secretion of IFN-γ and IL-4 in A549 cells. VA could inhibit the secretion of IFN-γ and increase the IL-4 level in MP-induced A549 cells. However, high concentration of VA had an inhibitory effect on the secretion of IL-4 as well as on the IFN-γ. These data provided a theoretical basis for the application of VA in MP pneumonia in the clinical practice.     

Modulation of Behavior and Glutamate Receptor mRNA Expression in Rats after Sub-chronic Administration of Benzo（a）pyrene

Objective The present study aimed to test whether exposure to benzo(a)pyrene [B(a)P] affects spatial learning and short-term memory by modulating the expression of the Gria1 and Grin2a glutamate receptor subunit genes in the hippocampus.Methods Thirty-six 21-24-day-old,male rats were randomly assigned into high-,medium-,and low-dose toxin exposure groups (6.25,2.5,and 1 mg/kg,respectively) and a control group,each containing nine rats.The behavioral performance of adult rats exposed to sub-chronic administr...     

Expression of USP15, TβR- Ⅰ and Smad7 in Psoriasis

Summary： The deubiquitinating enzyme ubiquitin specific peptidase 15 （USP15） is regarded as a regulator of TGFβ signaling pathway. This process depends on Smad7, the inhibitory factor of the TGFβ signal, and type Ⅰ TGFβ receptor （TβR- Ⅰ ）, one of the receptors of TGFβ. The expression level of USP 15 seems to play vital roles in the pathogenesis of many neoplasms, but so far there has been no report about USP15 in psoriasis. In this study, immunohistochemical staining of USP15, TβR- Ⅰ and Smad7 was performed in 30 paraffin-embedded psoriasis specimens and 10 normal specimens to investigate the expression of USP15, TβR- Ⅰ and Smad7 in psoriasis and to explore the relevance among them. And USP 15 small interfering RNA （USP 15 siRNA） was used to transfect Hacat cells to detect the mRNA expression of TβR- Ⅰ and Smad7. Of 30 cases of psoriasis in active stage, 28, 24 and 26 cases were positive for USP15, TβR- Ⅰ and Smad7 staining, respectively. The positive rates of USP15 and Smad7 were significantly higher in psoriasis specimens than in normal skin specimens （44.1%±26.0% vs. 6.1%±6.6%, 47.2%±27.1% vs. 6.6%±7.1%）, and positive rate of TβR- I （20.3%±22.2%） in psoriasis was lower than that in normal skin specimens （46.7%±18.2%）. There was a significant positive correlation between USP15 and Smad7 expression, and significant negative correlations between USP15 and TβR- Ⅰ expression, and between TβR- Ⅰ and Smad7 expression in psoriasis. After transfection of USP15 siRNA in Hacat ceils, the expression ofTβR- Ⅰ mRNA was up-regulated and that of Smad7 was down-regulated. It is concluded that USP15 may play a role in the pathogenesis of psoriasis through regulating the TβR- Ⅰ/Smad7 pathway and there may be other cell signaling pathways interacting with USP 15 to take part in the development of psoriasis.     

Qushi Huayu Decoction (祛湿化瘀方) Inhibits Protein and Gene Expression of Cathepsin B in HepG2 Cells Induced by Free Fatty Acids

Objective: To study the experimental efficacy of Qushi Huayu Decoction (祛湿化瘀方,QHD) on protein and gene expression of cathepsin B (ctsb) in HepG2 cells induced by free fatty acids (FFAs).Methods: The model of HepG2 steatosis and tumor necrosis factor-α (TNF-α) secretion was induced by long-chain FFAs.HepG2 cells were divided into 4 groups: control group (group C),model group (group M),low-dose QHD group (group L) and high-dose QHD group (group H ).Long-chain FFAs were added to groups M,L and H.The 10% blank-control serum was added to group C and M,while 5% and 10% QHD-containing sera were added to group L and H,respectively.The levels of serum TNF-α and cellular triglyceride (TG) were detected.Cellular p-IκB and ctsb expression were detected using Western blot and PCR.The expression and distribution of ctsb were observed by immunofluorescence.Results: After incubating with FFA for 24 h,TG deposition in HepG2,TNF-α content in cell supernatant,the protein expression of cellular ctsb and P-IκB,as well as mRNA expression of ctsb increased markedly in group M compared with group C (P0.05,P0.01).Compared with group M,TG deposition,the expression of cellular ctsb,P-IκB and ctsb mRNA in groups L and H,as well as TNF-α content in group H,decreased significantly (P0.05).Cell immunochemical fluorescence studies showed that ctsb was released from lysosomes and distributed in the cytoplasm extensively and diffusedly after being stimulated with FFA.In this study,these above-mentioned changes were inhibited markedly in groups L and H.Conclusion: QHD might have a direct inhibitory effect on the ctsb target in the FFA-ctsb-TNFα pathway of hepatic lipotoxicity.     

Astragaloside Ⅳ Protects Against Aβ1-42-induced Oxidative Stress,Neuroinflammation and Cognitive Impairment in Rats

Objective To investigate the neuroprotective action of astragaloside Ⅳ (AS-Ⅳ) on spatial learning and memory impairment induced by amyloid-beta 1-42 (Aβ1-42) in rats and elucidate its underlying molecular mechanisms. Methods Adult-male Sprague-Dawley rats (230-250 g) were divided into six groups randomly: control, Aβ1-42, AS-Ⅳ, Aβ1-42 plus 5 mg/kg·d AS-Ⅳ, Aβ1-42 plus 25 mg/kg·d AS-Ⅳ, and Aβ1-42 plus 50 mg/kg·d AS-Ⅳgroups. Aβ1-42 were delivered by intracerebroventricular injection under the guidance of a brain stereotaxic apparatus. The Morris water maze test (hidden platform test, probe trials, visible platform test) was performed one week after Aβ1-42 injection to obtain the ability of rat spatial learning and memory. AS-Ⅳ (5, 25 and 50 mg/kg·d) was administrated intraperitoneally once per day from the 8th day after Aβ1-42 injection for 5 consecutive days. Average escape latencies, distances for searching for the platform under water and the percentage of total time elapsed and distance swam in the right quadrant after removing platform were determined by behavior software system. The vision and swim speeds of rats were also determined to exclude the effect of these factors on the parameters of learning and memory. After behavioral tests, the rats were sacrificed immediately by decapitation. Hippocampus were collected. The enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-px) and catalase (CAT) in the hippocampus obtained from different-treated rat brain were measured by following the manufacturer's instructions. The levels of interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in tissue lysates were assayed with ELISA. Results The water maze test results indicated that chronic treatments with AS-Ⅳ effectively protected the rats from Aβ1-42-induced spatial learning and memory impairment. Furthermore, the activities of SOD, GSH-px and CAT decreased by Aβ1-42 were also restored by AS-Ⅳ treatment in the hippocampus of rats. In addition, AS-Ⅳsignificantly decreased the levels of IL-1β and TNF-α in the hippocampus of Aβ1-42-induced amnesia's rats. Conclusion Our findings suggest that AS-Ⅳ might be a useful chemical in improving the spatial memory and relieving the oxidative stress and neuroinflammation in Alzheimer patients.     

High-frequency stimulation of anterior nucleus thalamus improves impaired cognitive function induced by intra-hippocampal injection of Aβ1-40 in rats

Background The advent of brain stimulation techniques to treat movement disorders and psychiatric diseases has shown potential to decode the neural mechanism that underlies the cognitive process by modulating the interrupted circuit.Here,the present investigation aimed at evaluating the influence of deep brain stimulation of the anterior nucleus thalamus （ANT-DBS） on memory.Methods Thirty-two rats were randomized into phosphate buffer saline （PBS） group （n=8,rats received PBS injections without implantation of electrodes into the ANT）,Alzheimer＇s dementia （AD） group （n=8,rats received Aβ1-40 injections without implantation of electrodes into the ANT）,ANT sham stimulation group （n=8,rats received Aβ1-40 injections with implantation of electrodes into the ANT but without stimulation） and ANT stimulation group （n=8,rats received Aβ1-40 injections with implantation of electrodes into the ANT and stimulation）.A Morris maze test was used for determining the effect of electrical stimulation on cognitive function in rats.The data were assessed statistically with one-way analysis of variance （ANOVA） followed by Tukey＇s tests for multiple post hoc comparisons.Results The data showed that in the training test,PBS group and AD group managed to learn the hidden-platform faster and faster while AD group needed a significantly longer time to reach the platform than PBS group （P ＜0.05）.Meanwhile,ANT stimulation group demonstrated a significantly shorter time to reach the platform （P ＜0.05） compared to the AD group,while there was no significant difference between the ANT sham stimulation group and the AD group （P ＞0.05）.On the probe test,the AD group spent less time （（10.15±2.34） seconds） in the target quadrant than the PBS group （（28.20±2.75） seconds） （P ＜0.05）.And the times of platform-traversing of the AD group （3.35±1.12） significantly decreased compared with the PBS group （8.69±2.87） （P ＜0.05）.However,the times of platform-traversing and the time spent in the target quadrant of the ANT stimulation group significantly increased compared to the AD group （P ＜0.05）,while times of platformtraversing or the time spent in the target quadrant was not significantly different between the ANT sham stimulation group and the AD group （P ＞0.05）.Conclusion Bilateral high-frequency stimulation of the ANT may be useful as a potential therapeutic modality for cognitive dysfunction in AD.     

Effect of TGF-β1 on the Expression of IL-12, IL-15, IL-18, IL-4 and IL-10 in Heart Transplantation Rejection in Rats

To investigate the effect of TGF-β1 on the expressions of IL-12, IL-15, IL-18, IL-4 and IL-10 in heart transplantation rejection in rats, a model of rat cervical heterotopic heart transplantation was set up and the model rats were randomly divided into three groups： control group, transplant group and TGF-β1 group. The mRNA expression levels of IL-12, IL-15, IL-18, IL-4 and IL-10 were determined by RT-PCR at the 5th day after the transplantation. The mRNA expression levels of IL- 12, IL-15, IL-18 were increased obviously and those of IL-4, IL-10 were significantly decreased in the transplant group as compared with the control group （P〈0.01）. In the TGF-β1 group, the mRNA ex- pression levels of IL- 12, IL- 15, IL- 18 were significantly decreased and those of IL-4, IL- 10 were significantly increased as compared with the transplant group （P〈0.01）. The immunosuppressive effect of TGF-β1 on heart transplantation rejection was related to its inhibition of the expressions of Th1-type cytokines （IL-12, IL-15, IL-18 etc） and its promotion of the expressions of Th2-tpye cyto- kines （IL-4, IL-10）.     

The Effects of HBx Gene on the Expression of DNA Repair Enzymes hOGG1 and hMYHα mRNA in HepG2 Cells

To observe the alteration in the expression of DNA repair enzymes hOGG1 and hMYHa and the change in 8-OHdG levels in the HBx gene-transfected cells HepG2/HBx and to explore the mechanisms of the HBV-associated hepatocellular carcinoma, the gene-transfected cells HepG2/HBx which stably expressed HBx was established, and the effect of HBx on the cell cycle and proliferation of HepG2 was examined. By using the β-actin as the interior control, real-time polymerase chain reaction （Real-time qPCR） was employed to quantitatively detect the expression of DNA repair enzymes hOGG1 and hMYHα in the HepG2/HBx, the control cells HepG2 and HepG2 transfected with pcDNA3.1 vector （HepG2/pDNA3.1）. The 8-OHdG levels were determined by HPLC/ECD in the established gene-transfected cells HepG2/HBx and the control cells HepG2 and HepG2/pcDNA3.1. Our results showed that the expression of DNA repair enzyme hMYHα in the HepG2/HBx （0.021±0.007） was significantly lower than that of HepG2 （0.099±0.041） （P〈0.05） and HepG2/pDNA3.1 （0.121±0.005） （P〈0.05）. However, the no significant differences existed in the expression of DNA repair enzyme hOGG1 among the three cell strains （P〉0.05）. The 8-OHdG level in the HepG2/HBx was significantly higher than that in HepG2 and HepG2/pcDNA3.1 （P〈0.05）. It is concluded that HBx gene may inhibit the expression of DNA repair enzyme hMYHα mRNA to impair the ability to repair the intracellular DNA oxidative damage, to increase the oxidative DNA-adduct 8-OHdG and to affect the nucleotide excision repair function, thus participate in the occurrence and development of hepatocellular carcinoma.     

A study on the expressions and the correlation of TGF-β_1, and a-SMA in healing process of bile duct trauma

Objective: To explore the formation mechanism of benign biliary stricture. Methods: A model of trauma ofcommon bile duct was established in 28 dogs and then repaired. The anasomosis tissues were taken on the 1st week,3rd week and the 3rd month, 6th month respectively after operation and examined by using light microscopy and elec-tromicroscopy. Macrophage, TGF-β_1, and α-SMA were studied immunohistochemically. Results: The mucosal epitheli-um of common bile duct restored poorly, chronic inflammation lasted for a long time, fibroblasts proliferated actively,extracellular matrix overdeposited; and myofibroblasts functioned actively and existed during the whole healing process.Immunohistochemical test showed a high expression of macrophage, TGF-β_1, and α-SMA during healing process lastinga long duration. Macrophages were found in the lamina propria under mucosa, TGF-β_1 in the granulation tissue, fibro-blasts and endothelial cells of blood vesssels, while α-SMA in the myofiroblasts and smooth muscle     

红花注射液对低O2高CO2大鼠肝组织HIF-1 α与TGF-β1基因表达的影响

目的 观察慢性低O2高CO2大鼠肝组织低氧诱导因子1 α(HIF-1 α)与转化生长因子β1(TGF-β,)基因表达的变化及红花注射液对其的影响.方法 将30只SD大鼠随机分为A组(正常组)、B组(慢性低O2高CO2肺动脉高压模型组)和C组(红花注射液干预组),并观察各组肝组织病理学改变,同时分别采用免疫组化技术和RT-PCR技术检测HIF-1α、TGF-β,在肝内的表达、定位及其mRNA的含量.结果 (1)光镜下B组大鼠肝组织脂肪变性明显,而C组则不明显;(2)B组大鼠肝组织HIF-1 α、TGF-β1及其mRNA表达水平均高于A组,而C组大鼠上述指标均低于B组,差异均有统计学意义(P<0.0).结论 慢性低O2高CO2肺动脉高压状态下大鼠肝组织HIF-1 α、TGF-β,及其mRNA表达量增加,而红花注射液可下调其肝组织HIF-1 α及TGF-β,基因的表达.     

Expression Patterns of Sarcomeric α-Actin, α-Actinin and UCP2 in the Myocardium of Kunming Mice after Exposure to C-Terminal Polypeptide of Cardiotrophin-1

Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The e