共查询到20条相似文献,搜索用时 15 毫秒
1.
CHAI San-bao XU Shao-ping XUE Lin ZHANG Yong-gang PANG Yong-zheng TANG Chao-shu 《园艺学报》2001,17(2):116-119
AIM:To investigate the effect of endothelin(ET) on taurine transportation in rat cardiac myocytes in vitro.METHODS: In cultured cardiac myocytes of neonatal rats, taurine transportation velocity was measured by radio-ligand method. RESULTS: ET(10-10-10-8 mol/L) could inhibit taurine transportation in a dose-dependent manner.10-10,10-9 and 10-8mol/L of ET significantly decreased taurine transpotation by 13%, 38% and 71%, respectively (P<0.01), compared with control group. H7,BQ123 and Pre-PMA can reverse the inhibition of ET on taurine transportation dramatically(P<0.01).CONCLUSION:The binding of ET and ET-A receptor might activate protein kinase C,which inhibits taurine transportation in cultured myocytes of rats. 相似文献
2.
ZHANG Yu-xia YU Lun-yin LIU Ming-qiu ZHANG Zheng-bin TANG Zhi-jiao XIA Dong WANG Ming 《园艺学报》2002,18(1):32-35
AIM:To investigate the protein expression of cyclin D2 and p16 in proliferation and differentiation of cultured cardiac myocytes.METHODS:One-day-old Sparague-Dawley rats were used. Cardiac myocytes(CM) were collected by a trypsin-dispersal method and cultured. Cell growth line and fluorescence activated cell sorting (FACS) were used to investigate the proliferation of CM. Ultra-thin sections were made to observe the ultrastructure of CM under transmission electron microscope. The expression of cyclin D2 and p16 in CM were measured using immunocytochemistry and image analysis.RESULTS:①Results of cell growth line and FACS analysis showed that cultured CM could proliferate in the first 3 cultured days, but the ability decreased quickly, concomitant with differentiation. CM was obseved quiescent in cell cycle three days later. The ultrastructure of CM showed the large amount of myofilaments and mitochondrion. ②The protein expression of cyclin D2 in 3,4,5 day CM group was 0.89 times(P<0.05),0.80 times (P<0.05) and 0.56 times (P<0.01) of that in 1 day group, respectively. The expression of p16 in CM was increased during the culture process, 2,3,4,5 day group were 1.63 times, 1.72 times, 1.99 times and 2.84 times (P<0.01) of that in 1 day group, respectively.CONCLUSION:Cultured neonatal rat cardiac myocytes could proliferate during the first 3 days after incubation, but the ability of proliferation decreased, from the fourth day, concomitant with differentiation. Cyclin D2 and p16 play the key roles in CM postnatal development. Downregulation of cyclin D2 and upregulation of p16 may induce CM differentiation. 相似文献
3.
AIM:To investigate the role of proliferation and apoptosis in hypertensive left ventricular hypertrophy (LVH) and the effect of AT1 blockade with losartan. METHODS:Left ventricles (LV) from 12, 24-week-old SHR (SHR12, SHR24), 24-week-old SHR treated with losartan (15 mg·kg-1·d-1, SHR-L24) during 12 weeks, and age-matched WKY rats (WKY12, WKY24) were studied. Expression of PCNA was examined by immunohistochemistry. Apoptotic cells in LV sections were assessed by TUNEL method. Levels of fas mRNA were quantitated by RT-PCR. RESULTS: Compared with age-matched WKY, SHR12 and SHR24 showed increased LV hypertrophied index (HI), increased apoptotic index (AI) of myocytes (P<0.01), but decreased AI of fibroblasts (P<0.05). Moreover, SHR12 exhibited increased PCNA labeling of myocytes (P<0.05) with similar positive rates of fibroblasts.It was also showed that losartan reversed HI, significantly reduced the AI of myocytes and significantly increased the AI of fibroblasts. RT-PCR disclosed that levels of fas mRNA positively correlated with the frequency of apoptosis in LV of either SHR or WKY (r=0.52, P<0.05). CONCLUSION:The cellular changes of LVH in adult SHR manifest as the imbalance between proliferation and apoptosis of myocytes, and insufficient apoptosis of fibroblasts. The mechanisms of losartan on reversing LVH may be mediated through adjusting the abnormal amount of cells and the expression of fas gene. 相似文献
4.
AIM:To explore the role of tumor necrosis factor alpha(TNF-α) in the pathogenesis of liver fibrosis.METHODS:The proliferation and apoptosis of hepatic stellate cells (HSCs) in vitro were detected with flow cytometry, electron microscopy and TUNEL.RESULTS:The flow cytometry analysis showed that the cell proliferation index (PI) in the TNF-α(0.5 μg/L, 2.0 μg/L, 8.0 μg/L) groups was evidently lower than that in the control group (P<0.05). In the cell cycle distribution, the portion of G0/G1 phase in the TNF-α groups was significantly higher than that in the control group(P<0.05), but the portion of S phase in the TNF-α groups was evidently lower than that in the control group(P<0.05). These indicated that TNF-α interfered with HSCs entrance into S phase from G0/G1 phase whereupon the proliferation of HSCs was inhibited. The apoptotic rate in the TNF-α groups was evidently higher than that in the control group(P<0.05). The gene expression of bcl-2 and bax was also detected with flow cytometry. The expression of bcl-2 in the TNF-α groups was evidently lower than that in the control group(P<0.05), but the expression of bax in the TNF-α groups was significantly higher than that in the control group(P<0.05). TUNEL analysis showed the apoptotic rate of HSCs in the TNF-α(2.0 μg/L) group was 18.7%±2.5% compared with 5.3%±1.2% in the control group(P<0.05).CONCLUSIONS:TNF-α interfered with HSCs entrance into S phase from G0/G1 phase whereupon the proliferation of HSCs was inhibited. TNF-α down-regulated bcl-2 gene expression and up-regulated bax gene expression whereupon the apoptosis of HSCs was induced. 相似文献
5.
AIM: To investigate the effect of Salidroside on the proliferation, DNA synthesis, intracellular Ca2+ content of rabbit PASMC (pulmonary artery smooth muscle cells) under hypoxia. METHODS: Techniques of cell culture, MTT test, [3H][3H][3H]-TdR incorporation, fluo-3 and confocal laser scanning microscopy were used. RESULTS: The A value of MTT and [3H][3H]-TdR incorporation of PASMC increased significantly by 62% (P<0.05) and 138% (P<0.01) after 24 h hypoxia. Salidroside (32×10-5 mol/L) inhibited the action of hypoxia on the proliferation of PASMC, the A value of MTT and [3H][3H]-TdR incorporation declined significantly by 29% (P<0.05) and 37% (P<0.01) compared with hypoxia group. A calcium channel blocker, verapamil could also inhibit the accelerative effect of hypoxia on the proliferation of PASMC. The intracelluler Ca2+ content of PASMC raised markedly under hypoxia, but the effect of hypoxia on the intracelluler Ca2+ content could be inhibited by Salidroside. CONCLUSION: Salidroside inhibited the proliferation, DNA synthesis of PASMC induced by hypoxia. The inhibitory action of Salidroside on the increase in intracellular Ca2+ concentration under hypoxia might be one of the mechenisms. 相似文献
6.
AIM:To study the effects of exogenous metallothionein (MT) and ZnCl2-induced MT production on biological action of homocysteine(HCY)in vascular fibroblasts.METHODS:[3H]-TdR, [3H]-Pro incorporation and LDH leakage were measured, the cellular viabilities were calculated by trypan blue exclusion test and the intracellular contents of MT were assayed by [109Cd]-hemoglobin saturation method in cultured rat vascular fibroblasts.RESULTS:Proliferation, collagen production of vascular fibroblasts in HCY-treated group were significantly increased compared with control group in a concentration-depedant manner. HCY (500 μmol/L) increased LDH leakage and decreased the cellular viabilities (P<0.05 or P<0.01). [3H]-TdR incorporation, [3H]-Pro incorporation, collagen secretion and LDH leakage were all decreased in MT (1×10-5 mol/L, 1×10-4mol/L) plus HCY(500 μmol/L) incubated group, compared with HCY alone group, respectively (P<0.05 or P<0.01). MT content in ZnCl2 pretreatment group was increased compared with control group. Proliferation, collagen production and LDH leakage in HCY group pretreated with ZnCl2 were decreased whereas the cellular viabilities were increased compared with HCY alone group.CONCLUSIONS:The results shows that HCY induces proliferation and collagen production of vascular fibroblasts. Both exogenous MT and endogenous MT induced by ZnCl2 inhibite the above-mentioned effects of HCY on vascular fibroblasts. MT inhibites vascular fibroblast activation induced by HCY, which may be related to its vascular protection. 相似文献
7.
WANG Xiao-hong CHEN Ya-hong QI Yong-fen LI Shu-lian PANG Yong-zheng LIU Nai-kui TANG Chao-shu 《园艺学报》2001,17(3):193-195
AIM:To investigate the effect of endothelin (ET), angiotensin II (AngII) and homocysteine (Hcy) on C-type natriuretic peptide (CNP) synthesis and release. METHODS: Human endothelial cell was cultured; CNP was measured by radioimmunoassay method. RESULTS: ET and AngII could augment CNP synthesis in human endothelial cells. Compared with control group, 10-9,10-8,10-7 mol/L ET and Ang II increased CNP content of endothelial cells by 1%(P>0.05), 49%(P<0.05),117%(P<0.01) and 137% (P<0.01),165%(P<0.01),201%(P<0.01),respectively. A great dose of ET and Ang II also stimulated CNP release from cultured human endothelial cells. Hcy had no effect on CNP synthesis, but 10-9,10-8,10-7 mol/L Hcy enhanced CNP release from cultured human endothelial cells by 17%(P>0.05),84%(P<0.01) and 555%(P<0.01), respectively. CONCLUSION: ET, AngII and Hcy might be involved in the synthesis and release of human endothelial cell CNP.Fig 1 Time-course of CNP syntheis and release in cultured human endothelial cell ( ±s,n=6) 相似文献
8.
QI Yong-fen XIA Chun-fang CHEN Ya-hong XUE Lin PANG Yong-zheng TANG Chao-shu 《园艺学报》2002,18(3):230-232
AIM:To observe the effect of adrenomedullin(ADM)on proliferation of vascular smooth muscle cells(VSMC) induced by urotensin Ⅱ(UⅡ). METHODS:DNA synthesis of cultured rat aortic VSMC was measured by [3H]-TdR incorporation. The activities of mitogen activated protein kinase(MAPK) were determined by isotope tagged with [γ-32P]-ATP. RESULTS:UⅡ(10-8mol/L) significantly increased [3H]-TdR incorporation of VSMC and MAPK activities by 38%(P<0.05) and 260%(P<0.01) respectively compared with control group. Compared with UⅡ group, 10-10,10-9,10-8mol/L ADM decreased [3H]-TdR incorporation of VSMC by 7%(P>0.05), 32%(P<0.05)and 41%(P<0.01),respectively, and diminished MAPK activities by 24%(P>0.05), 32%(P<0.05)and 36%(P<0.05),respectively. CONCLUSION:ADM inhibits proliferation of VSMC induced by urotensin Ⅱ through inhibiting MAPK activation. 相似文献
9.
FU Min-gui CHEN Ya-hong LI Shu-lian XU Song PANG Yong-zheng LIU Nai-kui TANG Chao-shu 《园艺学报》2000,16(7):588-591
AIM: To study the role and regulation of calcineurin(CaN) in angiotensin II(AngⅡ)-stimulated cardiacmyocyte hypertrophy of rats. METHODS: Using AngⅡ to induce the cultured cardiac myocyte hypertrophy of rats, and investigating the effect of CaN inhibitor on [3H]-leucine incorporation of AngⅡ-stimulated cardiomyocytes and the regulation of various factors on CaN activity in cardiomyocytes.RESULTS: AngⅡ can stimulate the CaN activity in cultured neonatal rat cardiomyocytes in a dose- and time-dependent manner. In cardiac myocytes incubated with 10, 100, 1000 nmol·L-1 of AngⅡ for 12h, the CaN activities increased respectively by 13%,57%(P<0.05) and 228%(P<0.01) compared with that in non-stimulated cardiomyocytes. The CaN activities in AngⅡ-stimulated cardiomyocytes were significantly inhibited by losartan(50 μmol·L-1), H7(50 μmol·L-1)and Fura-2/AM(4 μmol·L-1),while no effect was observed with PD98059(50 μmol·L-1).The [3H]-leucine incorporation in AngⅡ-stimulated cardiomyocytes increased by 46%(P<0.01) compared with that in control group, which was dramatically inhibited by cyclosporin A(0.5~5μg/mL). CONCLUSIONS: Calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, may play an important role in AngⅡ-induced cardiac myocyte hypertrophy. The activation of CaN may dependent on the sustained increases of [Ca2+]i and be regulated by some protein kinases (such as PKC,etc.). 相似文献
10.
AIM:To investigate the effect of antisense oligonucleotides(ASON) of c-sis on cellular cycle and proliferation of pulmonary artery vascular smooth muscle cells(VSMC).METHODS:Tissue mass culture was done to get VSMC of pulmonary artery. Different concentrations of antisense oligonucleotides of c-sis were added into the cultures to observe the VSMC proliferation curve using MTT test. The changes of VSMC cellular cycle were also observed by flow cytometry.RESULTS:ASON with mid-to high concentrations restrained the proliferation of VSMC apparently with the peak of cell growth being attenuated or eliminated. Affected by mid-concentration ASON, PDGF-BB showed significant accelerating effect on the proliferation of VSMC. The ratio of G0/G1 in cellular cycle was increased significantly in VSMC culture with ASON in comparison with control. The G0/G1 ratio also showed significant differences among different concentration of ASON groups(P<0.05).CONCLUSION:Mid-to high concentration of ASON was a powerful inhibitor of cellular proliferation for pulmonary artery VSMC. ASON increased the ratio of G0/G1 significantly and the increase seems to be ASON dosage dependent. 相似文献
11.
AIM:To explore the effects of hydrogen sulfide (H2S) on proliferation of vascular smooth muscle cells (VSMC) stimulated by endothelin (ET-1, 10-7mol/L) and mitrogen-activated protein kinase (MAPK) activity in VSMCs.METHODS:Cultured VSMCs were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS groups, (5) serum+NaHS group, and (6) endothelin+NaHS group. VSMC proliferation was measured by[3H]-TdR incorporation and MAPK activity in VSMC was determined by radioactivity assay.RESULTS:ET-1 increased VSMC[3H]-TdR incorporation by 2.39 times (P<0.01) and MAPK activity by 1.62 times(P<0.01), as compared with control. H2S (5×10-5-5×10-4mol/L) decreased VSMC[3H]-TdR incorporation and MAPK activity by 16.8%-37.4% and 7.4%-33.6%, respectively (P<0.05 or P<0.01).CONCLUSION:This study demonstrates that H2S inhibits ET-1-induced proliferation of VSMC, which might be mediated by the inhibition of MAPK. 相似文献
12.
AIM: To investigate the roles of intermedin1-53 (IMD1-53) and exteracellular signal-regulated kinase (ERK) signal pathway in the proliferation of rat cardiac fibroblasts (CFBs).METHODS: Isolated and cultured CFBs from new born SD rats were randomly divided into control group, aldosterone (ALD) groups (at different concentrations) and ALD+IMD groups (IMD at different concentrations). The viability of CFBs was determined by MTT assay. Western blotting was used to observe the effect of IMD on ALD-induced ERK phosphorylation.RESULTS: IMD1-53 had no significant effect on the proliferation of CFBs in basal state, but inhibited the CFBs growth stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner. IMD1-53 also inhibited ERK phosphorylation stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner.CONCLUSION: IMD1-53 inhibits the proliferation of CFBs by ERK signal pathway. 相似文献
13.
AIM:To investigate the effect of Epstain-Barr virus latent membrane protein 1 (EBV-LMP1) on proliferation and cell cycle of nasopharyngeal carcinoma (NPC) cells. METHODS:The expression of EBV-LMP1 was detected by immunohistochemical method (LSAB). Proliferation of NPC cells was identified by MTT method. Cell cycle percentage was detected by flow cytometry analysis. RESULTS: OD value of EBV-LMP1 expressive NPC cells L-CEN1 was much higher than that of both EBV-LMP1 negative NPC cells V-CEN1 and CNE1 (P<0.01). Compared with the cell cycle percentage in both V-CNE1 and CNE1, the percentage of G1 was significantly decreased and the percentage of S was much increased in L-CNE1 (P<0.01). But no obvious differences were observed in all cell cycle percentage between V-CNE1 and CNE1 (P>0.05).CONCLUSION:The expression of EBV-LMP1 on NPC cell might cause some change of cell cycle and enhance cell proliferation. 相似文献
14.
AIM:To investigated the effect of 7-hydroxyisoflavone (7-HIF) on the proliferation, apoptosis and stem-like cell feature of colorectal cancer cells. METHODS:The effect of 7-HIF on the proliferation of HCT116 cells was detected by WST-1 assay and colony formation assay. The effects of 7-HIF on the cell cycle distribution and apoptosis in the HCT116 cells were analyzed by flow cytometry. The expression of cell-cycle related proteins and the stemness related proteins was determined by Western blot. RESULTS:After treated with 7-HIF (200 μmol/L), the viability of HCT116 cells was inhibited, and the size and number of the colony were decreased as compared with control group (P<0.05). The G0/G1 phase of the cell cycle was increased. The proportion of S phase was decreased and the cells were mainly arrested in G0/G1 phase. The apoptotic rate of HCT116 cells was 21.4%, which was significantly higher than that in the control group (1.1%). The results of Western blot revealed that the expression of inhibitor of differentiation 1(Id1) was significantly decreased (P<0.05). The expression of cell cycle markers cyclin D1 and cyclin E, the proliferative markers survivin and PCNA, and stem cell markers CD133, ALCAM and EpCAM were all down-regulated by 7-HIF treatment (P<0.05). CONCLUSION:7-HIF inhibits the proliferation and induces the apoptosis of colorectal cancer cells, and inhibits the stem-like cell feature, which may be related to Id1 inhibition. 相似文献
15.
AIM:To investigate the influences of bradykinin(BK)on left ventricular hypertrophy and cardiac function in angiotensin-converting enzyme inhibitor(ACEI) therapy in rats after myocardial infarction.METHODS:The effects of enalapril (500 μg·kg-1·d-1), enalapril (500 μg·kg-1·d-1)with BKB2 receptor antagonist (Hoe-140 500 μg·kg-1·d-1), losartan(3 mg·kg-1·d-1) on left ventricular end-diastolic pressure (LVEDP), maximum positive left ventricular pressure change (+dp/dtmax) and LVW/BW as well as V(m)n of noinfarcted area were examined after 4 weeks treatment in rats after myocardial infarction.RESULTS:The values of LVEDP, LVW/BW and V(m)n of three treatment groups were higher than that of untreated MI group (P<0.05),but the +dp/dtmax of three treatment groups were not significantly different compared with the untreated MI group. In addition, no significant difference in MAP was observed among the three treatment groups, but the LVW/BW and V(m)n of enalapril+Hoe-140-treated group were higher than that of enalapril-treated group (P<0.05) .CONCLUSION:Enalapril can prevent left ventricular hypertrophy and improve cardiac function independent of blood pressure after myocardial infarction, which is partly due to the inhibition of BK degradation. 相似文献
16.
AIM: To investigate the effect of decorin (DCN) on the proliferation and apoptosis of human pterygium fibroblasts (HPF) in vitro , and to compare the effect of mitomycin C (MMC) in order to search for a new method to prevent the recurrence after pterygium surgery. METHODS: Human pterygium fiborblasts were isolated from the caudomedial part of pterygium tissues in pterygium patients and then cultured in vitro using tissue inoculation method. The cells were treated with DCN and MMC at concentrations of 0.01, 0.1, 1, 5 and 10 mg/L. The morphological alterations of HPF were observed after 24 h, 48 h or 72 h of treatment. MTT method was used to assay the effects of the 2 drugs at different doses after 12 h, 24 h and 48 h on the proliferation of the cells. The expression of proliferating cell nuclear antigen (PCNA) in each group treated with different doses of DCN was detected by the method of immunohistochemistry after 48 h. The cell cycle distribution was determined by flow cytometry analysis. RESULTS: After administration of 10 mg/L DCN or 1 mg/L MMC for 12 h, the proliferation of HPF was significantly inhibited by both drugs in a dose- and time-dependent manner (P<0.05). After treated with 1~10 mg/L DCN for 48 h, the percentage of HPF in G0/G1 phase was increased, while the percentage of HPF in G2/M phase and S phase (G2/M%+S%) was decreased after treated with 5~10mg/L DCN for 48 h (P<0.05). The late-apoptotic cells were not found in DCN group and MMC group. DCN dose-dependently inhibited the expression of PCNA in HPF (P<0.05). CONCLUSION: Decorin significantly inhibits the proliferation of HPF, and blocks the cells in G1 phase. 相似文献
17.
AIM: To investigate the inhibitory effects of ATP on proliferation signaling in immortalized human fibroblasts. METHODS: Immortalized human fibroblasts were treated with ATP, ATP conbined with calcium or potassium channel antagonists, respectively. The intracelluar-free calcium ([Ca2+]i), inositol 1,4,5-trisphosphate(IP3) levels and cell viability were detected at different time points. RESULTS: ATP significantly increased the [Ca2+]i and decreased the IP3 level in immortalized human fibroblasts, especially at initial stage (P<0.01) . Compared to ATP alone, the proliferation rates remarkably increased when calcium or potassium channel antagonists were used (P<0.01, respectively) with ATP. CONCLUSION: The calcium and potassium channels and IP3 involved in the inhibitory effects of ATP on the proliferative signaling in immortalized human fibroblasts. 相似文献
18.
AIM:To study alterations of cardiac sarcoplasmic reticulum (SR) function in vitamin D3-induced calcium overload rats. METHODS: The Ca-overload rat models were prepared by vitamin D3 plus nicotine. Cardiac SR was seperated by centrifuging. The measurement of SR Ca2+uptake and Ca2+ release activities were preformed by the Millimore filtration technique. Specific SR -ryanodine binding capacity was measured by radioligand method. RESULTS: Compared with control,myocardial calcium content in calcium overload rats increased by 78%(P<0.01), SR Ca2+ uptake and Ca2+ release activities decreased by 64% and 40% respectively(P<0.01),and in the meantime ,the Ca2+-ATPase activity decreased by 65%(P<0.01).Maxmum value for -ryanodine binding decreased by 51%(P<0.01). CONCLUSION:The function of cardiac SR in calcium-overload rats was decreased. 相似文献
19.
AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of Gαq/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats (P<0.01). Protein Gαq/11 contents were not modified after 10 or 30 days of stenosis (P>0.05). At 10 days, the level of IP3 significantly increased in left ventricle of CA rats compared with the control animals (P<0.05), but there was no difference in IP3 level between CA and SO group after 30 days of operation. CONCLUSION: Phosphoinositide signaling pathway may play a role in the early stage of cardiac hypererophy induced by pressure overload. 相似文献
20.
YU Jun ZHU Miao-zhang PEI Jian-ming CHEN Bao-ying Lü Shun-yan DONG Ming-qing WEI Qi-ming 《园艺学报》2003,19(10):1311-1315
AIM:To investigate effect of hypoxia on the expression of proliferating cell nuclear antigen(PCNA) and phenotype of cardiac fibroblasts(CFs). METHODS:The purified cardiac fibroblasts were cultured and divided randomly into there groups :control group, moderate hypoxia(MH) group and severe hypoxia(SH) group. After 72 h, MTT method was used to investigate the proliferation of CFs, and the ultrastructure of fibroblasts were observed with transmission electron microscopy. The expression of PCNA and α-actin in cardiac fibroblasts were measured by the means of immunohistochemistry and laser scanning confocal microscopy, respectively. RESULTS: MTT A490 nmvalue of MH group was significantly higher than that of control group by (18.4±25.0)% (P<0.05), whereas MTT A490 nm value of MH group was significantly lower than that of control group by (15.8±25.0)% (P<0.05).The immunohistochemistry experiment showed that there was basal PCNA expression in control CFs, and it was increased in MH CFs(P<0.05 vs control group), but there was no significant difference between SH and control CFs. Observed with transmission electron microscopy, the control CFs had typical phenotype of fibroblasts: shuttle-shaped, abundant rough endoplasmic reticulums (RER) and golgi complexes, but few mitochondria or micromyofilaments in cytoplasm. After MH for 72 h, there appeared lots of micromyofilaments in cytoplasm, but there were little micromyofilaments in SH CFs. Observed with laser confocal scanning microscopy, there was lower expression of α-actin in CFs of control group, while many regular bundles of micromyofilaments and the expression of α-actin were signifiantly increased (P<0.05 vs control group) in CFs treated with MH. The α-actin expression in severe hypoxia CFs was not significantly different from control group. CONCLUSION:MH made CFs have the characteristics of myofibroblasts phenotype and enhanced PCNA expression. 相似文献