[Effect of Resveratrol on Isoproterenol Induced Cardiomyocyte Apoptosis Rats].

OBJECTIVE: To observe the effect and mechanism of resveratrol (Res) on isoprotere- nol (ISO) induced cardiomyocyte apoptosis rats. METHODS: Primary cultured neonatal cardiomyocyte ap- optosis rat model was established using ISO. Apoptosis cells were then randomly divided into 4 groups, i. e., the normal control group (non-serum DMEM culture fluid) , the model group (non-serum DMEM culture fluid + ISO 1 µmol/L for 48 h) , the Res + ISO group (ISO 1 µmol/L + Res 50 µmoI/L for 48 h) , the Res control group. (non-serum DMEM culture fluid + Res 50 l_mol/L). The apoptosis rate was measured by Hochest33258 staining. Ultrastructural changes of cardiomyocyte were observed by electron microscope. Leakage of lactate dehydrogenase (LDH) in the culture fluid was measured. Protein expressions of BcI-2 and Bax were detected using Western blot. Results The count of cardiomyocytes were reduced and the nucleus shape was irregular. The apoptosis bodies were visible and the apoptosis rate was increased in the model group. The cell membrane was complete with clear nuclear membrane in the Res + ISO group and the Res control group. Nuclear chromatin was concentrated and cell injured degree was attenuated in the Res +ISO group and the Res control group. Compared with the normal control group, the apoptosis rate and LDH leakage increased, the protein expression of Bcl-2 was down-regulated, and the expression of Bax was up-regulated in the model group (P <0. 05, P <0. 01). Compared with the model group, the apoptosis rate and LDH leakage decreased, the protein expression of Bcl-2 was up-regulated, and the expression of Bax was down-regulated in the Res + ISO group and the Res control group (P <0. 05). CONCLUSION: Res could obviously attenuate ISO induced cardiomyocyte apoptosis, and its mechanism might be associated with reversing protein expressions of Bcl-2 and Bax.

[Role of MEK1/ERK1, 2 pathways in the calcium-sensing receptor mediation of hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells].

OBJECTIVE: To explore the cell signal transduction pathway of calcium-sensing receptor (CaSR) mediated hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs). METHODS: The expressions of proliferating cell nuclear antigen (PCNA) and extracellular signal-regulated protein kinase 1, 2 (ERK1, 2) were analyzed by Western blot. Cell proliferation was tested by a 5-bromo-2-deoxyuridine (BrdU) incorporation assay. Cell cycle and proliferation index (PI) were analyzed by flow cytometry. RESULTS: Hypoxia significantly increased the expression of PCNA (0.528 ± 0.028), p-ERK1, 2 (1.12 ± 0.05, 0.91 ± 0.06), BrdU incorporation (143.3 ± 4.2) and cell proliferation index (12.5 ± 0.9) (all P < 0.05, versus control group, 0.243 ± 0.025, 0.47 ± 0.03, 0.40 ± 0.03, 100.0 ± 5.4, 7.5 ± 1.2). Gadolinium chloride (GdCl3, a CaSR agonist) amplified the effect of hypoxia (0.770 ± 0.039, 1.50 ± 0.06, 1.61 ± 0.05, 187.4 ± 3.9, 19.8 ± 0.6, all P < 0.05). PD98059 (a MEK1 inhibitor) decreased the up-regulation of PCNA expression, BrdU incorporation and the increase of cell proliferation index induced by hypoxia and GdCl3 in PASMCs (0.441 ± 0.020, 0.71 ± 0.07, 0.72 ± 0.06, 115.5 ± 4.0, 9.3 ± 1.1, all P < 0.05). CONCLUSION: Calcium-sensing receptor mediates hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells through ERK1, 2 pathways.

Ultrasonic destruction of albumin microbubbles enhances gene transfection and expression in cardiac myocytes.

BACKGROUND: It has been proven that ultrasonic destruction of microbubbles can enhance gene transfection efficiency into the noncardiac cells, but there are few reports about cardiac myocytes. Moreover, the exact mechanisms are not yet clear; whether the characteristic of microbubbles can affect the gene transfection efficiency or not is still controversial. This study was designed to investigate whether the ultrasound destruction of gene-loaded microbubbles could enhance the plasmids carried reporter gene transfection in primary cultured myocardial cell, and evaluate the effects of microbubbles characteristics on the transgene expression in cardiac myocytes. METHODS: The ß-galactosidase plasmids attached to the two types of microbubbles, air-contained sonicated dextrose albumin (ASDA) and perfluoropropane-exposed sonicated dextrose albumin (PESDA) were prepared. The gene transfection into cardiac myocytes was performed in vitro by naked plasmids, ultrasound exposure, ultrasonic destruction of gene-loaded microbubbles and calcium phosphate precipitation, and then the gene expression and cell viability were analyzed. RESULTS: The ultrasonic destruction of gene-loaded microbubbles enhanced gene expression in cardiac myocytes compared with naked plasmid transfection ((51.95 ± 2.41) U/g or (29.28 ± 3.65) U/g vs. (0.84 ± 0.21) U/g, P < 0.01), and ultrasonic destruction PESDA resulted in more significant gene expression than ASDA ((51.95 ± 2.41) U/g vs. (29.28 ± 3.65) U/g, P < 0.05). Ultrasonic destruction of microbubbles during calcium phosphate precipitation gene transfection enhanced ß-galactosidase activity nearly 8-fold compared with calcium phosphate precipitation gene transfection alone ((111.35 ± 11.21) U/g protein vs. (14.13 ± 2.58) U/g protein, P < 0.01). Even 6 hours after calcium phosphate precipitation gene transfection, ultrasound-mediated microbubbles destruction resulted in more intense gene expression ((35.63 ± 7.65) U/g vs. (14.13 ± 2.58) U/g, P < 0.05). CONCLUSIONS: Ultrasonic destruction of microbubbles might be a promising method for the delivery of non-viral DNA into cardiac myocytes, and the gene tranfection is related to the characteristics of microbubbles.

[Phospholamban antisense RNA transfer attenuates post-infarction remodeling and preserves cardiac functions].

OBJECTIVE: To investigate whether the gene transfer of phospholamban antisense RNA could inhibit remodeling and preserve cardiac function after myocardial infarction. METHODS: Wistar rats received a ligation of left coronary with a direct intramyocardial injection of phospholamban antisense RNA eukaryote vector PcDNA4-asPLB. The cardiac function, hemodynamics and ventricular geometry of three groups (shame, saline injection and PcDNA4-asPLB injection) were studied by echocardiography and left ventricle hemodynamic recording. The levels of phospholamban (PLB) and sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) were analyzed by Western blot and the expressions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) examined by RT-PCR. The histological study was performed to evaluate the collage content and cardiomyocyte fiber size. RESULTS: The PcDNA4-asPLB injection group had significantly better systolic cardiac function and diastolic function [LVEF (39.4 +/- 7.8)% vs (30.9 +/- 7.4)%, P < 0.05; dp/dt Max (1545 +/- 127) mm Hg x s(-1) vs (1172 +/- 91) mm Hg x s(-1), P < 0.05)]. Compared with saline injection, the PLB expression was inhibited by 50% in PcDNA4-asPLB injection group (PLB/beta-actin ratio, 0.28 +/- 0.07 vs 0.57 +/- 0.11, P < 0.05) and the function of SERCA2a was enhanced [(1.47 +/- 0.21) micromol x min(-1) x g(-1) protein vs (0.34 +/- 0.13) micromol x min(-1) x g(-1) protein, P < 0.05]. The expressions of ANP and BNP in the saline injection group were elevated as compared to those in the PcDNA4-asPLB injection group. Histological study also showed that the collage density and the cardiomyocyte fiber size in the saline injection group were worse than those in the PcDNA4-asPLB injection group. CONCLUSION: Intramyocardial injection of phospholamban antisense RNA eukaryote vector PcDNA4-asPLB after myocardial infarction results in PLB expression inhibition, attenuates ventricular remodeling and improves systolic and diastolic cardiac functions.

[Oxidized low density lipoprotein and peroxisome proliferator-activated receptor α induced endogenous fibroblast growth factor 21 upregulation is protective against apoptosis in cardiac endothelial cells].

OBJECTIVE: To investigate the effect of peroxisome proliferator-activated receptor (PPAR)α agonist bezafibrate and oxidized low density lipoprotein (ox-LDL) on fibroblast growth factor 21 (FGF21) expression and apoptosis in cardiac endothelial cells. METHODS: The mRNA level of FGF21 was determined by real time-PCR and the protein concentration of FGF21 in culture media was detected by enzyme-linked immunosorbent assay in cultured cardiac microvascular endothelial cells (CMECs) incubated with 10, 50, 100 µg/ml ox-LDL, 50, 100 or 200 µmol/L bezafibrate alone or in combination with 100 µg/ml ox-LDL. CMECs apoptosis in various treatment groups was also determined. RESULTS: FGF21 mRNA and protein expressions were significantly upregulated in proportion to increased ox-LDL, and 200 µmol/L bezafibrate alone also significantly upregulated FGF21 expression and CMECs apoptosis was significantly reduced in 200 µmol/L bezafibrate + 100 µg/ml ox-LDL group compared to 100 µg/ml ox-LDL group (P < 0.05). CONCLUSIONS: Our data suggest that bezafibrate and ox-LDL induced upregulation of FGF21 might mediate the protective effect against apoptosis. Endogenous FGF21 could thus play important roles in improving the endothelial function at the early stage of atherosclerosis and slowing the development of coronary heart disease.

[Using the combination of traditional risk factors and quantitative coronary angiography (QCA) in predicting the risk of individuals with subclinical artherosclerosis].

OBJECTIVE: To determine whether the combination of traditional risk factors and quantitative coronary angiography (QCA) assessment could provide accurate prognostic information on a population-based study including 1137 adults with subclinical artherosclerosis and with coronary risk factors. METHODS: Participants underwent coronary angiography examination before the minimal stenotic diameters, segment diameters, percent stenosis, plaque areas. Other parameters were analyzed by the computer-assisted Coronary Angiography Analysis System. The Framingham Risk Score for each participant was assessed. During the 1 year follow-up period, all kinds of endpoint cardiovascular events were screened. Endpoint events were defined as death from coronary heart disease, nonfatal myocardial infarction (MI) or unstable angina pectoris. RESULTS: During the 1 year of follow-up period, a total of 124 participants developed an endpoint event, which was significantly associated with the Framingham Risk Score, calcium of plaques and the plaque areas (all Ps<0.05). The QCA score incorporated with the QCA parameters was related to the endpoint events. The Framingham Risk Score was combined with QCA score through logistic regression for prediction of end-point events. Data from the ROC analysis showed the accuracy of this prediction algorithm was superior to the accuracy when variables themselves were used. The event-free survival rate was inferior to the control group in participates under high risk, when being screened with this prediction algorithm (P<0.05). CONCLUSION: The risk of cardiovascular attack in subclinical artherosclerosis individual seemed to be associated with the Framingham Risk Score, calcium of plaques and the plaque areas. When the traditional risk factors (the Framingham Risk Score) were combined with QCA, the new method could provide more prognostic information on those adults with subclinical artherosclerosis.

Fibroblast growth factor 21 as a possible endogenous factor inhibits apoptosis in cardiac endothelial cells.

BACKGROUND: Fibroblast growth factor 21 (FGF21) is a new member of FGF super family that is an important endogenous regulator for systemic glucose and lipid metabolism. This study aimed to explore whether FGF21 reduces atherosclerotic injury and prevents endothelial dysfunction as an independent protection factor. METHODS: The present study was designed to investigate the changes of FGF21 levels induced by oxidized-low density lipoprotein (ox-LDL), and the changes of apoptosis affected by regulating FGF21 expression. The FGF21 mRNA levels of cultured cardiac microvascular endothelial cells (CMECs) were determined by real time-PCR and the protein concentration in culture media was detected by enzyme-linked immunosorbent assay. We analyzed the different expression levels of untreated controls and CMECs incubated with ox-LDL, and the changes of CMECs apoptosis initiated by the enhancement or suppression of FGF21 levels. RESULTS: The secretion levels of FGF21 mRNA and protein were significantly upregulated in CMECs incubated with ox-LDL. Furthermore, FGF21 levels increased by 200 µmol/L bezafibrate could reduce CMECs apoptosis, and inhibit FGF21 expression by shRNA induced apoptosis (P < 0.05). CONCLUSIONS: FGF21 may be a signal of injured target tissue, and may play physiological roles in improving the endothelial function at an early stage of atherosclerosis and in stopping the development of coronary heart disease.

[Quantitative coronary angiography and intravascular ultrasound assessments on target lesion and reference vessel in patients with diabetes mellitus].

OBJECTIVE: To evaluate the accuracy of quantitative coronary angiography (QCA) assessment on target lesion and reference vessel in patients with diabetes mellitus with intravascular ultrasound (IVUS) measurements as golden standard. METHODS: QCA and IVUS were performed in 52 diabetes mellitus patients [35 males, mean age (62.3 +/- 7.1) years]. Regression equation was ascertained with the IVUS derived plaque burden as dependent and QCA derived vessel stenosis as independent variable. The measurement results derived from the two modalities on proximal and distal reference vessels were compared. RESULT: The regression equation (constant = 0.8286, P = 0.001) of plaque burden and vessel stenosis derived from two modalities were significantly correlated (r = 0.691, P < 0.001) but QCA overestimated the stenosis severity (57.9% +/- 15.5% vs. 53.5% +/- 12.9%, P < 0.01). Target vessels negative remodeling index in these patient was 0.87 +/- 0.23. QCA significantly underestimated the proximal and distal reference segments vessel diameters [(0.81 +/- 0.24) mm, (0.64 +/- 0.17) mm, all P < 0.05] as compared to IVUS results. CONCLUSION: Due to the significant negative vessel remodeling, QCA overestimated the stenosis severity and underestimated the reference segments vessel diameters in patients with diabetes mellitus.

[Value of intravascular ultrasound, 64 multi-detector computed tomography and quantitative coronary angiography on lesion of coronary artery in unstable angina pectoris patient].

OBJECTIVE: To compare the value of intravascular ultrasound (IVUS) and assess the value of quantitative coronary angiography (QCA) and 64 multi-detector computed tomography (MDCT) on unstable anginas (UAP) risk stratification. METHOD: A total of 61 UAP patients (low risk: 17, middle risk: 33 and high risk: 11) were recruited, 71 vessels were examined by MDCT, QCA and IVUS. Plaque characteristics (soft, fibrous, calcified and mixed plaques) and plaque burden at minimum area (< or = 50%, 51% - 74% and > or = 75%) were detected, calculated and analyzed. Results derived from various detection methods were compared. RESULTS: Plaque burden detection by QCA was comparable to IVUS results for low and middle risk UAP (r = 0.768 and r = 0.721, respectively; all P < 0.01) but not for high risk UAP (67% + or - 14% vs.75% + or - 16%, P < 0.01) due to significant positive vessel remodeling (remodeling index = 1.21 + or - 0.31). The high negative predict value of MDCT for stenosed coronary vessels (87.8% - 96.3%)was valuable for exclusion of coronary heart disease but MDCT was not able to identify fibrous cap (kappa = 0.235) and lipid core (kappa = 0.245). Extent of remodeling index, external elastic membrane area, minimum lumen area, plaque burden, plaque rupture and thrombosis increased in proportion to increasing risks of UAP patients. CONCLUSIONS: QCA is a suitable tool for assessing UAP patients with low and middle vessel stenosis but underestimated the stenosis degree in UAP patients with high vessel stenosis. MDCT is valuable for exclusion vessel disease but not useful for identifying soft and fibrous plaque. Soft plaque with positive remodeling index and minimum lumen area < 4 mm(2) derived from IVUS could correctly identify UAP patients with high degree of vessel stenosis.

Aspirin can elicit the recurrence of gastric ulcer induced with acetic acid in rats.

UNLABELLED: This study was supported by grants of New Ideas Capability for Backbone Teachers in Universities of Heilongjiang and of Scientific Research foundation in Qiqihar Medical College. BACKGROUND/AIMS: Ulcer recurrence and poor healing may be critically important to the development of serious gastrointestinal complications in patients with long-term non-steroid anti-inflammatory drugs (NSAIDs). The present study is to investigate the effects of aspirin on ulcer recurrence and healing quality and to explore the mechanism. METHODS: Gastric ulcers were induced with acetic acid in rats; aspirin was administrated by gavage from day 25 to day 54 after ulcer induction. The gastric juice volume, pH, gastric mucus, gastric mucosal blood flow (GMBF) and prostaglandin E(2) (PGE(2)) were measured. The mRNA transcription of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were analyzed with RT-PCR and protein expression with Western blot. RESULTS: The gastric juice volume was significantly increased in aspirin group compared with those of fasting or saline control groups (P<0.01); while the pH, mucus, GMBF and PGE(2) were significantly decreased in aspirin treated rats compared with those of other two groups (P<0.01). COX-2, evaluated with mRNA and protein expression, was significantly augmented in aspirin group compared with others. The quality of ulcer healing (QOUH) in Aspirin group was poorer than that of fasting or saline control groups. CONCLUSIONS: Aspirin enhance the recurrence of gastric ulcer. The inhibition of cycloxygenase, mucus secretion and mucosal blood flow may be involved. Aspirin also impair the quality of ulcer healing.

Cocultivation of umbilical cord blood CD34+ cells with retro-transduced hMSCs leads to effective amplification of long-term culture-initiating cells.

AIM: To establish a novel coculture system for ex vivo expansion of umbilical cord blood(UCB) hematopoietic progenitors using thrombopoietin (TPO)/Flt-3 ligand (FL)-transduced human marrow-derived mesenchymal stem cells (tfhMSCs) as feeder. METHODS: UCB CD34+ cells were isolated and cultured using four culture systems in serum-containing or serum-free medium. Suitable aliquots of cultured cells were used to monitor cell production, clonogenic activity, and long-term culture-initiating culture (LTC-IC) output. Finally, the severe-combined immunodeficient (SCID) mouse-repopulating cell (SRC) assay was performed to confirm ability of the cultured cells to reconstitute long-term hematopoiesis. RESULTS: There were no significant differences in the number of total nucleated cells among different culture systems in serum-containing medium during 21-d culture. However, on d 14, the outputs of CD34+ cells, CFU-C and CFU-GEMM in tfhMSCs coculture system were significantly enhanced. LTC-IC assay demonstrated that the tfhMSCs coculture system had the most powerful activity. The severe-combined immunodeficient (SCID) mouse repopulating cell (SRC) assay confirmed extensive ability of the expanded cells to reconstitute long-term hematopoiesis. Furthermore, PCR analysis demonstrated the presence of human hematopoietic cells in the bone marrow and peripheral blood cells of NOD/SCID mice. CONCLUSION: The TPO/FL-transduced hMSCs, in combination with additive cytokines, can effectively expand hematopoietic progenitors from UCB in vitro and the tfhMSCs coculture system may be a suitable system for ex vivo manipulation of primitive progenitor cells under contact culture conditions.

[The changes in the mRNA levels of calcium regulatory proteins in ischemia/reperfusion rat ventricles].

AIM: To investigate the changes in the expression of four kinds of calcium regulatory proteins mRNA on the isolated ischemia/ reperfusion (IR) hearts. METHODS: The rat hearts were divided into two groups: control group and IR group which received 45 min exposure to Krebs-Henseleit solution after 15 min zero-flow global ischemia. The indexes of left ventricular function, such as LVDP, +dp/dt(max), -dp/dt(max), and an arrhythmia scoring system were compared between the two groups. The messenger ribonucleic acid (mRNA) amount of sarcoplasmic reticulum (SR) Ca2+ ATPase (SERCA), phospholamban (PLB), inositol 1,4,5-trisphosphate receptor2 (IP3R2) and ryanodine receptor2 (RyR2) was measured by reverse transcription-polymerase chain reaction (RT-PCR) and normalized to the mRNA levels of beta-actin. RESULTS: In the IR group, LVDP, +dp/dt(max) and -dp/dt(min) of the isolated hearts were depressed and the high rate of arrhythmias occurred during reperfusion. The levels of SERCA, IP3R2, RyR2 mRNA were lower in the IR isolated hearts group than those in the control group, while there was no difference in the level of phospholamban. CONCLUSION: These data suggest that myocardial ischemia/reperfusion can induce the depression of cardiac performance and an increased risk of arrhythmias, concomitant with the decrease in SERCA, IP3R2, RyR2 mRNA steady state levels.

Construction of phospholamban antisense RNA recombinant adeno-associated virus vector and its effects in rat cardiomyocytes.

AIM: To construct a recombinant adeno-associated virus (rAAV) vector containing gene encoding phospholamban antisense RNA (asPLB), and analyse its effect on expression of PLB, expression and activity of sarco-endoplasmic reticulum Ca2+-ATPase (SERCA), and the change of intracellular free Ca2+ concentration ([Ca2+]i) in rat cardiomyocytes. METHODS: The target gene encoding PLB antisense RNA was inserted inversely into the adeno-associated virus plasmid pAAV-MCS digested by corresponding restricted endonuclease enzyme. The recombinant plasmid and pAAV-RC and pHelper were co-transfected into 293 cell. At the same time, a viral production positive control (rAAV-LacZ) and negative control were performed. The recombinant viruses were used to transfect the cultured rat cardiomyocytes. Site beta-Galactosidase staining were performed to observe the transfer efficiency. Reverse transcription-PCR and Western blot were used to determine the mRNA and protein expression of PLB and SERCA. The activity of SERCA and the [Ca2+]i were measured. RESULTS: The rAAV vectors were constructed successfully and were transfected into rat cardiomyocytes effectively. The PLB mRNA and protein expression were reduced in rat cardiomyocytes transfected by rAAV-asPLB compared with controls. The activity of SERCA was increased. In rest state, the level of [Ca2+]i in the rAAV-asPLB transfected group decreased. The level of [Ca2+]i increased when induced by isoproterenol. CONCLUSION: AAV-asPLB vector was constructed successfully, which disrupted the expression of PLB, enhanced the activity of SERCA, reduced the resting [Ca2+]i, and improved the cardiac function.

[Enhanced reporter gene transfer and expression in cardiac myocytes mediated by ultrasonic destruction of the microbubbles].

AIM: To determine if the diagnostic ultrasound and self-made microbubbles could be used to increase gene transfection and expression in cardiac myocytes by means of the ultrasound-mediated microbubbles destruction. METHODS: The perfluoropropane-exposed sonicated dextrose albumin(PESDA) microbubbles were made and mixed with indicated volume reporter gene encoding beta-galactosidase prior to gene transfection. Gene transfection into the cultured cardiac myocytes was performed by exposure to the various intense diagnostic ultrasound (1.3 MHz) in the presence of the gene-attached microbubbles. The calcium phosphate precipitation gene transfection was carried out alone or in combination with ultrasound-mediated destruction microbubbles. The cells were harvested 48 h after transfection and beta-galactosidase expression was detected by in situ staining and quantitive assay. RESULTS: Cardiac myocytes exposed to ultrasound with PESDA induced significantly increase in gene expression (60-fold compared with naked plasmids transfection, P < 0.01). Moreover, it was found that the reporter gene expression not only related with ultrasound intension but also with the microbubbles concentration. In combination with calcium phosphate precipitation gene transfection, ultrasound-mediated destruction microbubbles resulted in more intense gene expression even 6 hours after calcium phosphate precipitation gene transfection. CONCLUSION: The ultrasonic destruction of gene-loaded microbubble is a highly effective gene transfer method, and it not only acts on the gene entry into cells, but also on the intracellular exogenous DNA expression.

[Study of platelet membrane glycoprotein expression in mice with decompression sickness].

OBJECTIVE: To investigate the role of expression of platelet membrane glycoprotein CD31, CD61 and CD62p in the pathogenesis of decompression sickness. METHODS: Mice were randomly divided into decompression sickness group and normal control group. The animals in decompression sickness group were exposed to 600 kPa compressed air for 60 minute, then they were rapidly decompressed to normal pressure in one minute. At 60th minute after reducing to normal pressure, the expression of CD31, CD61 and CD62p on platelet membrane in mice was measured by flow cytometry. RESULTS: The mean fluorescence intensity of CD31, CD61 and positive percentage of CD62p on platelet membrane [(18.64 +/- 1.01), (271.06 +/- 24.25), (4.48% +/- 0.43%) respectively] in decompression sickness group were significantly increased compared with normal control group [(16.89 +/- 1.69), (234.09 +/- 15.96), (3.00% +/- 0.66%) respectively] (P < 0.05, P < 0.01). CONCLUSION: Inadequately rapid decompression may induce up regulation of platelet membrane glycoprotein CD31, CD61 and CD62p expression in mice, which may lead to thrombosis.

Short term effect of Salvia miltiorrhiza in treating rat acetic acid chronic gastric ulcer and long term effect in preventing recurrence.

AIM:To study the short-term effect of Danshen (Salvia miltiorrhiza) on acetic acid induced chronic gastric ulcer in rats and its long-term effect in preventing recurrence.METHODS:Rats with acetic acid-induced gastric ulcer were treated with Danshen and cimetidine for 30 days.Traditional gastric mucosal auto-radiography and (3)H-TdR incorporation into gastric mucosa in vitro were employed to study the effects of Danshen in rat acetic acid-induced chronic gastric ulcer, including ulcer index (UI), ulcer inhibitory rate (IR) and label rate (LR).RESULTS:On the day 5, 30 and 126 of ulcer-making, the UI in the Danshen group was obviously lower than that in the cimetidine group and the control group (42.3 ± 3.9, 3.6 ± 1.2, 4.4 ± 2.3; 49.1 ± 3.6, 5.9 ± 1.4, 9.2 ± 1.3; 61.0 ± 3.8, 8.9 ± 2.5, 12.4 ± 2.4, respectively, P < 0.01), the IR (%) in the Danshen group was obviously higher than that in the cimetidine group (31, 59, 64.8; 19, 33, 26, respectively), and the LR in the Danshen group was obviously higher than that in the cimetidine group and the control group (10.0 ± 0.5,16.2 ± 0.8, 15.0 ± 0.6; 9.0 ± 0.5, 13.9 ± 0.6, 10.8 ± 0.7; 6.5 ± 0.7, 10.1 ± 0.5, 8.0 ± 0.7, respectively, P < 0.01). There was no obvious difference in UI in the Danshen group on day 30 as compared with that on day 126.CONCLUSION:Danshen is effective in promoting ulcer healing and preventing recurrence. The mechanism of action is to strengthen the gastric mucosal barrier and to promote the gastric mucosal cell proliferation along the edge of the ulcer.