Distribution of Nogo in the heart and its role in cardiovascular disease / 解剖学报

As a member of the reticulin family, Nogo is mainly involved in processes such as tissue regeneration, apoptosis and tumor growth after tissue injury. Cardiovascular disease is one of the main diseases that threaten human health at present. In recent years, research on Nogo in the cardiovascular system has become increasingly extensive. Changes in the expression of Nogo during myocardial fibrosis, myocardial cell apoptosis and vascular remodeling suggest that it may play a certain role. This article reviews the distribution of Nogo in the heart and its role in cardiovascular disease, in order to reveal its possible role and mechanism in cardiovascular diseases.

Composition of Ophiopogon Polysaccharide, Notoginseng Total Saponins and Rhizoma Coptidis Alkaloids Inhibits the Myocardial Apoptosis on Diabetic Atherosclerosis Rabbit / 中国结合医学杂志

OBJECTIVE@#To investigate the effects of Composition of Ophiopogon polysaccharide, Notoginseng total saponins and Rhizoma Coptidis alkaloids (CONR) on myocardial apoptosis of diabetic atherosclerosis (DA) rabbits METHODS: Sixty male New Zealand white rabbits were randomly divided into 6 groups [control group, model group, CONR high-dose group (450 mg/kg), CONR medium-dose group (150 mg/kg), CONR low-dose group (50 mg/kg), and simvastatin group] by using a completely random method, 10 in each group. DA model was established by intravenously injected alloxan combined with high-fat diet and abdominal aortic balloon injury. After mediation for 10 weeks, fasting blood glucose (FBG), glycosylated hemoglobin (GHB), glycosylated serum protein (GSP), fructoseamine (FRA), aldose reductase (AR), advanced glycation end products (AGEs) in serum were measured by enzyme linked immunosorbent assay (ELISA) method; the expression of receptor of AGEs (RAGE) in myocardial tissue were observed by immunohistochemical method; and p-Jun N-terminal kinase (p-JNK), caspase-3, B-cell lymphoma-2 (bcl-2) protein expression in myocardial tissue were measured by Western blotting. The myocardial apoptosis was detected by TdT-mediated dUTPnick-end labeling (TUNEL) method, and apoptosis index (AI) was calculated.@*RESULTS@#Compared with the control group, serum FBG, GHB, GSP, FRA, AR, AGEs and the expression of myocardium RAGE, p-JNK, caspase-3 proteins, as well as apoptosis index (AI) were significantly increased and bcl-2 protein was significantly decreased in the model group (P<0.01). Compared with the model group, the levels of serum FBG, GHB, GSP, FRA and AR showed a significant decline in CONR high- and medium-dose groups (P<0.01). FBG and GHB showed a significant decline in CONR low-dose group (P<0.01). Compared with the model group, the expression of serum AGEs and myocardium RAGE, p-JNK and caspase-3 protein as well as AI were significantly decreased and bcl-2 protein was significantly up-regulated in all treatment groups (P<0.01); high-dose CONR had the most significant effect on abovementioned indices compared with other treatment groups (P<0.01). Middle-dose CONR had better effect on serum AGEs compared with the low-dose group (P<0.01); middle-dose CONR and simvastatin groups had better effect on the expression of caspase-3, bcl-2 protein, myocardium apoptosis compared with the CONR low-dose group (P<0.01).@*CONCLUSION@#CONR may effectively inhibit myocardial apoptosis on DA rabbits by intervening AGEs-RAGE and JNK, caspase-3, and bcl-2 protein expressions.

Myocardial apoptosis and anti-apoptotic mechanism of captopril on cardiac arrest after resuscitation of pulmonary embolism / 中华急诊医学杂志

Objective To observe the myocardial apoptosis and the molecular mechanism of captopril inhibiting myocardial apoptosis on cardiac arrest (CA) after resuscitation in a porcine acute pulmonary embolism (APE) model. Methods In this study, 29 inbred Beijing Landrace wererandomly (random number)divided into four groups (n=5, each group): control, APE-CA, restoration of spontaneous circulation (ROSC)-captopril, and ROSC-saline. The model of CA and ROSC was induced by APE through injection of thrombus followed by cardiopulmonary resuscitation and thrombolytic therapy (urokinase, 15000 U/kg, iv). Ten of 19 pigs with CA recovered to spontaneous circulation were divided randomly into the ROSC-captopril and ROSC-saline groups. Pigs in the ROSC-captopril group were treated with captopril (22.22 mg/kg) via porcine femoral vein at 30 min after ROSC. Pigs in the ROSC-saline group were treated with equal normal saline at 30 min after ROSC. The myocardial tissues were evaluated at 6 h after ROSC. Western blot was used to evaluate the protein levels of Bax, Bcl-2, Caspase-3, phosphorylated (p)-Src and phosphorylated extracellular regulated protein kinase (p-ERK1/2). Immunohistochemistry was used to evaluate the protein expression of p-Src and p-ERK1/2. Enzyme-linked immunosorbent assay was used to detect myocardial Na+-K+-ATPase levels. Statistical analysis was performed using one-way analysis of variance and pearson correlation test. Results Compared with the control group, the protein expression of Bax (0.25±0.01, 0.53±0.01, 0.37±0.05, F=14.16, P<0.05) and Caspase-3 (0.24±0.01, 0.33±0.01, 0.34±0.06, F=7.32, P<0.05) in the APE-CA and ROSC- saline group were increased significantly, and the Bcl-2 expression was significantly decreased (0.56±0.02, 0.19±0.01, 0.37±0.10, F=6.68, P<0.05). Captopril reduced the protein levels of Caspase-3 and Bax, while stimulated the Bcl-2 expression (all P<0.05). Compared with the control group, the protein expression of p-Src and p-ERK1/2 were higher and the Na+-K+-ATPase level was decreased on CA and ROSC induced by APE (all P<0.05). Compared with the APE-CA group, the p-Src expression in the ROSC-captopril group (0.46±0.01 vs. 0.35±0.06, P<0.05) was decreased significantly. Captopril inhibited the activation of p-ERK1/2 than saline group (0.41±0.10 vs. 0.26±0.07, P<0.05), but has no effect on the Na+-K+-ATPase level. The protein expression of p-Src and p-ERK1/2 were positively correlated with the Bax, and negatively correlated with the Bcl-2 respectively. The myocardial Na+-K+-ATPase level negatively correlated with Caspase-3 protein expression. Conclusions The molecular mechanism of cardiomyocyte apoptosis on CA and ROSC induced by APE might be related to decreased Na+-K+-ATPase level and activation of p-Src and p-ERK1/2. The cardiomyocyte apoptosis were inhibited by captopril through reducing the expression of p-Src and p-ERK1/2 in myocardium.

Effect of fracture of lower limbs with hemorrhage on myocardial injury and its mechanism in rats / 中国应用生理学杂志

OBJECTIVES@#To test whether myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage, in order to lay a foundation of myocardial injury after traumatic fracture for the follow-up study.@*METHODS@#Twenty SD rats were randomly divided into two groups, i. e. control group and trauma group(=10). A rat model of traumatic hemorrhage was establish, and a traumatic model of the original generation of myocardial cell culture was constructed . The level of interleukin-2(IL-2),IL-6,IL-10 and tumor necrosis factor-α(TNF-α) in rat serum was detected by ELISA at 0, 1, 2, 4, 8, 12, 16, 24 and 48 hour to find the most significant point. The pathological cardiac injury in rats was observed by HE staining under a microscope, and the apoptosis of cultured cardiomyocyte was detected by TUNEL methods. The expressions of apoptosis gene,(Bcl-2) and Bax, in myocardium of rat and cultured cardiomyocyte were detected by Western blot and RT-PCR.@*RESULTS@#At the 4 hour after trauma, IL-6 and IL-10 in the serum of rats reached its highest, IL-2 reached its lowest at the 8th hour after trauma, and TNF-αreached its highest at 1 hour after trauma, then all recovered to their normol level gradually. Myocardial HE staining indicated that cardiomyocyte was swelling, disordered derangement, inflammatory cell infiltrated; a large number of myocardial cell nuclei was dyedbrown in TUNEL test which proved that the apoptosis index increased (<0.05). Western blot and RT-PCR results showed that the expression of pro-apoptotic gene Bax was up-regulated (<0. 05), while expression of anti apoptosis gene Bcl-2 down-regulated (<0.05).@*CONCLUSIONS@#The myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage in rats, and then lead to myocardial injury.

Mangiferin alleviates hypoxia-induced cell apoptosis in rat primary cultural cardiomyocytes / 基础医学与临床

Objective To investigate the effect of mangiferin on the apoptosis of rat primary cardiomyocytes induced by hypoxia. Methods Rat primary cardiomyocytes were separated and cultured under aseptic condition. Cardiomyocytes were treated with hypoxia of 2, 4, 8 and 12 h, and then the time of hypoxia of cardiomyocyte apoptosis model was determined according to the apoptosis outcome.The cardiomyocytes were divided into normal group, hypoxia group and mangiferin intervention group, each group was subjected to 3 batches in parallel, and 3 holes were done in parallel with each batch. After the experiment, cardiomyocytes apoptosis was deteced by flow cytometry;apoptosis protease caspase-3 and caspase-9 activity in cell lysates was detected by spectrophotometry;the protein expression of Bax and Bcl-2 was detected by Western blot. Results After treated with hypoxia for 12 h, the cardio-myocytes apoptosis rate was significantly increased (P < 0.05), the apoptosis protease caspase-3 and caspase-9 activity was increased markedly (P＜0.05), the protein expression of proapoptotic protease Bax was increased notablely (P＜ 0.05 ) , and the protein expression of anti apoptotic protease Bcl-2 was decrease memorably (P＜0.05) in hypoxia group as compared with those in the control group. After mangiferin intervention, above indexes in mangiferin group can be significantly relieved as compared with those in the hypoxia group. Conclusions Mangiferin can significantly inhibit the apoptosis of rat primary cardiomyocytes induced by hypoxia.

The effect of Ulinastatin on myocardial cell apoptosis and Caspase-3 channel / 中华急诊医学杂志

Objective To investigate the effect of ulinastatin on myocardial injury in rats with sepsis.Methods Thirty male SD rats were randomly (random number) divided into 3 groups:sham operation group (Sham group,n=10),sepsis group (sepsis group,n=10) and ulinastatin group (UTI group,n=10).The sepsis model of the rats was subjected to cecal ligation and puncture (CLP).Rats of UTI group were given 200 000 U/kg ulinastatin at 6 hour after modeling,and dosing was repeated every 12 h.Blood samples were collected from inferior vena cava at 6,12,24,36 h after modeling for determination of cardiac troponin-Ⅰ (cTnI) and the inflammatory factor by ELISA,then the rats were sacrificed and hearts were removed for myocardial tissue stained with hematoxylin eosin (HE) staining,the expression of Bax/Bcl-2 protein level and myocardial cell apoptosis were detected by TUNEL.The level of caspase-3 protein in myocardial tissue was detected by Western-blot.Results The level of cTnI (ng/mL) in serum in UTI group at 6,12,24 and 36 h after modeling were significantly lower compared with sepsis group(P＜0.05).The protein expression levels of TNF-α and IL-6 (ng/mL) in group UTI were higher than those in Sham group,but was significantly lower than those in Sepsis group (P＜0.05).HE staining showed that inflammatory cell infiltration present in myocardial cells,edema and vacuole formation were observed in sepsis group,while those were significantly attenuated in UTI group compared with sepsis group.UTI increased the level of myocardial Bcl-2 protein in the rats (P＜0.05),and reduced the level of myocardial Bax protein (P＜0.05).TUNEL and HE staining showed apoptosis cells in UTI group was significantly reduced compared with sepsis group [(32.2±4.8)％ vs.(58.4±5.6)％,P＜0.05];Western-blot method showed the level of Caspase-3 protein in UTI group was higher than that in group sham (0.32±0.048) vs.(0.12±0.03),P＜0.05],but significantly lower than that of Sepsis group [(0.32±0.048) vs.(0.55±0.052),P＜0.05].Conclusions Ulinastatin can reduce proinflammatory mediators release in the blood of sepsis rats,and inhibit the apoptosis of myocardial cells protecting myocardial cells through the regulation of the Caspase-3 pathway during sepsis.

Effects of Moxibustion on Ventricular Mass Index and Expression of Apoptosis Related Proteins in Myocardium of Rats with Chronic Heart Failure / 针刺研究

OBJECTIVE: To observe the effect of moxibustion on cardiac function and the expression of B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), Fas, Fas ligand (FasL) in cardiomyocytes of chronic heart failure (CHF) rats, so as to explore its underlying mechanisms in preventing and treating CHF. METHODS: SD rats were randomly divided into normal control, model, moxibustion, Captopril and moxibustion ＋ Captopril (M＋C) groups (n＝12 rats/group). The CHF model was established by intraperitoneal injection of Adriamycin (ADR, from 1 to 4 mg/kg, once every other day for 15 days). Mild moxibustion was applied to bilateral"Feishu"(BL 13) and "Xinshu"(BL 15). Rats of the Captopril group was treated by gavage of Captopril suspension (5 mg/mL, 25 mL/kg), and those of the M＋C group treated by the combined two methods. All the treatments were given once a day for 3 weeks. The general conditions and behaviors of rats were observed. The left ventricular mass index (LVMI) and right ventricular mass index (RVMI) were detected for assessing the cardiac performance. Morphological changes of myocardium were observed by HE staining. Enzyme linked immunosorbent assay (ELISA) was used to detect the concentrations of B-type natriuretic peptide (BNP) and precursor N-terminal pro-brain natriuretic peptide (NT-pro BNP) in the serum. The expression levels of Bcl-2, Bax, Fas and FasL of the left ventricle of heart were detected by Western blot. RESULTS: After modeling, the pathological changes of myocardium (as myocardial cell swelling with vacuoles, myocardial fibre breakage, etc.) were obvious, the LVMI, RVMI, serum BNP and NT-pro BNP concentrations, and myocardial Bax, Fas and FasL protein expression levels were significantly increased in the model group compared with the normal group (P0.05)．. CONCLUSION: Moxibustion can reduce myocardial injury and improve cardiac function in CHF rats, which may be related to its effects in down-regulating the expression of myocardial Bax, Fas and FasL proteins, and up-regulating the expression of Bcl-2 protein to inhibit cardiomyocyte apoptosis.

Effects of Simvastatin on myocardial apoptosis and oxidative stress mechanism in immature rabbits with chronic heart failure / 中华实用儿科临床杂志

Objective To observe the effects of Simvastatin on myocardial apoptosis and oxidative stress mechanism in immature rabbits with chronic heart failure.Methods Thirty-six male New Zealand big-eared immature rabbits were randomly divided into 3 groups:Adriamycin(ADR) ± Simvastatin group(ADR-s group,n =12),in which ADR(1.5 mg/kg) received injection via the auricular vein of rabbits weekly,and the rabbits received oral Simvastatin [1.5 mg/(kg · d)] simultaneously for 12 weeks;ADR group (n =12),in which the rabbits received ADR like ADR-S group,and 9 g/L saline instead of Simvastatin;control group (CON group,n =12),which received the same amount of 9 g/L saline.Echocardiography examination was performed in 13th week.Myocardial fibrosis degree was detected by using MASSON staining,and the myocardial apoptosis was detected by using terminal deoxynucleotidyl transferase dUTP nick end labeling.Colorimetric method was used to detect the myocardial concentration superoxide dismutase (SOD) and malondialdehyde (MDA).Enzyme-linked immunosorbent assay was used to detect serum B-type brain natriuretic peptide (BNP) level.Results (1) In CON group,the immature rabbits were all alive.Four rabbits died in ADR group,and the survival rate was 66.7％,while 2 rabbits died in ADR-s group,and the survival rate was 83.3％.(2)Compared with CON group,the left ventricular end diastolic diameter (LVEDd) and left ventricular end systolic diameter (LVESd) in ADR-s group and ADR group increased [(11.90 ±1.09) mm,(ll.34 ±0.92) mm vs.(10.73 ±0.48) mm;(9.80 ±0.88) mm,(8.47 ± 1.23) mm vs.(7.31 ±0.36) mm];left ventricular fractional shortening(LVFS) and left ventricular ejection fraction(LVEF) decreased [(17.65 ± 1.70)％,(22.58 ± 2.19)％ vs.(31.79 ± 2.58) ％;(41.35 ± 3.19) ％,(49.17 ± 3.53) ％ vs.(64.34 ± 3.97) ％],and all the differences were significant(all P ＜ 0.05);LVEDd and LVESd in ADR-s group were lower than those of ADR group,while LVEF and LVFS in ADR-s group were higher than those of ADR group,and the differences were significant(all P ＜ 0.05).(3)MASSON staining:compared with ADR group,there was less myocardial cell hyperplasia of fibrous tissue in ADR-s group.(4) Compared with CON group,the apoptosis index was higher in ADR and ADR-s group [(34.25 ±11.13) ％,(24.00 ±6.85)％ vs.(16.58 ± 5.34)％],but ADR-s group had less than ADR group,and the differences were significant (all P ＜ 0.05).(5) Compared with ADR group,SOD activity of ADR-s group was higher [(13.40 ± 2.68) kU/L vs.(10.66 ± 2.99) kU/L],but MDA content was lower [(5.67 ± 1.36) μmol/mg vs.(7.08 ±0.98) μmol/mg],and the differences were significant (all P ＜0.05).(6) Serum BNP level in ADR group and ADR-s group was higher than that of the CON group[(33.28 ±9.58) μg/L,(26.71 ±6.72) μg/L vs.(13.56 ±2.82) μg/L],while was higher in ADR group than that of ADR-s group,and the differences were significant (all P ＜ 0.05).Conclusions Simvastatin can protect cardiac function of immature rabbits with chronic heart failure.The possible mechanism may be the up-regulation of myocardial SOD activity,reduction of cell lipid peroxidation and inhibition of myocardial apoptosis.

Protective effects of fentanyl preconditioning on cardiomyocyte apoptosis induced by ischemia-reperfusion in rats

We aimed to study the effect of fentanyl (Fen) preconditioning on cardiomyocyte apoptosis induced by ischemia-reperfusion (I/R) in rats. A total of 120 Sprague Dawley male rats (age: 3 months) were randomly divided into: sham operation group (S group), I/R group, normal saline I/R group (NS group), and fentanyl low, middle, and high dose groups (Fen1: 2 μg/kg; Fen2: 4 μg/kg; Fen3: 6 μg/kg). Heart rate (HR), mean arterial pressure (MAP), left ventricular developed pressure (LVDP), ±dp/dtmax, malondialdehyde (MDA), superoxide dismutase (SOD) activity, creatine phosphokinase-MB (CK-MB), and cardiac troponin-I (cTnI) were measured. Myocardial ischemic (MI) area, total apoptotic myocardial cells, and protein and mRNA expressions of B-cell lymphoma 2 (Bcl-2) and Bax were detected. HR and MAP were higher, while LVDP and ±dp/dtmax were close to the base value in the Fen groups compared to those in the I/R group. Decreased MDA concentration and CK-MB value and increased SOD activity were found in the Fen groups compared to the I/R group, while cTnI concentration was significantly lower in the Fen1 and Fen2 groups (all P<0.05). Myocardial damage was less in the Fen groups compared to the I/R group and the MI areas and apoptotic indexes were significantly lower in the Fen1 and Fen2 groups (all P<0.05). Furthermore, significantly increased protein and mRNA expressions of Bcl-2, and decreased protein and mRNA expressions of Bax were found in the Fen groups compared to the I/R group (all P<0.05). Fentanyl preconditioning may suppress cardiomyocyte apoptosis induced by I/R in rats by regulating Bcl-2 and Bax.

Research progress in pharmacological effects of ginsenoside on cardiovascular diseases in last decade / 中草药

There are abundant active substances in ginsenoside, which have been used effectually in many fields. Ginseng saponins are the effective components in the treatment of cardiovascular diseases. Many kinds of ginseng saponins have a positive therapeutic effect on inhibiting cardiomyocyte hypertrophy, improving myocardial ischemia, protecting the ischemia-reperfusion myocardium, stimulating angiogenesis, and inhibiting myocardial apoptosis and anti-arrhythmia. This article summarized the research progress in the pharmacological effects of ginsenoside on cardiovascular diseases in the last decade.

Valsartan Inhibits Myocardial Apoptosis by Down-regulating Myocardial X-box Binding Protein 1 Expression in Experimental Diabetic Cardiomyopathy Rat’s Model / 中国循环杂志

Objective: To study the relationship between myocardial X-box binding protein 1 (XBP1) expression and myocardial apoptosis in experimental diabetic cardiomyopathy (DCM) rat’s model and to clarify the mechanism of valsartan inhibiting myocardial apoptosis. Methods: A total of 50 Wistar rats were divided into 2 groups: Control group, the rats received intraperitoneal citrate buffer at 65mg/kg,n=10 and Streptozotocin group, the rats received intraperitoneal streptozotocin at 65mg/kg,n=40, all animals were treated for 7 days. DCM model was established in 37 rats (fasting blood glucose ≥ 16.7mmole/L) and they were further divided into 2 groups: DCM group, the rats received intragastric normal saline,n=20 and DCM + valsartan group, the rats received intragastric valsartan at 30mg/kg·day,n=17. The rats were treated for 16 weeks. The body weight, tail blood pressure, glucose and cardiac function were compared among 3 groups. Myocardial apoptosis was detected by TUNEL staining, RNA and protein expressions of myocardial cytochrome C, cleaved caspase 3, glucose regulation protein 78 (GRP78) and XBP1-s were examined by immunolfuorescence, real time RT-PCR and Western blot analysis. Results: Compared with Control group, DCM group showed disordered cardiac structure, more collagen content and myocardial apoptosis,P<0.05; increased RNA and protein expressions of GRP78, XBP1-s, cleaved caspase 3 and cytochrome C,P<0.05. Compared with DCM group, DCM + valsartan group had rather regularly arranged myocardiocytes, less interstitial ifbrosis and myocardial apoptosis,P<0.05; decreased RNA and protein expressions of GRP78, XBP1-s, cleaved caspase 3 and cytochrome C,P<0.05. Conclusion: Valsartan may inhibit myocardial XBP1 activation and therefore, reduce the myocardial apoptosis in experimental DCM rat’s model.

Protective effect of tanshinone II a on myocardial apoptosis in rats with sepsis / 中国药学杂志

OBJECTIVE: To explore the effect of tanshinone II A (Tan II A) on the myocardial apoptosis in rats with sepsis. METHODS: The sepsis rat model was established by cecal ligation and puncture operation (CLP), and the Tan II A was given for 12 consecutive hours. Then, the following indices were measured such as the activities of Na+-K+-ATPase and SOD, the contents of TNF-α, IL-1β, calcium, MDA, apoptotic index and the protein level of Bcl-2, Bax, Fas, caspase-3, calcincurin in myocardial. RESULTS: CD Compared with sham group, CLP treatment can result in decreased myocardial activities of Na+-K+-ATPase and SOD, elevated the contents of IL-1β, calcium, MDA (P<0.05); Tan II A treatment can improve the above aberrant indices. (2) Compared with sham group, CLP treatment can elevated the myocardial apoptotic index (P<0.05), and Tan II A treatment can decrease the elevation of apoptotic index by CLP treatment (P<0.05); (3)Compared with sham group, the protein level of Bax, Fas, caspase-3 and calcincurin significantly increased, and protein level of Bcl-2 decreased (P<0.05) in CLP group, and Tan II A treatment can improve exceptional expression of the above proteins (P<0.05). CONCLUSION: Tanshinone II A shows a protective effect on the myocardial apoptosis in septic rats maybe by depressing inflammatory infiltration and oxidative stress reaction, relieving calcium overload and partly improving the exceptional expression of the proteins such as Bax, Bcl-2, Fas, caspases-3 and calcincurin.

Effect of levothyroxine and vitamin E treatment on oxidative stress and myocardial apoptosis in rats with hypothyroidism / 中华内分泌代谢杂志

Objective To investigate the oxidative stress status and cardiac myocyte apoptosis in rats with propylthiouracil-induced hypothyroidism and to examine the effect of levothyroxine ( LT4 ),vitamin E ( VitE ),and both supplementation on this experimental model.Methods Male Sprague Dawley rats were divided into normal control group( NC),propylthiouracil group( PTU ),LT4 treatment group( PTU + LT4 ),VitE treatment group ( PTU +VitE),LT4 and VitE combination therapy group (PTU + LT4 + VitE).Serum T3,T4,TSH levels,serum and myocardial superoxide dismutase ( SOD ) activity and malondialdehyde ( MDA ) content were determined.Cardiac myocyte apoptotic index was made with TUNEL.Results ( 1 ) Compared with NC group,T3 and T4 levels were significantly lower and TSH level was significantly higher in PTU group and PTU+VitE groups( P＜0.05 ).Compared with PTU group,T3 and T4 levels were significantly higher and TSH level was significantly lower in PTU + LT4 group and PTU + LT4 + VitE group( P＜0.05 ).There were no statistical differences in T3,T4,and TSH levels between PTU group and PTU + VitE group( P＞0.05 ).( 2 ) Compared to NC group,serum and myocardial MDA levels in PTU group increased significantly( P＜0.05 ),serum SOD activity decreased significantly ( P＜0.05 ),while myocardial SOD activity showed no significant difference( P＞0.05 ).( 3 ) Compared with NC group,myocardial apoptosis index was significantly higher in PTU and PTU + VitE groups( P＜0.05 ).Compared with PTU group,myocardial apoptosis index was significantly lower in PTU + LT4 group and PTU + LT4 + VitE group( P＜0.05 ).Conclusion LT4,VitE,and their combined treatment of hypothyroidism in rats reduce the myocardial cells apoptosis,which may be related to the improvement of thyroid function and amelioration of oxidative stress.

An Anti-apoptotic Protein Expressed Specifically and Highly in The Cardiac Tissue:ARC / 生物化学与生物物理进展

Many apoptosis-related heart diseases such as myocardial infarction, cardiomyopathies, and heart failure severely impair human's health and life. Currently, a key focus for the medical researchers is to find out effective ways to prevent or treat these heart diseases. ARC (apoptosis repressor with caspase recruitment domain) is the first anti-apoptotic protein so far identified to be highly and specifically expressed in the cardiac tissue. ARC could be structurally phosphorylated and involved in various signaling pathways during apoptosis.

The Effect of Bone Marrow Mononuclear Cells Transplantation on Myocardial Apoptosis after Acute Myocardial Infarction in Rats / 医学研究杂志

Objective To observe the effect of allogenic bone marrow mononuclear cells(BM-MNCs) transplantation on myocardial apoptosis after acute myocardial infarction(AMI) in rats.Methods 40 Wistar rats were randomly divided into control group(n=20) and transplantation group(n=20).Myocardium around the infarcted left ventricular area of the rats in transplantation group were injected with BM-MNCs suspension beneath the epicardium.Myocardium the area of control group was injected with culture solution.Results After 4 weeks of the operation,the myocardial apoptosis index,the TNF-? content and the PDCD5 mRNA of transplantation group were all notably less than those of control group(P