人参皂苷Rb3及Rb2组合物对大鼠实验性心肌梗死的保护作用

目的研究人参皂苷Rb,及Rb,组合物对大鼠急性心肌梗死的保护作用。方法采用大鼠结扎左冠状动脉前降支制备急性心肌梗死模型,计算急性心肌梗死24h后的心肌梗死面积（MIS）,测定血清肌酸磷酸激酶（CK）、乳酸脱氢酶（LDH）、天门冬氨酸氨基转换酶（AST）、超氧物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH—Px）活力,丙二醛（MAD）及一氧化氮（NO）含量。结果人参皂苷Rb,及Rb：组合物5、10、20mg／kg均可明显缩小急性心肌梗死大鼠的MIS,降低血清CK、LDH、AST活性及MAD含量,提高血清SOD、GSH—Px活性及NO含量。结论人参皂苷Rb,及Rb：组合物对大鼠急性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少氧自由基对心肌的损伤等机制有关。     

重金属致植物矿质营养元素代谢异常的生理效应

重金属胁迫会导致植物体细胞的矿质营养元素缺乏、代谢过程紊乱,甚至可引起植物的死亡。综述了重金属导致植物体的某些矿质元素代谢异常的生理效应。     

Alteration of serum interleukin-6 and tumor necrosis factor-α after ischemic stimulation of coronary artery in PTCA

AIM: Inflammatory responses play an important role in the post- percutaneous transluminal coronary angioplasty (PTCA) restenosis and has been demonstrated occuring immediately after PTCA. Interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) are the main inflammatory cytokines. We try to compare the changes in interleukin-6(IL-6) and TNF-α after PTCA in the patients with and without collateral circulation to probe into the pathogenesis of early inflammatory response. METHODS: The extent of myocardial ischemia induced by balloon inflation was quantified by a scoring system referring to the Leaman coronary score. The IL-6、TNF-α levels of coronary heart disease group and control group before and after PTCA are calculated. RESULTS: The concentrations of IL-6 and TNF-α were (9.592±1.847) ng/L and (26.959±1.967) ng/L, respectively, and were significantly increased 4 hours after PTCA. CONCLUSION: IL-6 and TNF-α are sensitive indicators of the early inflammatory response after PTCA. Ischemia scores reflected the extent of ischemia reperfusion injury during PTCA. Collateral circulation decreased the early inflammatory response after PTCA.     

Cardiac troponins in canine babesiosis

This study compared the sensitivity of ECG and cardiac troponins to predict cardiac histopathological changes, clinical severity, and survival in canine babesiosis. One control group (n = 9) and 4 groups of dogs with mild uncomplicated babesiosis (n = 8), severe uncomplicated babesiosis (n = 9), complicated babesiosis (n = 8), and babesiosis and concurrent immune-mediated hemolytic anemia (IMHA) (n = 9) were studied. A 1-minute lead II ECG was recorded, and cardiac troponin I (cTnI) and T (cTnT) concentrations in plasma were measured. cTnI concentrations were significantly higher in the complicated (mean, 9.9; SE, +/-5.76) and concurrent IMHA (mean, 6.53; SE, +/-4.32) groups and in the 3 dogs that died of the disease (mean, 22.17; SE, +/-12.85) than in the control dogs (concentration below detection limit of test, -0.3 ng/mL). The 3 nonsurvivors had the most severe cardiac histopathological changes, but no arrhythmia and minimal other ECG changes. Dogs with babesiosis developed a variety of ECG abnormalities, but the abnormalities were not associated with disease severity, outcome, or plasma cardiac troponin concentrations. The exception was the presence of ventricular premature complexes (VPCs), which were associated with high cardiac troponin concentrations. This study showed an association between cTnI concentration and histological changes, clinical severity, and survival and no correlation between ECG abnormalities and histological changes or biochemical evidence of myocardial damage as reflected by cTnI concentrations. From this study, it was concluded that the analysis of plasma cTnI is a feasible and sensitive test and is superior to cTnT in diagnosing cardiac involvement in dogs with babesiosis.     

Effects of celecoxib on cardiac myocyte apoptosis after myocardial infarction

AIM: To investigate the effects of celecoxib, a selective cyclooxygenase-2 inhibitor, on antioxidative capability and apoptosis of cardiac myocytes after myocardial infarction. METHODS: 24 New Zealand rabbits were divided into three groups randomly (8 in each group): sham-operated group (sham group), myocardial infarction group (MI group), celecoxib group (Cele group, 10 mg kg^-1·d^-1, qd, with the drugs gastric gavage for six weeks). The NO concentration, total antioxidative capability (T-AOC), the activity of constitutive nitric oxide synthase (cNOS) and inducible NOS (iNOS) in cardiac tissue homogenate, adjacent to the infracted area, were detected. The pathological changes were observed by light microscope and electron microscopy. The expressions of Bcl-2 and Bax protein in myocytes were observed using immunohistochemistry, and the degree of apoptosis were examined by TUNEL. RESULTS: Cardiac tissue in MI group presented interstitial edema, fibroplastic proliferation, inflammatory cellular infiltration, and vacuolar degeneration in cardiac myocytes. The results of electron microscopy showed that myocytes presented more changes caused by ischemic injury: widened interspace of myofibril, disordered myofibrillae, focal lysis of myofilament, ectasia of sarcoplasmic reticulum. In Cele group, the pathological changes were light, the NO^-₂/ NO^-₃ concentration, the activity of iNOS were lower (P<0.05), while the activity of cNOS and T-AOC were higher (P<0.05) than those in MI group. The expression rate of Bcl-2 protein in Cele group was higher than that in MI group, while the Bax was lower (P<0.01). The number of apoptotic myocytes was lower than that in MI group (P<0.01).CONCLUSION: Celecoxib decreases the number of apoptotic cardiomyocytes and increases the antioxidative capability after myocardial infarction.     

Myocardial dysfunction resulting from coronary microembolization

Coronary microembolization is a significant and frequent complication of primary percutaneous coronary intervention in the patients with acute myocardial infarction. More importantly, coronary microembolization is a main reason of dysfunction of microcirculation. The mechanism of myocardial disfunction resulting from coronary microembolition was associated with the vascular active materials released from platelet, platelet aggregation, which aggravate microembolization in microcirculation, endothelial dysfunction and inflammation.     

The effects of 17β-estradiol on cardiomyocyte hypertrophy induced by endothelin

AIM:To investigate the effect of 17β-estradiol (E₂) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism. METHODS:Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17β-estradiol on myocardial hypertrophy were observed. The role of ERK1/2 in the effects of 17β-estradiol was also detected. RESULTS:Compared with control group,ET-1 increased cell protein content,cell surface area and ［³H］^-Leucine ［³H］^-Leu) incorporation. Pretreatment with E₂ for 24 h could inhibit the increase in cell protein content,cell surface area and ［³H］^-Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E₂.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E₂. The ability of ET-1 to stimulate ［³H］^-Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E₂ on the increase of ［³H］^-Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION:E₂ can inhibit cardiomyocyte hypertrophy induced by ET-1. This effect is mediated by estrogen receptor. ERK1/2 signal pathway is closely correlated with the inhibitory effect of E₂ on cardiomyocyte hypertrophy induced by ET-1.     

Effects of atorvastatin on cardiac myocyte hypertrophy of neonatal rat induced by angiotensinⅡ in vitro and TLR4 expression

AIM: To assess effects of atorvastatin (Ator) on cardiac myocytes (CM) hypertrophy of neonatal rat induced by angiotensinⅡ (AngⅡ) in vitro and Toll like receptor 4 (TLR4) expression for theoretical bases of preventing and treating myocardial hypertrophy.METHODS: CM of neonatal Sprague-Dawley (SD) rats were isolated with trypsin digestion method and those growth-arrested cells were stimulated with 10^-7 mol/L AngⅡ in the presence of various concentrations of Ator.The method of coomassie brilliant blue was adopted to evaluate the protein contents of CM.The changes in β-MHC,AT₁ receptor and TLR4 mRNA expression were observed by RT-PCR.RESULTS: ① AngⅡ increased the protein content of CM and β-MHC mRNA expression significantly,upregulated AT₁ receptor and TLR4 gene expression.② In a dose-dependent manner,Ator inhibited the increases in the protein contents of CM and β-MHC mRNA expression induced by AngⅡ.③ In a dose-dependent manner,Ator downregulated the AT₁ receptor and TLR4 mRNA expression of CM hypertrophy of neonatal rat induced by AngⅡ.CONCLUSION: Ator inhibits CM hypertrophy,downregulates the AT₁ receptor and TLR4 gene expression.     

Cardiomyocyte apoptosis and expression of Bcl-2, Bax protein after acute myocardial infarction and late reperfusion in dogs

AIM: To study the effect of late reperfusion on apoptotic cardiomyocytes in the risk area of acute myocardial infarctin in dogs. METHODS: The experiment was divided into three groups: sham operation group, acute myocardial infarction (AMI) group, and late reperfusion (LR) group. Apart from sham operation group, the other two groups were subjected to left anterior descending branch of coronary artery ligation. The acute myocardial infarction group was only subjected to ligation for 12 hours, late reperfusion group was subjected to ligation for 6 hours following by 6 hours of reperfusion. The cardiomyocyte apoptosis was measured by TUNEL assay. Immunohistochemistry and Western blotting analysis were used to detect the expression of Bcl-2 and Bax protein. RESULTS: The number of apoptotic cardiomyocytes in late reperfusion group was much less than acute myocardial infarction group (P<0.05), and increased significantily as compared with sham operation group (P<0.01). The expression of Bcl-2 protein was enhanced gently in late reperfusion group in contrast to acute myocardial infarction group, but no significant difference in the two groups (P>0.05) was observed, although it was much more in the two groups than that in sham operation group (P<0.01). The expression of Bax protein in late reperfusion group was much higher than that in sham operation group (P<0.01), and was lower than that in acute myocardial infarction group (P<0.05). CONCLUSION: Late reperfusion reduces cardiomyocyte apoptosis in the risk area of acute myocardial infarction. The mechanism may be that late reperfusion can decrease the expression of Bax protein.     

大庆石油化工大气污染对几种大豆幼苗的伤害初探

用大庆石油化工（以下称石化）污染大气，对四个品种大豆幼苗进行熏气处理试验的结果可见，叶片浸液的电导率和Ｋ＾＋外渗率都明显增大；叶片叶绿素、可溶性糖、蛋白质和核酸的含量却显著下降；过氧化物酶同工酶的含量的和活性升高。这表明石化大气污染对大豆幼苗具有伤害作用。但是，不同品种的大豆幼苗对其伤害的反应不同，所测试的四个品种大豆中，合丰２５和嫩丰４抗性较强，而黑河５和嫩丰１１则抗性较弱。这为石化大气污染对植