Cardioprotective effects of saponins from Panax japonicus on acute myocardial ischemia against oxidative stress-triggered damage and cardiac cell death in rats

Aim

To study the cardioprotective effects of saponins from Panax japonicus (SPJ) on acute myocardial ischemia injury rats induced by ligating of the left anterior descending branch (LAD), on the basis of this investigation, the possible mechanism of SPJ was elucidated.

Materials and methods

SPJ was identified by high performance liquid chromatography-evaporative light scattering detection. Male Sprague-Dawley rats (200–220 g) were randomly divided into four groups: sham-operated, LAD, LAD + l-SPJ (SPJ, 50 mg/kg/day, orally) and LAD + h-SPJ (SPJ, 100 mg/kg/day, orally). Before operation, the foregoing groups were pretreated with homologous drug once a day for 7 days, respectively. After twelve hours in LAD, the cardioprotective effects of SPJ were evaluated by infarct size, biochemical values, hemodynamic, and histopathological observations and the antioxidative and antiapoptotic relative gene expressions.

Results

SPJ significantly improved heart function and decreased infarct size; remarkably decreased levels of serum lactate dehydrogenase, creatine kinase, xanthine oxide and malondialdehyde content, increased contents of serum total antioxidant capacity, superoxide dismutase (SOD), glutathione peroxidase, catalase; quantitative real-time PCR results showed that SPJ might markedly reverse the down-regulated mRNA expressions of the SOD1, SOD2 and SOD3, ameliorate the increased Bax and caspase-3 mRNA expressions and decreased Bcl-2 mRNA expression and ratios of Bcl-2 to Bax. Histopathological observations provided supportive evidence for biochemical analyses, and with the dose of SPJ increasing, the aforesaid improvement became more and more strong.

Conclusions

The studies demonstrated that in ischemic myocardium, oxidative stress caused the overgeneration and accumulation of reactive oxygen species (ROS), which was central of cardiac ischemic injury. SPJ exerted beneficially cardioprotective effects on myocardial ischemia injury rats, mainly scavenging oxidative stress-triggered overgeneration and accumulation of ROS, alleviating myocardial ischemia injury and cardiac cell death.     

葡萄籽提取物抗氧化作用人体实验研究

目的研究葡萄籽提取物原花青素对人体丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的影响情况。方法选择年龄45~65岁的受试者120名,分为试食组和对照组。试食组每人每天2粒服用受试样品,连续3个月,对照组按同法给予安慰剂。比较实验前后受试者的MDA、SOD、GSH-PX改善情况。结果试食组血清中MDA平均下降4.80%;SOD平均升高2.31%;GSH-PX平均升高2.45%,;试食组自身实验前后比较及与对照组组间比较差异均有统计学意义(均P0.01)。结论在研究剂量范围内可见葡萄籽提取物原花青素具有抗氧化功能。     

康泰仙对小鼠肝脑组织SOD、GSH-Px、CAT、MDA影响的实验研究

目的通过测定小鼠肝脑组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)的活性和丙二醛(MDA)含量来研究康泰仙(KOTAIS)对小鼠抗衰老的作用。方法采用D-半乳糖制作的衰老模型,将小鼠随机分为正常组、模型组、药物低、中、高剂量组。连续给药灌胃60d后,检测肝脑组织中的SOD、GSH-Px、CAT、MDA指标。结果各剂量组能提高小鼠肝组织中SOD、GSH-Px、CAT的活性,并能降MDA的含量,以低、中剂量组尤其明显。结论康泰仙(KOTAIS)具有较好的消除自由基、抗衰老的作用。     

过氧化苯甲酰对小鼠肝脏组织损伤作用

目的 探讨面粉增白剂过氧化苯甲酰(benzoyl peroxide,BPO)对小鼠肝脏组织的损伤作用。方法 64只昆明种小鼠随机分为对照组和低、中、高剂量BPO组,分别灌胃给予BPO 50,100和200 mg/kg,每组16只,雌雄各半;灌胃6周后,测定各组肝脏组织中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量及三磷酸腺苷(ATP)酶活力。结果 高、中剂量BPO组SOD活力分别为(40.15±7.13),(46.01±6.69)U/(mg·prot),与对照组(53.15±6.55)U/(mg·prot)比较,差异有统计学意义(P<0.05);高剂量BPO组与对照组MDA含量分别为(1.93±0.37)和(1.57±0.33)nmol/(mg·prot),差异有统计学意义(P<0.05);高剂量BPO组Mg²⁺-ATP、Ca²⁺-ATP酶活力分别为(1.58±0.11)和(1.48±0.09)μmol Pi/(mg·prot),与对照组比较明显降低,差异有统计学意义(P<0.05);各剂量BPO组GSH-Px活力与对照组比较差异无统计学意义(P>0.05)。结论 BPO在一定程度上可降低小鼠肝脏抗氧化及Ca²⁺、Mg²⁺-ATP酶活力。     

三种饮用水对小鼠抗过氧化酶影响比较

目的比较不同饮用水对小鼠的抗过氧化酶的影响。方法ICR小鼠随机分为三组,每组雌雄各半,分别用矿泉水、自来水和纯净水喂养。经过一年时间喂养后,取其肺、肝、脑、心制成匀浆测定谷胱甘肽过氧化物酶(GSH-Px)、总超氧化物歧化酶(SOD)活力。结果矿泉水组小鼠的心匀浆GSH-Px活力较纯净水组高,有显著差异(P<0.05);而SOD活力矿泉水组除在肺匀浆中明显高于其他两组(P<0.05),肝中SOD纯净水组高于矿泉水组。结论不同饮用水对小鼠组织器官的抗氧化酶影响不同,表现出不同的抗氧化/致氧化效应。     

l-Theanine prevents alcoholic liver injury through enhancing the antioxidant capability of hepatocytes

l-Theanine is a unique amino acid in green tea. We here evaluated the protective effects of l-theanine on ethanol-induced liver injury in vitro and in vivo. Our results revealed that l-theanine significantly protected hepatocytes against ethanol-induced cell cytotoxicity which displayed by decrease of viability and increase of LDH and AST. Furthermore, the experiments of DAPI staining, pro-caspase3 level and PARP cleavage determination indicated that l-theanine inhibited ethanol-induced L02 cell apoptosis. Mechanically, l-theanine inhibited loss of mitochondrial membrane potential and prevented cytochrome c release from mitochondria in ethanol-treated L02 cells. l-Theanine also prevented ethanol-triggered ROS and MDA generation in L02 cells. l-Theanine restored the antioxidant capability of hepatocytes including GSH content and SOD activity which were reduced by ethanol. In vivo experiments showed that l-theanine significantly inhibited ethanol-stimulated the increase of ALT, AST, TG and MDA in mice. Histopathological examination demonstrated that l-theanine pretreated to mice apparently diminished ethanol-induced fat droplets. In accordance with the in vitro study, l-theanine significantly inhibited ethanol-induced reduction of mouse antioxidant capability which included the activities of SOD, CAT and GR, and level of GSH. These results indicated that l-theanine prevented ethanol-induced liver injury through enhancing hepatocyte antioxidant abilities.     

Lowered Glutathione-Peroxidase Activity in Asthmatic Patients with Food and Aspirin Intolerance

In analogy with findings from animal experiments, people with low glutathione-peroxidase (GSH-Px) activity could be expected to have altered sensitivities to effects of drugs, chemicals and possibly food. We have investigated GSH-Px activity in 12 patients with intrinsic asthma and food and aspirin intolerance. Ten of the 12 patients had very low or low GSH-Px activity and the frequency of low GSH-Px activity in this group was statistically significant (P less than 0.001) compared with the control material of age- and sex-matched healthy individuals. Our finding of lowered GSH-Px activity in patients with aspirin intolerance may indicate the involvement of hitherto unknown mechanisms in the pathogenesis of asthmatic disorders.     

黑木耳硒多糖对小鼠血脂、血硒及过氧化物酶的影响

目的　探讨黑木耳硒多糖对血脂、血硒浓度及谷胱甘肽过氧化物酶活性的影响。方法昆明系雄性小白鼠随机分成四组 :正常对照组 ( )、高脂对照组 ( )、亚硒酸钠组 ( )、硒多糖组( )。 和 组饲喂高脂饲料。并每日每鼠分别灌胃亚硒酸钠或硒多糖水溶液 1 ml(1 .95μg Se/ml) ,共 2 1 d。结果　与 组比 , 、 组小鼠血清 TC显著降低 (P<0 .0 0 1 ) ,GSH- Px活性显著增强 (P<0 .0 0 1 ) ; 组小鼠血清 TG显著降低 (P<0 .0 5) ,血硒浓度显著提高 (P<0 .0 1 ) ; 组小鼠血清 TG显著降低 (P<0 .0 1 ) ,血硒浓度显著提高 (P<0 .0 0 1 ) ;与 组比 , 组硒血浓度显著提高(P<0 .0 0 1 ) ,GSH- Px活性显著增强 (P<0 .0 1 )。结论　硒多糖较亚硒酸钠具有更好的降血脂、提高血硒浓度和增强 GSH- Px活性的作用 ,对高血脂症有一定的预防作用     

慢性冷暴露过程中SD大鼠RBC抗氧化系统和膜行为的变化

本研究以SD大鼠为模型,对慢性冷暴露过程中RBC过氧化与抗氧化机制的变化及膜部分行为的改变进行了动态观察。结果表明:(1) 冷适应初期抗氧化机制相对不足,过氧化占主导地位,过氧化物的堆积有可能造成一定的损伤而减弱机体的抗寒能力,而进一步抗氧化能力的增强则可能是冷适应建立的重要机制之一。(2) RBC在冷适应过程中抗氧化系统加强,包括SOD活性的升高与GSHPx活性的增强。(3) 慢性冷暴露过程中,SD大鼠RBC膜发生一定的组成变化和功能调整,而膜流动性变化却不显著。本实验为冷适应过程中脂质过氧化物(LPO)的存在提供了有力依据,为冷适应机理的研究与耐寒能力的探讨,提供了一条新的途径。     

Alleviation of the acute doxorubicin-induced cardiotoxicity by Lycium barbarum polysaccharides through the suppression of oxidative stress

The present study aims to investigate whether Lycium barbarum polysaccharides (LBP) could protect against acute doxorubicin (DOX)-induced cardiotoxicity. Rats received daily treatment of either distilled water (4 ml/kg) or LBP (200 mg/kg) for 10 days and then followed by an intravenous injection at day 7 of either saline (10 ml/kg) or DOX (10 mg/kg). DOX induced significantly myocardial damage in rats, which were characterized as conduction abnormalities, decreased heart-to-body weight ratio, increased serum CK, and myofibrillar disarrangement. DOX treatment also increased MDA and decreased SOD and GSH-Px activity in cardiac tissues. Pretreatment with LBP significantly reduced DOX-induced oxidative injury in cardiac tissue, suggesting by the fact that LBP significantly attenuated DOX-induced cardiac myofibrillar disarrangement and LBP was effective in decreasing the levels of serum CK and thus improving conduction abnormalities caused by DOX. LBP treatment significantly increased SOD and GSH-Px activity and decreased the MDA level of heart tissues damaged by DOX exposure in rats. Furthermore, the cytotoxic study showed that LBP protect against cytotoxicity of DOX in cardiac myoblasts H9c2 but dose not attenuate the anti-tumor activity of DOX. In summary, our evidence indicates that LBP elicited a typical protective effect on DOX-induced acute cardiotoxicity via suppressing oxidative stress.