慢性低压低氧对大鼠肺组织HIF-1ɑ、COX1蛋白及氧化应激反应的影响

目的探讨慢性低压低氧环境对大鼠肺组织细胞色素C氧化酶1(COX1)蛋白及氧化应激反应的影响。方法将大鼠随机分为常氧组(1 500 m)和低氧组(4 300 m),低氧组大鼠暴露低氧30 d后采集标本。用Western blot检测肺组织COX1蛋白的表达及ELISA检测肺组织和血清HIF-1ɑ、血浆ROS、肺组织SOD和CAT酶。用生理信号采集系统测定肺动脉压(PAP)。结果在低氧组的大鼠血清和肺组织内HIF-1α蛋白显著高于常氧组(P0.01);ROS含量显著低于常氧组(P0.01);COX1蛋白在低氧组的大鼠肺组织中表达显著下降(P0.01);血清总抗氧化能力升高(P0.01)。结论高海拔对机体的影响可能是直接性的损伤,而并非仅仅是氧化应激反应所致。     

异甘草素对低氧诱导的大鼠肺动脉结构重建的影响

目的 观察异甘草素对缺氧性肺动脉高压（HPH）大鼠模型的肺动脉压力的变化,右心室肥厚程度及肺血管结构重建的影响,探讨异甘草素对HPH的抑制作用及其可能机制。方法 雄性SD大鼠30只随机分为对照组、HPH组、异甘草素组,每组各10只。HPH组和异甘草素组大鼠置于缺氧箱中建立大鼠HPH模型。异甘草素组中,每只大鼠腹腔注射异甘草素剂量为10 mg/(kg·d),从缺氧前1周开始给药直到缺氧结束。对照组和HPH组大鼠腹腔注射等体积0.5% DMSO。测定各组大鼠平均右心室压力(RVSP);称重法测得各组大鼠右心室游离壁（RV）及左心室加室间隔（LV+S）质量,以及RV/（LV+S）;HE染色观察肺动脉病理形态改变,计算血管厚度百分比(WT%)及面积百分比(WA%);ELISA法检测各组大鼠血清及肺组织中的超氧化物歧化酶(SOD)及丙二醛(MDA)的含量。Real-time PCR检测各组大鼠肺组织中的NADPH氧化酶4(NOX4) mRNA的表达。结果 HPH组大鼠RVSP、RV/LV+S、WT%,以及WA%明显高于对照组大鼠（P<0.01）,然而异甘草素组大鼠RVSP、RV/LV+S、WT%,以及WA%均明显低于HPH组大鼠（P<0.01）。HPH组大鼠肺组织及血清中的SOD含量较对照组明显降低,而MDA含量则明显增高（P<0.01）。异甘草素组大鼠肺组织及血清中的SOD含量较HPH组大鼠明显增高,而MDA含量则明显降低（P<0.01）。 Real time PCR结果显示,异甘草素有效抑制了低氧诱导的大鼠肺组织中NOX4 mRNA的高表达（P<0.01）。结论 异甘草素抑制由低氧诱导的HPH大鼠肺动脉压力升高、右心室肥厚,以及肺动脉管壁的增厚,可能与异甘草素抑制HPH大鼠体内的氧化损伤有关。     

Effect of Methylsulfonylmethane on Paraquat-Induced Acute Lung and Liver Injury in Mice

Methylsulfonylmethane (MSM) is a natural organosulfur compound that exhibits antioxidative and anti-inflammatory effects. This study was carried out to investigate the effect of MSM on paraquat (PQ)-induced acute lung and liver injury in mice. A single dose of PQ (50 mg/kg, i.p.) induced acute lung and liver toxicity. Mice were treated with MSM (500 mg/kg/day, i.p.) for 5 days. At the end of the experiment, animals were euthanized, and lung and liver tissues were collected for histological and biochemical analysis. Tissue samples were used to determine malondialdehyde (MDA), myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and tumor necrosis factor-α (TNF-α) levels. Blood samples were used to measure plasma alanine transaminase (ALT), γ-glutamyl transferase (GGT), and alkaline phosphatase (ALP). Histological examination indicated that MSM decreased lung and liver damage caused by PQ. Biochemical results showed that MSM treatment significantly reduced tissue levels of MDA, MPO, and TNF-α, while increased the levels of SOD, CAT, and GSH compared with PQ group. MSM treatment also significantly reduced plasma levels of ALT, GGT, and ALP. These findings suggest that MSM as a natural product attenuates PQ-induced pulmonary and hepatic oxidative injury.     

L-肉碱对NAFLD脂肪肝大鼠肝脏线粒体能量代谢及抗氧化能力的影响

研究L-肉碱对NAFLD脂肪肝大鼠肝脏线粒体能量代谢及抗氧化能力的影响.脂肪肝大鼠48只,随机分为对照组、肉碱组、运训组和肉碱+运训组.运训组和肉碱+运训组进行6周运动,肉碱组和肉碱+运训组每日灌胃一次肉碱(500 mg/kg).6周后各组大鼠进行力竭运动,即刻麻醉取出肝脏提取线粒体,测定线粒体呼吸链酶RCCI~IV活性及自由基代谢相关指标.与对照组比,肉碱组大鼠肝脏线粒体呼吸链RCCII,运训组RCCI、RCCIII,肉碱+运训组RCCI、RCCII、RCCIII活性均显著提高.与肉碱组比,肉碱+运训组RCCI、RCCIII活性显著提高.与运训组比,肉碱+运训组RCCI活性显著提高.与对照组比,肉碱组、肉碱+运训组大鼠肝脏线粒体GSH-Px活性显著提高;与对照组比,三组SOD 活性显著提高,MDA含量降低.与肉碱组比,肉碱+运训组SOD活性显著提高;与运训组比,肉碱+运训组GSH-Px活性显著提高.补充L-肉碱、运动、L-肉碱+运动均可提高非酒精性脂肪肝大鼠肝脏线粒呼吸链酶活性,提高线粒体能量代谢速率及抗氧化损伤能力,补充L-肉碱结合运动训练组效果更加显著.     

电磁脉冲辐照对大鼠脑线粒体功能的影响

为研究电磁脉冲（EMP）对大鼠脑线粒体功能的损伤，大鼠经过连续不同场强EMP辐照后测定了脑线粒体膜功能随辐照时间的变化，并分离脑线粒体，测定线粒体肿胀度、膜流动性、膜磷脂含量、呼吸功能、线粒体呼吸酶、超氧化物歧化酶（SOD）、丙二醛（MDA）、Ca^2＋等指标以显示线粒体功能、抗氧化能力的变化。结果表明，EMP辐照后大鼠脑线粒体明显肿胀，膜磷脂降解、膜流动性下降，呼吸功能衰减，呼吸酶、SOD活性降低，Ca^2＋、MDA含量升高。由此认为，EMP可造成大鼠脑线粒体功能受损，其机制可能与脑线粒体膜损伤后继发的自由基生成增加、脑线粒体能量代谢障碍有关。     

红景天甙减轻大鼠酒精性肝损伤

目的:探讨红景天甙对大鼠酒精性肝损伤的作用及其可能机制。方法:将100只SD大鼠随机分为5组:对照组、模型组、联苯双酯滴丸组及红景天甙低剂量(20 mg/kg)和高剂量(40 mg/kg)组,除空白组给予生理盐水外,其余各组均给予56%乙醇灌胃,建立酒精性肝损伤大鼠动物模型,给药组同时予以相应药物灌胃,于末次给药后12 h采血,处死动物后取出肝脏,采用全自动生化仪测定血清甘油三酯(TG)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平,苏木素-伊红(HE)染色观察肝组织病理学改变,试剂盒测定肝组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,ELISA法测定各组大鼠血清中肿瘤坏死因子α(TNF-α)和核因子κB(NF-κB)水平,Western blot法和RT-PCR测定肝组织TNF-α和NF-κB的蛋白和mRNA表达。结果:与模型组比较,红景天甙高、低剂量组肝组织损伤程度明显减轻;红景天甙对酒精性肝损伤大鼠血清TG、ALT及AST水平均具有明显抑制作用(P0.05),并可降低肝组织MDA含量,增强肝组织SOD活性(P0.05);红景天甙各剂量组大鼠血清TNF-α和NF-κB含量降低(P0.05)。结论:红景天甙能够改善大鼠酒精性肝损伤病理变化,减轻肝组织炎症反应,增加抗氧化酶的活性,降低脂质过氧化,该作用可能与调节NF-κB介导的炎症反应有关。     

GRP78在肝硬化大鼠肠源性内毒素血症引发心脏病变中的作用

目的: 探讨葡萄糖调节蛋白78(GRP78)在肝硬化大鼠肠源性内毒素血症引发心脏病变中的作用。方法: 51只Wistar雄性大鼠随机分为肝硬化模型4周组、6周组、8周组和同期正常对照组。于第8周检测大鼠心功能;检测各组心肌组织匀浆中肿瘤坏死因子α(TNF-α)和丙二醛(MDA)水平;甲苯胺蓝染色和van Giesan染色分别观察心肌细胞数量的变化和计算心肌胶原容积分数(CVF);免疫组化法检测心肌组织GRP78和缺氧诱导因子1α(HIF-1α)蛋白表达情况。结果: 随肝硬化病程进展:(1)肝硬化8周组大鼠左室舒张末期压(LVEDP)及左室内压最大上升和下降速率(±LV dp/dt_max)均较对照组降低(P<0.05);(2)心肌组织中TNF-α、MDA、CVF、GRP78蛋白和HIF-1α蛋白水平均逐渐升高并显著高于正常对照组(P<0.05);(3)甲苯胺蓝染色显示模型各组心肌细胞数量逐渐减少并显著低于正常对照组(P<0.05);(4)血浆中内毒素水平分别与丙氨酸氨基转移酶(ALT)、同型半胱氨酸(Hcy)、TNF-α、GRP78和MDA呈显著正相关(P<0.05);(5)GRP78蛋白分别与HIF-1α、Hcy、MDA、ALT和CVF呈显著正相关(P<0.05)。结论: 肝硬化大鼠伴发的肠源性内毒素血症通过直接或间接作用引起内质网应激和GRP78表达增加,后者可能是引起心肌重构、导致心脏功能变化的关键分子。     

脑梗死患者血浆Hcy水平与脂质过氧化的关系

目的：探讨了脑梗死患者血浆同型半胱氧酸（Hcy）水平与脂质过氧化的炎系。方法：应用发光免疫分析测定54例脑梗死患者血浆Hcy水平和化学比色法测定血浆丙二醛（MDA）．超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—PX）,并与35名正常健康人作比较。结果：脑梗死患者血浆Hcy水平和MDA水平非常显著地高于正常人组（P〈0．01）,而SOD、GSH—PX、SOD／MDA水平则低于正常人组（P〈0.01）,相关分析显示：患者Hcy水平与SOD、GSH-Px水平呈负相关（r=-0．4018、-0．4412,P〈0．01）,而与MDA水平成正相关（r=0.6012,P〈0．01）。结论：脑梗死患者血浆Hcy水平的增高与活性氧代谢紊乱有关。     

原卟啉钠对急性肝损伤小鼠肝组织SOD、MDA的影响

 目的 探讨原卟啉钠对四氯化碳（CCl4）致急性肝损伤小鼠血清转氨酶和肝组织超氧化物歧化酶（SOD）、脂质过氧化产物丙二醛（MDA）的影响。方法 60只ICR小鼠随机分为正常对照组、CCl4模型组、联苯双酯组、原卟啉钠低、中、高剂量组。各治疗组每天灌胃给药及造模16h后,摘眼球取血测定血清中谷丙转氨酶（ALT）和谷草转氨酶（AST）活性,剖腹取肝测定肝脏SOD活力和MDA含量。结果 CCl4模型组小鼠血清ALT和AST活力分别为（1879±1219）、（2210±1585）U/L,与正常对照组比较,降低显著（P<0.01）;联苯双酯组、原卟啉钠低、中、高剂量组的SOD活力和MDA含量分别为（207.61±16.02）、（184.35±13.42）、（190.88±17.77）、（199.38±14.43）U/mgprot和（1.08±0.15）、（1.35±0.26）、（1.07±0.16）、（0.92±0.18）nmol/mgprot,与CCl4模型组比较,差异有统计学意义（P<0.05～P<0.01）。结论 原卟啉钠能有效阻止CCl4致急性肝损伤小鼠肝组织SOD活性降低,脂质过氧化产物MDA含量升高,具有一定的保肝降酶作用。     

Effects of erdosteine on acetaminophen-induced hepatotoxicity in rats

We investigated the effects of erdosteine on acetaminophen (APAP)-induced hepatotoxicity in rats. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), AST (aspartate aminotransferase), and ALT (alanine transaminase) activities, and malonyldialdehyde (MDA) and nitric oxide levels as oxidant/antioxidant biochemical parameters were investigated with light microscopic evaluation in adult female Wistar Albino rats. APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. MDA and NO levels increased in the APAP group, and erdosteine treatments prevented these increases. Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Light microscopic evaluation of livers showed that there were remarkable centrilobular (zone III) hepatic necrosis and mild to moderate sinusoidal congestion in the APAP group, whereas in the erdosteine group, cellular necrosis was minimal and the hepatocytes maintained a better morphology when compared to the APAP group. Erdosteine prevented APAP-induced liver injury and toxic side effects probably through the antioxidant and radical scavenging effects of erdosteine.     

再灌注前干预肥大细胞功能对大鼠肠缺血再灌注后早期肝损伤的影响

 目的：探讨肠缺血后再灌注前干预肥大细胞功能对SD大鼠继发肝脏损伤的影响及机制。方法：35只大鼠随机分成5组：假手术组（S组）、缺血再灌注组（IR组）、缺血再灌注＋色甘酸钠组（IR+C组）、缺血再灌注＋酮替芬组（IR+K组）和缺血再灌注＋compound 48/80 组（IR+CP组）。复制大鼠肠缺血再灌注模型,IR+C、IR+K和IR+CP组分别在再灌注前5 min经尾静脉给予相应药物,S和IR组给予等量生理盐水。再灌注4 h后处死大鼠,观察各组肝脏病理变化及评分,测定血清丙氨酸氨基转移酶（ALT）活性、天冬氨酸氨基转移酶（AST）活性和组胺含量,检测肝脏乳酸脱氢酶（LDH）活性、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性和肿瘤坏死因子α（TNF-α）、白细胞介素8（IL-8）水平。结果：与S组相比,IR组肝脏病理损伤明显（P<0.05）,血清ALT、AST水平、组胺含量、肝LDH活性、MDA、TNF-α、IL-8水平升高,SOD活性减弱（P<0.05）。与IR组相比,IR+C和IR+K组肝脏损伤减轻,以上指标呈相反趋势（P<0.05）,IR+CP组则加重肝损伤及恶化检测结果（P<0.05）。结论：再灌注前抑制肥大细胞功能可以减轻肠缺血再灌注后早期肝脏损伤,其机制可能与组胺释放、氧化损伤和炎症反应有关。     

红景天苷对非酒精性脂肪性肝炎大鼠肝组织氧化应激的抑制作用

 目的：观察红景天苷（salidroside ,SDS）对大鼠非酒精性脂肪性肝炎（NASH）肝组织氧化应激的影响。方法：以高脂高胆固醇饮食14周诱导建立大鼠NASH模型,药物干预组在造模第8周末时给予SDS 300 mg·kg-1·d-1体重灌胃连续6周,在14周末检测大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇（TC）和甘油三酯（TG）,以及肝组织TC、TG、丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽（GSH）含量的变化,ELISA检测8-异前列腺素F2α(8-iso-PGF2α)的水平变化, HE染色观察肝组织病理学变化,免疫组化观察8-羟基脱氧鸟苷酸（8-OHdG）表达的变化。结果：在14 周末, NASH模型组大鼠肝组织病理学检查显示肝组织呈中重度脂肪变性并同时伴有炎症细胞浸润;与正常对照组相比,NASH模型组大鼠血清ALT、AST、TG和TC,以及肝TG、TC和MDA的含量显著上升,而肝SOD和GSH的含量显著下降,8-iso-PGF2α的水平显著上升,免疫组化显示8-OHdG表达的阳性细胞数显著增多。与模型组相比,SDS药物干预组大鼠ALT、AST、TG、TC、MDA和8-iso-PGF2α的含量均显著下降,而肝SOD和GSH的含量显著上升,肝病理学变化得到显著改善,8-OHdG表达的阳性细胞数明显减少。结论：SDS对高脂高胆固醇饮食诱导的NASH有较好的抑制效果,其机制可能与SDS的抗氧化作用有关。     

Study of the effect of Cannabis sativa on liver and brain damage caused by thioacetamide

Cannabis sativa preparations are the most widely used illicit drugs worldwide. The present study aimed to examine the effect of C. sativa extract on liver injury caused by thioacetamide in the rat. Thioacetamide was administered at 50 mg/kg twice weekly via subcutaneous route (s.c.) for 2 weeks. Starting from the first dose of thioacetamide, rats were treated with either C. sativa at doses of 10 or 20 mg/kg (expressed as Δ⁹-tetrahydrocannabinol), silymarin (25 mg/kg) or saline, once daily s.c., for 2 weeks. Reduced glutathione (GSH), lipid peroxidation (malondialdehyde; MDA) and nitric oxide concentrations were measured in the liver and brain. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), paraoxonase 1 activities (PON1) and total proteins were determined in serum. Hepatic injury was also determined via histological examination of liver sections. The administration of only cannabis to saline-treated rats had no significant effect on serum liver enzymes or on the hepatic levels of GSH, MDA or nitric oxide. Serum PON1 decreased by 21.9 % by 20 mg/kg cannabis. The level of MDA and nitric oxide in brain decreased by only cannabis administration. In thioacetamide-treated rats, the administration of cannabis extract (10 or 20 mg/kg) did not alter the level of MDA, GSH or nitric oxide in hepatic tissue. Serum ALT or AST were not significantly altered, but ALP increased significantly by 38.9 % after treatment with 20 mg/kg cannabis. Serum PON1 activity which showed marked decrease in thioacetamide-treated rats, increased by 18.9 and 151 % after C. sativa treatment. Serum proteins increased after the administration of cannabis (by 20.4 and 21.3 %, respectively). In brain tissue, both MDA and nitric oxide were significantly decreased by cannabis. Meanwhile, treatment with silymarin resulted in significant decrease in MDA and increased GSH in the liver tissue. Serum AST, ALT and ALP were significantly decreased, while PON1 activity was increased after silymarin. In brain, MDA decreased by 27.9 % after silymarin. Cannabis alone caused histological liver damage and fibrosis and neuronal degeneration. The liver tissue damage and brain degeneration caused by thioacetamide were enhanced by cannabis but almost prevented by silymarin treatment. It is concluded that the administration of C. sativa exacerbates the thioacetamide-induced liver and brain injury.     

Effect of Zingiber officinale on liver oxidative status and biochemical parameters in rats exposed to paraquat

Oxidative stress caused by reactive oxygen species is one of the major pathogenesis of important diseases of animals and human. Paraquat is widely used as herbicide. The toxicity of paraquat is through induction of oxidative processes in biological systems. Biochemically, this herbicide interferes with intracellular electron transfer system leading to the formation of superoxide anion. Zingiber officinale (ginger) is widely used as a spice and medical treatment for various diseases. The objective of this study was to assess the effect of different levels of ginger extract on antioxidant status and serum metabolites of rats. Sixty male albino Wistar rats were divided in six groups as follows: control (saline); ginger; paraquat; paraquat with 100, 200, and 400 ginger. After 30 days of treatment, the blood was collected by cardiac puncture. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), reduced glutathione (GSH), and lipid peroxidation were estimated. In paraquat-treated group, the serum levels of ALT, AST, and malondialdehyde (MDA) were markedly raised. Administration of ginger extract with paraquat reduced the serum levels of ALT, AST, and MDA. Hepatic SOD, CAT, GPx, GST, and GSH activities were significantly decreased in paraquat-treated group compared to those of control. However, concurrent administration of paraquat with all concentrations of ginger extract had the opposite effect, where it increased the hepatic SOD, CAT, GPx, GST, and GSH activities near to control. The present study demonstrates that administration of ginger extract to rats modulates the antioxidant enzymes and suggests a possible adaptive mechanism to counteract oxidative stress situation.     

Tissue-specific mtDNA lesions and radical-associated mitochondrial dysfunction in human hearts exposed to doxorubicin

Doxorubicin causes a chronic cardiomyopathy. Although the exact pathogenesis is unknown, recent animal data suggest that somatically acquired alterations of mitochondrial DNA (mtDNA) and concomitant mitochondrial dysfunction play an important role in its onset. In this study, skeletal and myocardial muscles were examined from human autopsies. Compared to controls (n = 8), doxorubicin-exposed hearts (n = 6) showed low absolute enzyme activity of mtDNA-encoded nicotinamide adenine dinucleotide hydrogen dehydrogenase (NADH DH, 79% residual activity, p = 0.03) and cytochrome c oxidase (COX, 59% residual activity, p < 0.001), but not of succinate dehydrogenase (SDH), which is encoded exclusively by nuclear DNA. NADH DH/SDH and COX/SDH ratios were 37% (p < 0.001) and 27% (p < 0.001) of controls. Expression of the mtDNA-encoded subunit II of COX was reduced (82%, p = 0.04), compared to its unchanged nucleus-encoded subunit IV. MtDNA-content was diminished (56%, p = 0.02), but the 'common' mtDNA-deletion was increased (9.2-fold, p = 0.004). Doxorubicin-exposed hearts harboured numerous additional mtDNA rearrangements lacking direct repeats. They contained elevated levels of malondialdehyde (MDA) (p = 0.006, compared to controls), which correlated inversely with the COX/SDH ratio (r = -0.45, p = 0.02) and the mtDNA-content (r = -0.75, p = 0.002), and correlated positively with the levels of the 'common' deletion (r = 0.80, p < 0.001). Doxorubicin-exposed hearts also contained the highest levels of superoxide (p < 0.001, compared to controls), which correlated negatively with the mtDNA-encoded respiratory chain activities, such as the COX/SDH ratio (r = -0.57, p = 0.02) and the NADH/SDH ratio (r = -0.52, p = 0.04), as well as with the mtDNA content (r = -0.69, p = 0.003), and correlated positively with the frequency of the 'common' deletion (r = 0.76, p < 0.001) and the MDA levels (r = 0.86, p < 0.001). Doxorubicin-exposed hearts contained electron-dense deposits within mitochondria. Hearts exposed to other anthracyclines (n = 6) or skeletal muscle (all groups) had no mitochondrial dysfunction. Doxorubicin, unlike other anthracyclines, augments lipid peroxidation, induces mtDNA mutations and decreases mtDNA content in human hearts. These lesions have an impact on mitochondrial function and could be of importance in the pathogenesis of clinical cardiomyopathy.     

螺旋藻对大鼠高同型半胱氨酸血症的影响

目的：研究螺旋藻(SP)对大鼠高同型半胱氨酸血症(hyper homocysteinemia,HHcy)的影响。方法：用高蛋氨酸饮食复制HHcy大鼠模型,给予叶酸或SP干预12周。以高压液相色谱法测定血浆Hcy浓度,硫代巴比妥酸反应比色法测定血浆丙二醛(MDA)浓度,黄嘌呤氧化酶法测定血浆超氧化物歧化酶(SOD),并采用链霉亲和素-过氧化物酶(S-P)免疫组化染色法检测动脉平滑肌增殖细胞核抗原(proliferating cell nuclear antigen,PC- NA)的表达。结果：HHcy模型组血浆Hcy浓度、MDA水平、SOD活力及平滑肌PCNA阳性细胞率明显高于正常对照组,经叶酸及SP干预后,上述指标都比模型组降低。结论：螺旋藻在体内可减低血浆Hcy和MDA浓度,有效消除氧化自由基,降低动脉平滑肌增殖指数,保护HHcy血症损伤的内皮细胞。     

肝炎康对D-氨基半乳糖所致大鼠急性肝损伤的保护作用

目的:观察肝炎康对D-氨基半乳糖(D-GalN)所致大鼠急性肝损伤的保护作用。方法:建立D-GalN致大鼠急性肝损伤模型,设正常对照组,模型对照组,云芝多糖阳性对照组和肝炎康大、中、小剂量治疗组。检测大鼠血清中谷丙转氨酶(ALT)、天门冬氨酸转氨酶(AST)活性和肝组织均浆中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,并观察肝脏组织病理学变化,以评价肝炎康对肝脏的保护作用。结果:肝炎康能明显降低由D-GalN所致急性肝损伤大鼠血清中ALT、AST活性,降低肝组织中MDA含量,提高SOD活性,并能明显改善肝脏组织病理损伤。结论:肝炎康对D-GalN所致大鼠急性肝损伤具有一定的保护作用。