肌肽对肉鸡血清部分生化指标的影响

1日龄AA肉鸡160只,随机分成4组。1~4组饮水中肌肽添加剂量分别为0(对照组)、20(低剂量组)、40(中剂量组)、60(高剂量组)mg/L,试验期6周。于2、4、6周末每组随机取6只肉鸡心脏采血,测定血清中的谷丙转氨酶(ALT)、谷草转氨酶(AST)活力和总胆固醇(TC)的含量。结果表明:肌肽各剂量组ALT活力在2、4、6周龄时均低于对照组,但组间差异均不显著(P>0.05)。4周龄时各剂量组AST的活力均高于对照组,2、6周龄均低于对照组(P<0.05或P<0.01)。生长中期肌肽组血清胆固醇含量有所上升,生长后期略微下降,肌肽对肝脏功能没有明显的影响。     

布鲁杆菌病患者血清酶变化及其临床意义

目的:探讨急性期布鲁杆菌病患者血清酶的变化及其临床意义.方法:采用全自动生化分析仪测定30例急性期布鲁杆菌病患者治疗前后血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(HBDH)水平,并与正常对照组进行比较.结果:急性期布鲁杆菌病患者上述各个酶均较正常对照组升高(P<0.05),治疗后恢复正常.结论:血清ALT、AST、LDH、HBDH的测定,有助于判断急性期布鲁杆菌病的病情和疗效.     

冬虫夏草对大鼠运动能力的影响

通过建立一次性力竭游泳训练动物模型,分别测定了谷草转氨酶、谷丙转氨酶和肌酸激酶的活性,血红蛋白和血糖的含量.训练组与对照组比较实验的结果显示,服药训练组大鼠的GOT、GPT和CK的活性明显降低(P<0.05),而Hb(P<0.05)和BS(P<0.01)有显著性升高.以上研究结果表明,冬虫夏草对运动造成的骨骼肌细胞膜的损伤有明显的保护作用,提高运动过程中糖的储备和血红蛋白含量,可提高运动能力.     

决明子乙酸乙酯提取物对肝纤维化小鼠脂质过氧化水平的影响

目的:研究决明子乙酸乙酯提取物对肝纤维化小鼠脂质过氧化水平的影响.方法:采用腹腔注射0.1%的CCl4花生油溶液建立小鼠肝纤维化模型,采用试剂盒测定血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)和碱性磷酸酶(ALP)的含量;采用分光光度法测定肝组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)的活性.结果:结果表明,决明子乙酸乙酯提取物低剂量(0.10g/kg)组、中剂量(0.15g/kg)组能减少小鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)和碱性磷酸酶(ALP)的含量,并可减少肝脏中丙二醛(MDA)含量,抑制肝脏中超氧化物歧化酶(SOD)的活性.结论:决明子乙酸乙酯提取物对肝纤维化小鼠有一定的保护作用,其作用机制可能与抑制脂质过氧化有关.     

海藻多糖抗氧化作用的实验研究

目的:研究海藻多糖(Polysaechrides from Spirulina Platensis,PSP)对小鼠肝损伤动物模型与肝匀浆脂质过氧化模型的抗氧化作用。方法:采用腹腔注射CCL4的方法,制造小鼠肝损伤动物模型,金氏法测定血清谷氨酸丙酮酸转氨酶(SGPT)和肝脏的过氧化脂质(Lipoper-oxides,LPO)含量;Fenton反应诱导小鼠肝匀浆脂质过氧化动物模型,采用硫代巴比妥酸(TBA)法测定肝匀浆LPO。结果:在体外,海藻多糖可剂量依赖性地抑制Fenton反应导致的CCL4毒化小鼠肝匀浆中LPO的生成,其IC50为1.6×10-4。在体内,灌胃250mg/kg的海藻多糖组可明显降低CCL4毒化小鼠血清SGPT活性(P<0.01)。结论:海藻多糖对体内外的肝组织有一定程度的抗氧化作用。     

和营安心方对过氧化氢损伤大鼠胚胎心肌细胞的保护作用

目的：探讨和营安心方对过氧化氢（hydrogen peroxide,H2O2）所致大鼠胚胎心肌细胞损伤的保护作用。方法：建立H2O2致大鼠胚胎心肌细胞氧化应激损伤模型,设正常对照组（Control）、过氧化氢（200μmol·L-1）模型组（Model）、和营安心方（500、250、125 mg·kg-1）三个剂量组,四甲基偶氮唑盐（3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl tetrazolium bromide,MTT）代谢率检测心肌细胞细胞活性,测定细胞培养液中乳酸脱氢酶（lactate dehydrogenase,LDH）及丙二醛（malondialdehyde,MDA）的含量。结果：H2O2组细胞活性显著性降低（P<0.01）, LDH及MDA含量显著性升高（P<0.01）;和营安心方可显著提高H2O2损伤心肌细胞的活性,减少MDA 含量（P<0.05）,降低LDH 活性（P<0.05）。结论：和营安心方对H2O2损伤的心肌细胞具有明显的保护作用,其机制可能与抑制脂质过氧化有关。     

针剌手厥阴心包经穴对力竭大鼠心肌过氧化损伤的保护作用

目的:观察针刺手厥阴心包经穴对大鼠自由基代谢的影响,探讨针灸对力竭运动心脏的保护作用.方法:24只SD大鼠随机分为安静对照组、力竭运动组、针刺力竭运动组.针刺力竭运动组每日针刺双侧内关穴和郄门穴一次,连续20天后,力竭运动组、针刺力竭运动组做力竭游泳实验.运动后即刻处死各组大鼠,取心脏备用.分别测定其心肌线粒体SOD活性、GSH和MDA含量.结果:力竭运动组与安静对照组相比,GSH、SOD下降明显(P<0.01),而MDA显著升高(P<0.01).针刺力竭运动组MDA明显低于力竭运动组(P<0.01),SOD显著高于力竭运动组(P<0.01),GSH略高于力竭运动组,无统计学意义.结论:针刺内关、郄门穴能增强心肌细胞清除自由基能力,抑制力竭运动时心肌脂质过氧化反应而起到保护心肌的作用.     

泉州湾桐花树种群抗氧化能力的比较

比较研究了泉州湾桐花树种群构件水平和个体水平不同龄级叶的脂质过氧化程度及抗氧化物含量,结果表明：在桐花树种群叶构件水平上过氧化程度较严重的是植株基部老叶,其次是中上部叶,膜脂质过氧化程度较低的是顶叶;从个体种群水平看植株叶的脂质过氧化程度较高的是刚进入繁殖期的植株;在构件水平上植株顶叶GSH含量和CAT活性表现最高,中部叶片次之,基部老叶较低,NO含量呈现与之相反的变化趋势;在个体种群水平上桐花树叶的GSH含量和CAT活性表现为开花期植株比未开花植株高,2~6片叶幼苗植株叶的抗氧化物含量最低.桐花树种群抗氧化能力的研究结果显示,进入繁殖生长的植株和2~6片叶幼苗植株宜作为泉州湾桐花树林的重点保护对象.     

抗肝细胞脂质堆积模型药物最佳筛选条件的研究

目的：利用小檗碱研究抗脂质堆积肝细胞模型药物的最佳实验条件.方法：将培养12h的HepG2细胞分为正常对照组（Con）、模型对照组（Model）和阳性对照药组（Ber）.Con细胞仅用培养液培养,Model和Ber加入脂质堆积诱导液,后者再加不同浓度的小檗碱,分别观察不同的诱导时间对肝细胞脂质堆积的影响和对小檗碱治疗作用的影响.以油红0染色观察细胞内脂滴形成状况,并检测细胞内TG的含量.结果：1mM油酸钠、50nM胰岛素共同诱导48 h的实验条件可见肝细胞内有典型的脂滴形成,肝细胞内TG含量显著升高,差异有统计学意义（P〈0.01）,终浓度10-5M小檗碱与模型对照组比较,能明显改善肝细胞脂质堆积,差异具有统计学意义（（P〈0.001）可为对照阳性药,此条件比较适合样品的筛选.结论：确定了该细胞模型用于药物筛选的最佳实验条件.     

苦菜水提取物对力竭运动训练大鼠血脂和血液生化指标的实验研究

目的:研究苦菜水提取物对力竭运动训练大鼠血脂和血液生化指标的影响。方法:大鼠游泳运动训练至力竭后测定大鼠总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)和极低密度脂蛋白(VLDL)含量、超氧化物歧化酶(SOD)、谷草转氨酶(GOT)、谷丙转氨酶(GPT)活性及血糖(BS)、丙二醛(MDA)和全血血红蛋白(Hb)含量。结果:苦菜水提取物能使力竭运动训练大鼠TC的含量显著下降;HDL的含量显著升高;LDL和VLDL的含量显著下降;SOD活性、BS、Hb含量显著升高;MDA含量、GOT活性显著下降。结论:苦菜水提取物对力竭运动训练大鼠可显著降低血脂、清除运动产生的脂质过氧化物和提高BS、Hb含量。苦菜水提取物可延缓大鼠运动性疲劳的发生。     

感染旋毛虫兔血清酶变化与虫体密度关系

目的：探讨旋毛虫病时肌酸激酶（CK）、醛缩酶（ALD）、丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）和乳酸脱氢酶（LDH）与虫体密度的关系,为旋毛虫病血清酶的检测分析提供参考资料。方法：将实验用兔随机分成三组：轻度感染组、重度感染组和对照组,感染后不同时间检测血清CK、AI,D、ALT、AST和LDH活性,处死后用人工消化法进行肌幼虫计数。。结果：兔旋毛虫病时五种血清酶（CK、ALD、ALT、AST和LDH）均升高,五种血清酶与宿主腓肠肌虫体密度有相关性。结论：CK、AI．D、ALT、AST及LDH与宿主腓肠肌虫体密度有相关性。     

Chlorogenic acid prevents acetaminophen-induced liver injury: the involvement of CYP450 metabolic enzymes and some antioxidant signals

Chlorogenic acid (CGA), a polyphenolic compound, is abundant in fruits, dietary vegetables, and some medicinal herbs. This study investigated the prevention of CGA against acetaminophen (AP)-induced hepatotoxicity and its engaged mechanisms. CGA reversed the decreased cell viability induced by AP in L-02 cells in vitro. In addition, CGA reduced the AP-induced increased serum levels of alanine/aspartate aminotransferase (ALT/AST) in vivo. The effect of CGA on cytochrome P450 (CYP) enzymatic (CYP2E1, CYP1A2, and CYP3A4) activities showed that CGA caused very little inhibition on CYP2E1 and CYP1A2 enzymatic activities, but not CYP3A4. The measurement of liver malondialdehyde (MDA), reactive oxygen species (ROS), and glutathione (GSH) levels showed that CGA prevented AP-induced liver oxidative stress injury. Further, CGA increased the AP-induced decreased mRNA expression of peroxiredoxin (Prx) 1, 2, 3, 5, 6, epoxide hydrolase (Ephx) 2, and polymerase (RNA) II (DNA directed) polypeptide K (Polr2k), and nuclear factor erythroid-2-related factor 2 (Nrf2). In summary, CGA ameliorates the AP-induced liver injury probably by slightly inhibiting CYP2E1 and CYP1A2 enzymatic properties. In addition, cellular important antioxidant signals such as Prx1, 2, 3, 5, 6, Ephx2, Polr2k, and Nrf2 also contributed to the protection of CGA against AP-induced oxidative stress injury.     

Hypothetical mode of action of earthworm extract with hepatoprotective and antioxidant properties

The hepatoprotective potential of earthworm extract (EE) (Lampito mauritii, Kinberg) was evaluated against paracetamol-induced liver injury in Wistar albino rat, in comparison with silymarin, the standard hepatoprotective drug. We observed a reduction in liver antioxidants, such as glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx),and catalase (CAT) and in serum total protein, and an increase in serum alkaline phosphatase (ALP), serum aspertate aminotranferase (AST), serum alanine aminotranferase (ALT), bilirubin and liver thiobarbituric acid reactive substances (TBARS) due to liver injury in the paracetamol-administered rats (2 g/kg). On the contrary, increased activities of liver GSH, SOD, GPx,CAT and serum total protein level, and decrease in the contents of serum ALP, AST, ALT, bilirubin and liver TBARS were observed in rats administered with different doses of EE (100, 200 and 300 mg/kg), which are similar to the activities of hepatoprotective drug silymarin (150 mg/kg). The mode of action of EE as evidenced by the above parameters may suggest that EE, on the one hand, prevents the formation of the reactive oxygen groups, or scavenges these groups, thereby preventing the damage on the hepatic cells, and, on the other hand, modulates the genes responsible for synthesis of antioxidant enzymes such as GPx, CAT and SOD in liver tissue and decreases the serum enzymatic activities such as ALP, AST and ALT.     

Ferulic acid prevents liver injury and increases the anti-tumor effect of diosbulbin B in vivo

The present study is designed to investigate the protection by ferulic acid against the hepatotoxicity induced by diosbulbin B and its possible mechanism, and further observe whether ferulic acid augments diosbulbin B-induced anti-tumor activity. The results show that ferulic acid decreases diosbulbin B-increased serum alanine transaminase/aspartate transaminase (ALT/AST) levels. Ferulic acid also decreases lipid peroxide (LPO) levels which are elevated in diosbulbin B-treated mice. Histological evaluation of the liver demonstrates hydropic degeneration in diosbulbin B-treated mice, while ferulic acid reverses this injury. Moreover, the activities of copper- and zinc-containing superoxide dismutase (CuZn-SOD) and catalase (CAT) are decreased in the livers of diosbulbin B-treated mice, while ferulic acid reverses these decreases. Further results demonstrate that the mRNA expressions of CuZn-SOD and CAT in diosbulbin B-treated mouse liver are significantly decreased, while ferulic acid prevents this decrease. In addition, ferulic acid also augments diosbulbin B-induced tumor growth inhibition compared with diosbulbin B alone. Taken together, the present study shows that ferulic acid prevents diosbulbin B-induced liver injury via ameliorating diosbulbin B-induced liver oxidative stress injury and augments diosbulbin B-induced anti-tumor activity.     

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease （NAFLD） in rats

Objective： The prevalence of non-alcoholic fatty liver disease （NAFLD） has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone （PGZ） acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. Methods： The rats were separated randomly into 6 groups： model group Ⅰ were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/（kg.d） simultaneously, while control group Ⅰ were fed normal food for 8 weeks; model group Ⅱ were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/（kg.d） orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group Ⅱ were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, alkaline phosphatase （ALP）, tumor necrosis factor alpha （TNF-α）, fasting blood glucose （FBG）, fasting plasma insulin （FINS）, HOMA （homeostasis model assessment） insulin resistance index （HOMA-IR）, and the liver histology of rats of all groups were assayed. Results： After 8 weeks, the liver in model group Ⅰ showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-α were significantly increased （P〈0.05） compared with control group Ⅰ. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased （P〈0.05） compared with model group Ⅰ. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group Ⅱ rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels ofALT, AST, ALP, FINS and HOMA-IR were significantly increased （P〈0.05） in model group Ⅱ compared with control group Ⅱ. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-α and HOMA-IR were significantly decreased compared with model group Ⅱ. Conclusion： Insulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.     

Protection of plasma transfusion against lipopolysaccharide/<Emphasis Type="SmallCaps">d</Emphasis>-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice

Fulminant hepatic failure is a severe clinical condition associated with extremely poor outcomes and high mortality. A number of studies have demonstrated the ability of plasma transfusion to successfully treat fulminant hepatic failure, but the underlying mechanisms are not well understood. The aim of the present study is to define the mechanisms of plasma transfusion treatment in lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced mice. LPS/D-GalN treatment in mice causes significant hepatic failure, including increasing serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, histopathological changes in centrilobular necrosis and inflammatory cells, and the up-regulation of inflammation (tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)). When LPS/D-GaIN-induced mice were treated with plasma, these changes were halted. Results showed that plasma transfusion significantly reduced mortality, and decreased the levels of AST, ALT, and inflammation factors such as TNF-α and IL-6. The expression levels of cleaved Caspase-3, BAX, and p53 were down-regulated and Bcl-2 was up-regulated, suggesting that plasma can reduce LPS/D-GalN-induced apoptosis. The protective mechanism of plasma against LPS/D-GalN-induced fulminant hepatic failure is related to the inhibition of the inflammatory response and the reduction in apoptosis through the down-regulation of the p53-induced apoptotic pathway.     

Effects of astaxanthin on oxidative stress induced by Cu<Superscript>2+</Superscript> in prostate cells

Astaxanthin (AST), a carotenoid molecule extensively found in marine organisms and increasingly used as a dietary supplement, has been reported to have beneficial effects against oxidative stress. In the current paper, the effects of AST on viability of prostate cells were investigated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay; cell apoptosis and intracellular reactive oxygen species (ROS) levels were determined by flow cytometry; the mitochondrial membrane potential (MMP) was measured by fluorospectrophotometer; and activities of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were evaluated by a detection kit. The results show that copper ion (Cu²⁺) induced apoptosis, along with the accumulation of intracellular ROS and MDA, in both prostate cell lines (RWPE-1 and PC-3). AST treatments could decrease the MDA levels, increase MMP, and keep ROS stable in RWPE-1 cell line. An addition of AST decreased the SOD, GSH-Px, and CAT activities in PC-3 cell line treated with Cu²⁺, but had a contrary reaction in RWPE-1 cell lines. In conclusion, AST could contribute to protecting RWPE-1 cells against Cu²⁺-induced injuries but could cause damage to the antioxidant enzyme system in PC-3 cells.     

Evaluation of the hepatoprotective and antioxidant activities of Rubus parvifolius L

The hepatoprotective and antioxidant activities of the n-butanol extract of Rubus parvifolius L. (RPL), a widely used medicinal plant, were evaluated. Results demonstrated that RPL extract possessed pronounced hepatoprotective effects against carbon tetrachloride (CCl₄)-induced hepatic injury in mice, which was at least partially attributed to its strong antioxidant capacity. Treatment with RPL extract markedly attenuated the increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels caused by CCl₄ intoxication. It also significantly prevented the decrease in superoxide dismutase (SOD) activity and the increase in malondialdehyde (MDA) content of liver tissue. Meanwhile, histopathological changes of hepatic damage were also remarkably ameliorated. Phytochemical analysis based on high-performance liquid chromatography/tandem mass spectrometry (HPLC-MS/MS) revealed the presence of various phenolic compounds, including caffeic acid conjugates, ellagic acid glycosides, and flavonol glycosides, which might be responsible for the hepatoprotective and antioxidant activities of RPL.     

山莨菪碱清除氧自由基和抗脂质过氧化作用

山莨菪碱对Fenton反应生成的·OH具育较强的直接清除作用,其IC_(50)为276mg.L~(-1),作用比·OH特异性清除剂甘露醇(IC_(50)为1349mg·L~(-1)强。对黄嘌呤-黄嘌呤氧化酶系统产生的O(?)也有较强的清除作用,其IC_(50)126mg·L~(-1)。山莨菪碱对自由基发生系统(FRGS)诱导离体大鼠心肌匀浆组织产生的脂质过氧化(LPO)作用有明显的抑制效应。对FRGS诱导离体大鼠心肌线粒体膜LPO也有一定的抑制作用。结果提示山莨菪碱的抗脂质过氧化作用与清除氧自由基作用有关。