Hydroxysafflor yellow A protects against thioacetamide-induced liver fibrosis in rats via suppressing proinflammatory/fibrogenic mediators and promoting hepatic stellate cell senescence and apoptosis

Objective:To evaluate the effect of hydroxysafflor yellow A(HSYA)on thioacetamide-induced liver fibrosis.Methods:Thioacetamide was administered to rats intraperitoneally in doses of 200 mg/kg twice a week for 12 weeks.Thioacetamide-intoxicated rats were given silymarin(50 mg/kg)or HSYA(5 mg/kg)orally every day for 8 weeks.Liver enzymes,fibrosis markers,histological changes as well as immunohistochemistry of TNF-α,IL-6,p21,α-SMA,and caspase-3 were examined.The effect of HSYA on HSC-T6 activation/proliferation and apoptosis was also determined in vitro.Results:HSYA decreased liver enzymes,TNF-α,IL-6,and p21 expressions,hepatic PDGF-B,TIMP-1,TGF-β1,and hydroxyproline levels,as well as fibrosis score(S2 vs.S4)compared to the thioacetamide group.HSYA also downregulatedα-SMA while increasing caspase-3 expression.Surprisingly,at 500μg/mL,HSYA had only a slightly suppressive effect on HSC proliferation,with a 9.5%reduction.However,it significantly reduced TGF-β1,inhibitedα-SMA expression,induced caspase-3 expression,and promoted cell senescence.Conclusions:HSYA may be a potential therapeutic agent for delaying and reversing the progression of liver fibrosis.More research on HSYA at higher doses and for a longer period is warranted.

Effects of endotoxin on expression of ras, p53 and bcl-2 oncoprotein in hepatocarcinogenesis induced by thioacetamide in rats

AIM To evaluate the relationship between expression of ras, p53, bcl 2 gene products, and hepatocarcinogenesis since endotoxemia produced from lipopolysaccharide admi nistration and/or the hypophagocytic state of splenectomy significantly accelerated hepatocarcinogenesis induced by thioacetamide. 〖WTH4〗METHODS〓〖WTXFZ〗The hepatocarcinoma model was induced by oral intake of 0 03% thioacetamide for six months. During the induction of hepatocarcinoma model, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The techniques of flow cytometry, immunohistochemistry and immunoelectronmicroscopy were applied to quantitative analysis of the expression of oncogene proteins. RESULTS In this model system, overexpression of ras p21 protein mainly occurred on precancerous cell population or in early stage of hepatocyte transformation. And the levels of ras p21 declined when nuclear DNA aneuploid increased. Expression of bcl 2 protein slowly and steadily rose with more hepatocytes staying in S+G2M phases as the hepatocarcinoma became more malignant. P53 was moderately expressed during the hepatocarcinogenesis. There was no statistical correlation between endotoxemia levels and the changes of ras, p53 and bcl 2 gene products. CONCLUSION Over expression of oncogene ras p21 was likely to be a precursor of the premalignant hepatocytes and it might be responsible for the initiation of hepatocarcinogenesis. Bcl 2 protein expression is proportional to the severity of the malignancies. P53 may be a key pathway on the transformation and development of hepatocarcinoma. This study confirmed the hypothesis that there are multiple genes and multiple steps involved in hepatocarcinogenesis. Expressions of oncogene proteins reflected the properties of the premalignant and malignant cells, but not directly related to endotoxemia statistically.[JP]

Protective effects of Phyllanthus acidus(L.) Skeels leaf extracts on acetaminophen and thioacetamide induced hepatic injuries in Wistar rats

Objective:To investigate and compare the hepatoprotective effects of crude ethanolic and aqueous extracts of Phyllanthus acidus（L.） Skeels（P.acidus） leaves on acetaminophen（APAP） and thioacetamide（TAA） induced liver toxicity in wistar rats.Silymarin was the reference hepatoprotective agent.Methods:In two different sets of experiments,the P.acidus extracts （200 and 400 mg/kg,body weight） and silymarin（100 mg/kg,body weight） were given orally for 7 days and a single dose of APAP（2 g/kg,per oral） or TAA（100 mg/kg,subcutaneous） were given to rats.The level of serum aspartate transaminase（AST）,alanine transaminase（ALT）,alkaline phosphatase（ALP）,total bilirubin and total protein were monitored to assess hepatotoxicity and hepatoprotection.Results:APAP or TAA administration caused severe hepatic damage in rats as evident from significant rise in serum AST,ALT,ALP,total bilirubin and concurrent depletion in total serum protein.The P.acidus extracts and silymarin prevented the toxic effects of APAP or TAA on the above serum parameters indicating the hepatoprotective action.The aqueous extract was found to be more potent than the corresponding ethanolic extract against both toxicants.The phenolic and flavonoid content（175.02±4.35 and 74.68±1.28,respectively） and 2,2-diphenyl-1- picrylhydrazil（DPPH）[IC50=（33.2±0.31）μg/mL]scavenging potential was found maximum with aqueous extract as compared to ethanolic extract.Conclusions:The results of present study suggests that the aqueous extract of P.acidus leaves has significant hepatoprotective activity on APAP and TAA induced hepatotoxicity,which might be associate with its high phenolic and flavonoid content and antioxidant properties.

Tetrandrine stimulates the apoptosis of hepatic stellate cells and ameliorates development of fibrosis in a thioacetamide rat model

AIM： To investigate the therapeutic effect of tetrandrine on liver fibrosis induced by thioacetamide in rats in vivo and in vitro. METHODS： In vitro study： we investigated the effect of tetrandrine on the apoptosis of rat hepatic stellate cells transformed by simian virus 40 （T-HSC/CI-6）, which retains the features of activated cells. In vivo study： hepatic fibrosis was induced in rats by thioacetamide. Tetrandrine was given orally to rats at doses of 5, 10 or 20 mg/kg for 4 wk compared with intraperitoneal injection of interferon-r. RESULTS： In vitro study： 5, 10 or 25 μg/mL of tetrandrine-induced activation of caspase-3 in t-HSC/CI-6 cells occurred dose-dependently. In vivo study： tetrandrine treatment as well as interferon-r significantly ameliorated the development of fibrosis as determined by lowered serum levels of aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, total bilirubin （T-Bil） and the levels of liver hydroxyproline （Hyp）, hyaluronic acid （HA）, laminin （LN） and also improved histological findings. The effects of tetrandrine at the concentration of 20 mg/kg were better than the other concentration groups. CONCLUSION： Tetrandrine promotes the apoptosis of activated HSCs in vitro. Tetrandrine administration can prevent liver fibrosis and liver damage induced by thioacetamide in rats in vivo, indicating that it might exert a direct effect on rat HSCs.

Atorvastatin and rosuvastatin do not prevent thioacetamide induced liver cirrhosis in rats

AIM:To examine whether the administration of atorvastatin and rosuvastatin would prevent experimentallyinduced hepatic cirrhosis in rats.METHODS:Liver cirrhosis was induced by injections of thioacetamide(TAA).Rats were treated concurrently with TAA alone or TAA and either atorvastatin(1,10 and 20 mg/kg) or rosuvastatin(1,2.5,5,10 and 20 mg/kg) given daily by nasogastric gavage.RESULTS:Liver fibrosis and hepatic hydroxyproline content,in the TAA-treated group was significantly higher than those of the controls [11.5 ± 3.2 vs 2.6 ± 0.6 mg/g protein(P = 0.02)].There were no differences in serum aminotransferase levels in the TAA controls compared to all the groups treated concomitantly by statins.Both statins used in our study did not prevent liver fibrosis or reduce portal hypertension,and had no effect on hepatic oxidative stress.Accordingly,the hepatic level of malondialdehyde was not lower in those groups treated by TAA + statins compared to TAA only.In vitro studies,using the BrdU method have shown that atorvastatin had no effect of hepatic stellate cells proliferation.Nevertheless,statin treatment was not associated with worsening of liver damage,portal hypertension or survival rate.CONCLUSION:Atorvastatin or rosuvastatin did not inhibit TAA-induced liver cirrhosis or oxidative stress in rats.Whether statins may have therapeutic applications in hepatic fibrosis due to other etiologies deserve further investigation.

Protective effect of aqueous extract of Feronia elephantum correa leaves on thioacetamide induced liver necrosis in diabetic rats

Objective:To evalueate hepatoprotective effects Feronia elephantum(F.elephantum)correa against thioacctamide(TA)induced liver necrosis in diabetic rats.Methods:Male wistar rats were made diabetic with alloxan(160 mg/kg)on day 0 of the study.They were intoxicated with hepatotoxicant(thioacetamide,300 mg/kg,ip)on day 9 of study to produce liver necrosis.Effects of 7 day daily once administration(day 2 to day 9)of EF(400 and 800 mg/kg,po)were evaluated on necorosis of liver in terms of mortality,liver volume,liver weight,serum aspartate aminotransferase(AST)and serum alanine transaminase(ALT),and histopathology of liver sections(for signs of necorosis and inflammation)on day-9 of the study.Separate groups of rats with treated only with alloxan(DA control),thioacetamide(TA control)and both(TA+DA control)were maintained.Results:FE significantly lowered the mortality rate and showed improvement in liver function parameters in TA-induced diabetic rats without change in liver weight,volume and serum glucose levels.Conclusions:FE showed promising activity against TA-induced liver necorsis in diabetic rats and so might be useful for prevention of liver complications in DM.

Involvement of P53 and Bax/Bad triggering apoptosis in thioacetamide-induced hepatic epithelial cells

AIM： Thioacetamide （TAA） has been used in studying liver fibrosis and cirrhosis, however, the mechanisms of TAA-induced apoptosis in liver are still unclear. The hepatic epithelial cell line clone 9 was cultured and treated with TAA to investigate the causes of cell death. METHODS： The cell viability of TAA-induced clone 9 cells was determined using MTT assay. Total cellular GSH in TAA-induced clone 9 cells was measured using a slight modification of the Tietze assay. The activity of caspase 3 in TAA-induced clone 9 cells was monitored by the cleavage of DEVD-p-nitroanaline. TUNEL assay and flow cytometry were applied for the determination of DNA fragmentation and the proportion of apoptosis in TAA- induced clone 9 cells, respectively. The alterations of caspase 3, Bad, Bax and Phospho-P53 contents in TAA- induced clone 9 cells were measured by Western blot. RESULTS： The experimental data indicated that TAA caused rat hepatic epithelial cell line clone 9 cell death in a dose-and time-dependent manner; 60% of the cells died （MTT assay） within 24 h after 100 rag/1 TAA was applied. Apoptotic cell percentage （TUNE1 assay） and caspase 3 activities were highest after 100 rag/1 TAA was added for 8 h. The release of GSH and the elevation in caspase content after TAA treatment resulted in clone 9 cell apoptosis via oxidative stress and a caspasedependent mechanism. The phospho-p53, Bax and Bad protein expressions in clone 9 cells were increased after TAA treatment. CONCLUSION： These results reveal that TAA activates p53, increases caspase 3, Bax and Bad protein contents, perhaps causing the release of cytochrome c from mitochondria and the disintegration of membranes, leading to apoptosis of cells.

Chrysanthemum indicum ethanol extract attenuates hepatic stellate cell activation in vitro and thioacetamide-induced hepatofibrosis in rats

Objective:To investigate the antifibrotic effects of Chrysanthemum indicum ethanol extract(CIEE)against activated hepatic stellate cells(HSC)and thioacetamide(TAA)-induced hepatofibrosis in rats.Methods:Cell viability and proliferation of HSC-T6 cells were measured using MTT assay.Primary HSCs were used to study morphology.TAA(200 mg/kg)was used to induced hepatic fibrosis in rats.CIEE(100 and 500 mg/kg)and silymarin(50 mg/kg)were administered orally.Liver functions including alanine transaminase,aspartate transaminase,glutathione,and hydroxyproline levels were measured using commercial kits.Liver sections and fibrotic biomarker expression were measured using hematoxylin and eosin staining and real-time polymerase chain reaction.Results:In vitro study revealed that CIEE(0.1,0.25,and 0.5 mg/mL)inhibited the proliferation of activated HSCs exposed to transforming growth factor(TGF)-β and restored the activated primary HSC morphology.In in vivo studies,TAA-induced increase in liver/body weight ratio(5.46±0.26)was significantly reduced(4.13±0.22)by CIEE(P<0.05 at 500 mg/kg).CIEE(100 and 500 mg/kg)improved the liver functions by significantly attenuating changes in alanine transaminase,aspartate transaminase,glutathione,and hydroxyproline levels(P<0.05).Further,CIEE(100 and 500 mg/kg)ameliorated the histological changes in liver tissue and TGF-β expression significantly(P<0.05)in TAA-induced rats.Conclusions:CIEE significantly protects against TAA-induced liver damage in rats and can be used in the treatment of liver fibrosis.

Protective effect of Amorphophallus campanulatus(Roxb.) Blunie.tuber against thioacetamide induced oxidative stress in rats

Objective:To identify the phytochemical constituents of Amorphopkallus campanulatus(A. campanulatus) tuber and to evaluate its antioxidant potential through in vitro and in vivo models. Methods:Phytochemical screening and in vitro antioxidant activities of A.campanulatus tuber n-hexane extract(ACHE) and methanolic extract(ACME) were evaluated using DPPH,hydroxyl radical,reducing power and total antioxidant capacity assays.The total phenolic and flavonoid contents were also investigated.The protective potential of two different doses of ACME(125 and 250 mg/kg) was also evaluated against thioaeetamide(TAA) induced oxidative stress in rats. Silymarin used as a standard drug control.Hepatotoxicitv was assessed by quantifying the serum levels of aspartate aminotransferase(AST),alanine aminotransferase(AIT),alkaline phosphatase (ALP) and lactate dehydrogenase(LDH).The antioxidant potential of ACME were also evaluated by the estimation of catalase(CAT),glutathione peroxidase(GPx),glutathione reductase (OR),glutathione-S-transferase(GST),reduced glutathione(GSH) and lipid peroxidation (Thiobarbituric acid reactive substances) in hepatic and renal tissues.Histopathologic changes of liver were also evaluated.Results:In vitro studies revealed that ACME has higher antioxidant and radical scavenging activity than ACHE,which may be attributed to its higher phenolic and flavonoid content.ACME significandy prevented the elevation of serum AST,ALT.ALP,LDH,and tissue malondialdehyde levels(P 【 0.05).Hepatic and renal GSH.GST.GR,GPx,and catalase levels were remarkably increased by the treatment with the extract.Quantification of histopathological changes also supported the dose dependent protective effects of ACME.Conclusions:The results do suggest that A.campanulatus tuber could be considered as a potential source of natural antioxidant.

Protective effect of Pisonia aculeata on thioacetamide induced hepatotoxicity in rats

Objective:To evaluate the protective effect of Pisonia aculeata(P.aculeata) on thioacetamide induced hepatotoxicity in rats.Methods:Male Wistar rats were administered 250 or 500 mg/kg p.o.of P.aculeata extract for 21 days and simultaneously administered thioacetamide(TAA) 50 mg/kg bw s.c.1 h alter the respective assigned treatments every 72 h.At the end of all experimental methods,all the animals were sacrificed by cervical decapitation.Blood samples were collected.Serum was separated and analyzed for various biochemical parameters.Results:TAA induced a significant rise in aspartate amino transferase(AST),alanine amino transferase(ALT),alkaline phosphatase(ALP),total bilirubin,gamma glutamate transpeptidase(GGTP),lipid peroxidase(LPO)with a reduction of total protein,superoxide dismutase(SOD),catalase,glutathione peroxidase(GPx) and glutathione S-transferase(GST).Treatment of rats with different does of plant extract(250 and 500 mg/kg) significantly(P<0.001) altered serum marker enzymes and antioxidant levels to near normal against TAA treated rats.The activity of the extract at a dose of 300 tug/kg was comparable to the standard drug,silymarin(50 mg/kg.p.o.).Conclusions:It can be concluded that P.aculeata extract possesses a remarkable hepaloprolective and antioxidant activity against TAA induced hepatotoxicitv.Wore research is required lo derive an optimal therapeutic dose.

Effect of dichloromethylene diphosphonate on liver regeneration following thioacetamide-induced necrosis in rats

AIM: To study the effect of dichloromethylene diphos-phonate (DMDP), a selective Kupffer cell toxicant in reference to liver damage and postnecrotic liver regeneration in rats induced by sublethal dose thioacetamide (TA). METHODS: Rats, intravenously (iv ) pre-treated with a single dose of DMDP (10 mg/kg), were intraperitoneally (ip ) injected with TA 6.6 mmol/kg (per 500 mg/kg body weight). Hepatocytes were isolated from rats at 0, 24, 48 and 72 h following TA intoxication and blood and liver samples were obtained. To evaluate the mecha-nisms involved in the postnecrotic regenerative state, DNA distribution and ploidy time course were assayed in isolated hepatocytes. Circulating cytokine tumor necrosis factor-alpha (TNF-α) was assayed in serum and determined by reverse transcriptase-polymerase chain reaction in liver extract. RESULTS: The effect of DMDP induced noticeable changes in postnecrotic regeneration, causing an increased percentage of hepatocytes in the cell cycle S phase. The increase at 24 h in S1 population in rats pretreated with DMDP + TA was significantly (P < 0.05) different compared with that of the TA group (18.07% vs 8.57%). Hepatocytes increased their proliferation as a result of these changes. Also, TNF-α expression and serum level were increased in rats pre-treated with DMDP. Thus, DMDP pre-treatment reduced TA-induced liver injury and accelerated postnecrotic liver regeneration. CONCLUSION: These results demonstrate that Kupffer cells are involved in TA-induced liver, as well as in post-necrotic proliferative liver states.

An unexpected reaction of cyanothioacetamide:Novel preparation of pyrazolo[3,4-b]-pyridine derivatives under MWI

An unexpected multi-component reaction of cyanothioacetarnide with aldehyde and aminopyrazole under MWI was reported. Through this reaction, a series of pyrazolo[3,4-b]-pyridine derivatives was prepared in high yields via simple operational procedure.

Endotoxins enhance hepatocarcinogenesis induced by oral intake of thioacetamide in rats

AIM To clarify whether endotoxin is of pathogenic importance for hepatocarcinogenesis, or the increased cancer risk results solely from the cirrhotic process. METHODS The rat model of hepatoma was treated by the intake of 0 03% thioacetamide in drinking water for six months. During induction of hepatoma, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The liver nuclear DNA index and proliferation index were quantitatively analyzed by flow cytometry. Hepatic histology was examined with light and electron microscopes. Plasmic endotoxin concentration and γ glutamyl transpeptidase activity were measured, and hepatoma incidence was recorded. RESULTS Thioacetamide induced cirrhosis and hepatoma in Wistar rats with histology or regenerative nodule, fibrosis and neoplastic foci were quite similar to the pathogenic process of human cirrhosis leading to hepatoma. In comparison with TAA controls (DNA index: 1 15±0 21), exo endotoxin increased the DNA index by 7 8% (1 24±0 25, P <0 02) and hepatoma rate by 16 7. Splenectomy induced enteric endotoxemia increased the DNA index by 25% (1 44±0 15, P <0 01) and hepatoma rate by 33%. A summation of the effects of these two factors increased the DNA index by 36% ( P <0 01)and hepatoma incidence by 50%, moreover, the level of endotoxemia showed a close relation with DNA index ( r =0 96, P <0 01), as well as with the occurrence rate of hepatoma ( r =0 00, P <0 01). Histological findings further verified such alterations. CONCLUSION Lipopolysaccharide administration and/or splenectomy induced enterogenic endotoxemia may enhance rat hepatocarcinogenesis induced by oral intake of thioacetamide.

Co-administration of cyclosporine A alleviates thioacetamide-induced liver injury

AIM: To investigate the effects of cyclosporine A (CsA)on thioacetamide (TAA)-induced liver injury.METHODS: CsA was co-administrated (7.5 μg/kg body weight per day, i.p.) into rat to investigate the role of CsA on TAA-(200 mg/kg body weight per 3 d for 30 d, i.p.)induced liver injury.RESULTS: The data show that TAA caused liver fibrosis in rat after 30 d of treatment. CsA alleviates the morphological changes of TAA-induced fibrosis in rat liver. The blood glutamyl oxaloacetic transaminase (GOT)/glutamyl pyruvic transaminase (GPT) in the TAA-injury group is elevated compared to that of the normal rat. Compared with the TAA-injury group, the blood GOT/GPT and TGFβ1 (by RT-PCR analysis) are reduced in the CsA plus TAA-treated rat. The level of the transforming growth factor receptor I (TGFβ-R1) in the CsA plus TAA-treated group shows higher than that in the TAA only group, but shows a lower level of the fibroblast growth factor receptor 4 (FGFR4)in the CsA plus TAA-treated group, when using the Western blot analysis. After immunostaining of the frozen section,TGFβ-R1 and FGFR4 are more concentrated in rat liver after CsA plus TAA injury.CONCLUSION: This result suggests that CsA has an alleviated effect on TAA-induced liver injury by increasing the multidrug resistance P-glycoprotein and could be through the regulation of TGFβ-R1 and FGFR4.

赢创完成向SABO出售TAA衍生物业务

赢创完成向意大利化学品公司SABO出售三丙酮胺(TAA)衍生物业务。这一举措标志着公司在持续优化产品组合、专注于特种化学品方面更进一步。意大利化学品公司SABO是世界领先的光稳定剂制造商之一,TAA衍生物是生产光稳定剂的原材料。本次收购的具体金额不作披露。本次交易于2022年10月中旬公布,并于2022年12月29日正式完成交易。

TAA致大鼠急性肝衰竭的胃肠功能及病理改变

目的了解大鼠急性肝衰竭时胃肠功能及病理组织学变化。方法以硫代乙酰胺(TAA)腹腔注射SD大鼠制备急性肝衰竭模型,观察其一般情况、肝脏生化指标、肝脏与胃肠组织学变化及全胃肠道钡剂通过时间。结果模型组大鼠出现典型消化道症状及肝性脑病,肝脏生化指标较对照组显著升高(P<0.01),肝脏组织坏死、肠壁损伤。肠蠕动功能减低,较对照组显著延长(P<0.01)。结论急性肝衰竭大鼠确实存在着胃肠功能的障碍,且胃肠功能障碍与肝衰竭密切相关。

蒙药地格达-4味汤对TAA所致小鼠化学性肝损伤的实验研究

目的:观察蒙药地格达-4味汤对硫代乙酰胺(TAA)所致小鼠肝损伤的防治作用。方法:将地格达-4味汤组和护肝片组分别灌胃7天,腹腔注射TAA80mg.kg-1引起小鼠急性肝损害,24h后取血,分离血清,检测血清ALT、AST活性;取肝组织,观察肝脏形态学的变化。结果:地格达-4味汤组可明显降低因TAA所致肝损伤小鼠的ALT及AST(P<0.01)。模型组肝组织学改变主要表现为碎片状坏死;护肝片组可见散在点状及小碎片状坏死;地格达-4味汤组可见散在点状坏死,有炎细胞浸润。结论:地格达-4味汤对硫代乙酰胺(TAA)所致肝损伤模型,有一定的防治作用。

民族药马蹄金提取物对D-GlaN、TAA、ANIT所致小鼠化学性肝损伤的药理作用研究

目的 :观察马蹄金对D 半乳糖胺 (D GlaN)、硫代乙酰胺 (TAA)、异硫氰酸 1 萘酯(ANIT)所致小鼠肝损伤的防治作用。方法 :以联苯双酯作阳性对照 ,用不同肝毒剂造成小鼠急性肝损伤 ,分别测定动物血清相关指标及肝脏病理切片 (D GlaN组 ) ,用t检验法比较各组间差异。结果 :马蹄金各剂量组 (32 5g·kg- 1、 16 3g·kg- 1及 8 2g·kg- 1)可降低因AN IT所致胆汁郁积型黄疸小鼠升高的血清总胆红素 (Tbil)及血清转氨酶 (ALT及AST) ;明显降低因TAA所致肝损伤小鼠的ALT (P <0 0 1) ;明显降低因D GlaN所致肝损伤小鼠的ALT及AST (P <0 0 5及P <0 0 1) ,亦明显降低肝组织中甘油三酯 (TG)含量 (P <0 0 5 ) ,病理检查显示给药组小鼠肝脏损伤程度较模型组明显减轻。结论 :马蹄金对以上不同肝损伤模型 ,有一定的防治作用 ,似为该药的功效及应用提供了实验依据。

澳大利亚TAA培训包能力体系及其考评标准评价

澳大利亚TAA培训包包括教学环境协调模块、教学设计模块、授课与学习辅导模块、考评鉴定模块、培训咨询服务模块、语言和数理表达模块、通用模块等8个能力模块及55个能力单元,其考评鉴定过程强调有效性、可靠性、灵活性和公正性等原则,这些都对我国职业教育师资队伍建设和人才培养具有一定的借鉴意义。

带类型注解的汇编器TAAS的设计与实现

给出了一种带类型注解的汇编器 TAAS的设计与实现 .TAAS分析带有类型注解的汇编代码 ,把类型注解映射进目标文件和可执行文件中 ,产生带有类型注解的二进制代码 ,同时不影响代码的执行语义 .TAAS分析 AT&T语法的汇编程序 ,产生 EL F格式的 x86机器代码 ,并且与 GNU