Enhancing metformin-induced tumor metabolism destruction by glucose oxidase for triple-combination therapy

Despite decades of laboratory and clinical trials,breast cancer remains the main cause of cancer-related disease burden in women.Considering the metabolism destruction effect of metformin(Met)and cancer cell starvation induced by glucose oxidase(GOx),after their efficient delivery to tumor sites,GOx and Met may consume a large amount of glucose and produce sufficient hydrogen peroxide in situ.Herein,a pH-responsive epigallocatechin gallate(EGCG)-conjugated low-molecular-weight chitosan(LC-EGCG,LE)nanoparticle(Met–GOx/Fe@LE NPs)was constructed.The coordination between iron ions(Fe3+)and EGCG in this nanoplatform can enhance the efficacy of chemodynamic therapy via the Fenton reaction.Met–GOx/Fe@LE NPs allow GOx to retain its enzymatic activity while simultaneously improving its stability.Moreover,this pH-responsive nanoplatform presents controllable drug release behavior.An in vivo biodistribution study showed that the intracranial accumulation of GOx delivered by this nanoplatform was 3.6-fold higher than that of the free drug.The in vivo anticancer results indicated that this metabolism destruction/starvation/chemodynamic triple-combination therapy could induce increased apoptosis/death of tumor cells and reduce their proliferation.This triple-combination therapy approach is promising for efficient and targeted cancer treatment.

Effects of Terpinen-4-ol on Four Metabolic Enzymes and Polyphenol Oxidase (PPO) in Mythimna separta Walker

To study insecticidal mechanism of terpinen-4-ol, a main insecticidal composition in the essential oil of Sabina vulgaris, the 5th instar larvae of Mythimna separta, were investigated with terpinen-4-ol by topical application. The activities of phosphatase, glutathione S-transferase （GSTs）, cytochrome P450 （P450）, and polyphenol oxidase （PPO） of tested insects were determined in all poisoning stages, including exciting stage, convulsing stage, paralysis stage, and recover stage. The result showed that the activities of both acid phosphatase （ACP） and alkaline phosphatase （AKP） in treated insects were induced by terpinen-4-ol, but ACP was inhibited in paralysis stage. The activities of GSTs were inhibited in exciting stage, convulsing stage, and paralysis stage, but gradually recovered in recover stage. O-demethylase activity of cytochrome P450 was inhibited by terpinen-4-ol, and the inhibition rate in all poisoning stages were 26.27, 46.03, 80.24, and 90.22%, respectively. PPO activities were strongly inhibited by terpinen-4-ol both in vitro and in vivo. In conclusion, the activities of P450, GSTs, and PPO could have relation with toxicity of terpinen-4-ol against larvae of the Mythimna separta, but recover stage of the poisoning insects might be related to GSTs induced. As a new insecticide or synergist, terpinen- 4-ol has a potential value in field of insecticide resistance management.

Linking uric acid metabolism to diabetic complications

Hyperuricemia have been thought to be caused by the ingestion of large amounts of purines, and prevention or treatment of hyperuricemia has intended to prevent gout. Xanthine dehydrogenase/xanthine oxidase(XDH/XO) is rate-limiting enzyme of uric acid generation, and allopurinol was developed as a uric acid(UA) generation inhibitor in the 1950 s and has been routinely used for gout prevention since then. Serum UA levels are an important risk factor of disease progression for various diseases, including those related to lifestyle. Recently, other UA generation inhibitors such as febuxostat and topiroxostat were launched. The emergence of these novel medications has promoted new research in the field. Lifestyle-related diseases, such as metabolic syndrome or type 2 diabetes mellitus, often have a common pathological foundation. As such, hyperuricemia is often present among these patients. Many in vitro and animal studies have implicated inflammation and oxidative stress in UA metabolism and vascular injury because XDH/XO act as one of the major source of reactive oxygen species Many studies on UA levels and associated diseases implicate involvement of UA generation in disease onset and/or progression. Interventional studies for UA generation, not UA excretion revealed XDH/XO can be the therapeutic target forvascular injury and renal dysfunction. In this review, the relationship between UA metabolism and diabetic complications is highlighted.

Regio- and Substrate-Specific Oxidative Metabolism of Terpinolene by Cytochrome P450 Monooxygenases in <i>Cupressus lusitanica</i>Cultured Cells

Many of monoterpenes produced in plants contribute to defenses against herbivores, insects and microorganisms. Among those compounds, β-thujaplicin formed in Cupressaceae plants has a unique conjugated seven-membered ring and some useful biological activities, e.g. fungicide, repellent, insecticide and so on. The biosynthesis pathway of β-thujaplicin has not yet been revealed;we have been trying to uncover it using Cupressus lusitanica cultured cells as a model. In our previous study, terpinolene was identified as a potential β-thujaplicin intermediate at the branching point to terpenoids. In this article, terpinolene metabolism in C. lusitanica cultured cells was investigated, and it was shown that the microsomal fraction from cells oxidized terpinolene into the hydroxylated compound, 5-isopropylidene-2-met-hylcyclohex-2-enol (IME). Then, IME was further oxidized by microsomal fraction to the epoxidized compound, 1,6-epoxy-4(8)-p-menthen-2-ol (EMO). These were the only two products detected from the microsomal reactions, respecttively. Moreover, microsomal reactions with monoterpenes other than terpinolene produced nothing detectable. These results show that the enzymes of these reactions had strict substrate specificity and regio-selectivity. Experiments on kinetics and with specific inhibitors confirmed that these reactions were caused by cytochrome P450 monooxygenases, respectively. These results support our hypothesis that terpinolene is a putative intermediate of β-thujaplicin biosynthesis and show that IME and EMO are also putative intermediates.

Enzymes of Phenylpropanoid Metabolism Involved in Strengthening the Structural Barrier for Providing Genotype and Stage Dependent Resistance to Karnal Bunt in Wheat

The role of lignifications and enzymes involved in the phenylpropanoid (PP) biosynthesis i.e. phenylalanine ammonia lyase (PAL), Peroxidase (POD), Polyphenol oxidase (PPO) in providing resistance to Karnal Bunt (KB) during different developmental stages of resistant (HD-29) and susceptible genotype (WH-542) and its recombinant inbred lines (RILs) of wheat were investigated. The enzymes of PP pathway were expressed constitutively in both the susceptible and resistant genotype. However, the activity was higher in all the developmental stages of resistant genotype and its RILs, indicating that this genotype has a significant higher basal level of these enzymes as compared to the susceptible line and could be used as marker(s) to define KB resistance. The activity of PAL and POD was significantly higher in WSv stage (Z = 16) while the specific activity of PPO was higher in WS3 (Z = 77) stage as compared to the other physiological stages in both the genotypes. In resistant genotype the lignin content increased two-fold and three-fold at WS2 and WS3 stage, respectively, while in susceptible genotype no significant increase in lignin content was observed. The pathway might be associated with the enhancement of structural defense barrier due to lignifications of cell wall as evident from the enhanced synthesis of lignin in all the stages of resistant genotype. Our results clearly indicate the possible role of enzymes of PP metabolism provides genotype and stage dependant structural barrier resistance in wheat against KB.

Inhibition of xanthine oxidase alleviated pancreatic necrosis via HIF-1α-regulated LDHA and NLRP3 signaling pathway in acute pancreatitis

Acute pancreatitis(AP)is a potentially fatal condition with no targeted treatment options.Although inhibiting xanthine oxidase(XO)in the treatment of AP has been studied in several experimental models and clinical trials,whether XO is a target of AP and what its the main mechanism of action is remains unclear.Here,we aimed to re-evaluate whether XO is a target aggravating AP other than merely generating reactive oxygen species that trigger AP.We first revealed that XO expression and enzyme activity were significantly elevated in the serum and pancreas of necrotizing AP models.We also found that allopurinol and febuxostat,as purine-like and non-purine XO inhibitors,respectively,exhibited protective effects against pancreatic acinar cell death in vitro and pancreatic damage in vivo at different doses and treatment time points.Moreover,we observed that conditional Xdh overexpression aggravated pancreatic necrosis and severity.Further mechanism analysis showed that XO inhibition restored the hypoxia-inducible factor 1-alpha(HIF-1α)-regulated lactate dehydrogenase A(LDHA)and NOD-like receptor family pyrin domain containing 3(NLRP3)signaling pathways and reduced the enrichment of^(13)C_(6)-glucose to^(13)C_(3)-lactate.Lastly,we observed that clinical circulatory XO activity was significantly elevated in severe cases and correlated with C-reactive protein levels,while pancreatic XO and urate were also increased in severe AP patients.These results together indicated that proper inhibition of XO might be a promising therapeutic strategy for alleviating pancreatic necrosis and preventing progression of severe AP by downregulating HIF-1α-mediated LDHA and NLRP3 signaling pathways.

铜代谢相关基因COX17与头颈部鳞状细胞癌不良预后相关

目的:探讨铜代谢相关基因细胞色素c氧化酶铜伴侣17(COX17)对头颈部鳞状细胞癌(HNSCC)发生发展及预后的影响。方法:运用生物信息学分析COX17在HNSCC与正常组织中的表达差异;通过构建列线图验证COX17在预测HNSCC预后中的作用;采用KEGG和GO分析对COX17相关基因进行功能富集分析以及利用ssGSEA分析COX17表达与HNSCC组织中免疫细胞浸润丰度的关系;采用实时定量聚合酶链反应(RT-qPCR)验证COX17在HNSCC细胞系与永生化正常上皮细胞系中的表达差异;细胞活力试剂盒(CCK-8)和Transwell实验分别用于检测COX17对细胞增殖、侵袭能力的影响。结果:COX17在HNSCC中表达显著上调(P<0.05)。预后分析表明COX17与HNSCC患者总生存期(OS)密切相关(P<0.05)。免疫浸润相关性分析显示,COX17与多种免疫细胞浸润丰度呈负相关关系(均P<0.001)。敲低COX17可显著抑制HNSCC细胞SCC-9、SAS细胞的增殖及侵袭能力。结论:COX17的表达可影响HNSCC细胞的增殖和侵袭,并与HNSCC组织中免疫细胞浸润存在潜在关联;作为线粒体铜代谢分子标记物,COX17可能是评估HNSCC预后的有效指标和潜在治疗靶点。

NOX4 promotes tumor progression through the MAPK-MEK1/2-ERK1/2 axis in colorectal cancer

BACKGROUND Metabolic reprogramming plays a key role in cancer progression and clinical outcomes;however,the patterns and primary regulators of metabolic reprogramming in colorectal cancer(CRC)are not well understood.AIM To explore the role of nicotinamide adenine dinucleotide phosphate oxidase 4(NOX4)in promoting progression of CRC.METHODS We evaluated the expression and function of dysregulated and survival-related metabolic genes using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Consensus clustering was used to cluster CRC based on dysregulated metabolic genes.A prediction model was constructed based on survival-related metabolic genes.Sphere formation,migration,invasion,proliferation,apoptosis and clone formation was used to evaluate the biological function of NOX4 in CRC.mRNA sequencing was utilized to explore the alterations of gene expression NOX4 over-expression tumor cells.In vivo subcutaneous and lung metastasis mouse tumor model was used to explore the effect of NOX4 on tumor growth.RESULTS We comprehensively analyzed 3341 metabolic genes in CRC and identified three clusters based on dysregulated metabolic genes.Among these genes,NOX4 was highly expressed in tumor tissues and correlated with worse survival.In vitro,NOX4 overexpression induced clone formation,migration,invasion,and stemness in CRC cells.Furthermore,RNA-sequencing analysis revealed that NOX4 overexpression activated the mitogen-activated protein kinase-MEK1/2-ERK1/2 signaling pathway.Trametinib,a MEK1/2 inhibitor,abolished the NOX4-mediated tumor progression.In vivo,NOX4 overexpression promoted subcutaneous tumor growth and lung metastasis,whereas trametinib treatment can reversed the metastasis.CONCLUSION Our study comprehensively analyzed metabolic gene expression and highlighted the importance of NOX4 in promoting CRC metastasis,suggesting that trametinib could be a potential therapeutic drugs of CRC clinical therapy targeting NOX4.

The role of temperature as a driver of metabolic flexibility in the Red-billed Leiothrix(Leiothrix lutea)

Background:The thermoregulatory ability of animals is strongly influenced by the temperature of their environment.Acclimation to cold requires a range of physiological and morphological adjustments.In this study,we tested the hypothesis that a small passerine,the Red-billed Leiothrix(Leiothrix lutea),can maintain homeothermy in cold conditions by adjusting the physiology and biochemistry of its tissue and organs and return to its former physiological and biochemical state when moved to a warm temperature.Methods:Phenotypic variation in thermogenic activity of the Red-billed Leiothrixs(Leiothrix lutea)was investigated under warm(35℃),normal(25℃)or cold(15℃)ambient temperature conditions.Oxygen consumption was measured using an open-circuit respirometry system.Mitochondrial state-4 respiration and cytochrome-c oxidase(COX)activity in liver,kidney heart and pectoral muscle were measured with a Clark electrode.Results:Birds acclimated to an ambient temperature of 15℃ for 4 weeks significantly increased their basal metabolic rate(BMR)compared to a control group kept at 25℃.Birds acclimated to 35℃ decreased their BMR,gross energy intake(GEI)and digestible energy intake(DEI).Furthermore,birds acclimated to 15℃ increased state-4 respiration in their pectoral muscles and cytochrome-c oxidase(COX)activity in their liver and pectoral muscle,compared to the 25℃ control group.Birds acclimated to 35℃ also displayed lower state-4 respiration and COX activity in the liver,heart and pectoral muscles,compared to those kept at 25℃.There was a positive correlation between BMR and state-4 respiration,and between BMR and COX activity,in all of the above organs except the liver and heart.Conclusions:Our study illustrates that the morphological,physiological,and enzymatic changes are associated with temperature acclimation in the Red-billed Leiothrix,and supports the notion that the primary means by which small birds meet the energetic challenges of cold conditions is through metabolic adjustments.

Relationships between interspecific differences in the mass of internal organs,biochemical markers of metabolic activity,and the thermogenic properties of three smallpasserines

Background:The capacity for thermogenesis is considered part of an animal's adaptive strategy for survival,and basal metabolic rate(BMR) is one of the fundamental physiological standards for assessing the energy cost of thermoregulation in endotherms.BMR has been shown to be a highly flexible phenotypic trait both between,and within,species,but the metabolic mechanisms involved in the regulation of BMR,which range from variation in organ mass to biochemical adjustments,remain unclear.In this study,we investigated the relationship between organ mass,biochemical markers of metabolic tissue activity,and thermogenesis,in three species of small passerines:wild Bramblings(Fringilla montifringilla),Little Buntings(Emberiza pusilla) and Eurasian Tree Sparrows(Passer montanus),caught in Wenzhou,southeastern China.Methods:Oxygen consumption was measured using an open-circuit respirometry system.Mitochondrial state-4 respiration and cytochrome c oxidase(COX) activity in liver and pectoral muscle were measured with a Clark electrode.Results:Our results show that Eurasian Tree Sparrows had significantly higher BMR,digestive organ mass,mitochondrial state-4 respiration capacity and COX activity in liver and muscle,than Bramblings and Little Buntings.Furthermore,interspecific differences in BMR were strongly correlated with those indigestive tract mass,state-4 respiration and COX activity.Conclusions:Our findings suggest that the digestive organ mass,state-4 respiration and COX activity play an important role in determining interspecific differences in BMR.

温阳益髓方对膝骨关节炎模型大鼠膝关节软骨、骨代谢及NOX2/ROS/NF-κB水平的影响

目的:探讨温阳益髓方对膝骨关节炎模型大鼠膝关节软骨、骨代谢及NOX2/ROS/NF-κB水平的影响。方法:选取40只SPF级SD雄性大鼠,随机分为正常组、模型组、低剂量温阳益髓方(低剂量)组、高剂量温阳益髓方(高剂量)组。除正常组外,其余3组均采用膝关节腔注射0.05 mL(20 mg/mL)碘乙酸钠,建立膝骨关节炎模型。建模成功后,低、高剂量组分别以6、24 mg/kg温阳益髓方汤剂灌胃,正常组、模型组以同体积生理盐水灌胃。采用H-E染色、光镜观察各组膝关节软骨组织的形态结构;ELISA法检测血清骨代谢相关指标水平;二氢乙锭荧光探针检测膝关节软骨组织活性氧(ROS)水平;免疫印迹检测膝关节软骨组织NADPH氧化酶2(NOX2)、核因子-κB(NF-κB)水平。结果:模型组膝关节软骨组织边缘的软骨基质减少、软骨囊结构不清、软骨细胞减少,且出现钙化灶。与模型组比较,低、高剂量组上述结构变化明显改善。与正常组比较,模型组Mankin评分显著升高;与模型组比较,低、高剂量组Mankin评分显著降低,且高剂量组低于低剂量组。与正常组比较,模型组血清骨钙素(OCN)、Ⅰ型胶原C末端肽(CTX-Ⅰ)水平显著降低,软骨寡聚基质蛋白(COMP)水平显著升高;与模型组比较,低、高剂量组血清OCN、CTX-Ⅰ水平显著升高,且高剂量组高于低剂量组,COMP水平显著降低,且高剂量组低于低剂量组。与正常组比较,模型组ROS水平显著升高;与模型组比较,低、高剂量组ROS水平显著降低,且高剂量组低于低剂量组。与正常组比较,模型组NOX2、NF-κB水平显著升高;与模型组比较,低、高剂量组NOX2、NF-κB水平显著降低,且高剂量组低于低剂量组。结论:温阳益髓方可改善膝骨关节炎模型大鼠膝关节软骨、骨代谢,其机制可能与其降低膝关节软骨组织NOX2/ROS/NF-κB水平有关。

花色苷及其调控尿酸代谢的研究进展

花色苷是一种广泛存在于花卉、蔬果中的天然食用功能性色素,具有多方面生理活性,对人体健康起到积极作用。最新的体内外实验表明花色苷还具有调控尿酸代谢作用,这为其多元化开发提供了新方向。本文系统归纳了花色苷的结构、成分分析、生理功能及尿酸合成代谢过程,探究花色苷调控尿酸代谢的作用机制,为其在健康食品与疾病调控方面的研究与开发提供参考。

代谢相关脂肪性肝病患者血清YKL-40 NOX2表达与肝纤维化的关系

目的 探究代谢相关脂肪性肝病(MAFLD)患者血清几丁质酶样蛋白40(YKL-40)、烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)表达水平,并分析其与肝纤维化的关系。方法 选取2020年4月至2021年12月于保定市人民医院就诊的108例MAFLD患者为MAFLD组,选取同期该院108例健康体检者为对照组。肝纤维化程度评估根据瞬时弹性成像技术所得肝脏硬度值分为非纤维化组(60例,肝脏硬度值<8.0 k Pa)和纤维化组(48例,肝脏硬度值≥8.0 k Pa)。比较研究对象YKL-40、NOX2及临床资料差异。logistic回归分析MAFLD患者发生肝纤维化的影响因素。受试者工作特征(ROC)曲线评价YKL-40、NOX2对肝纤维化的预测效能。结果 MAFLD组血清YKL-40、NOX2水平高于对照组,差异有统计学意义(P<0.05)。纤维化组YKL-40、NOX2水平高于非纤维化组,差异有统计学意义(P<0.05)。回归分析显示,年龄(OR=1.647,95%CI:1.053~2.575,P=0.029)、HOMA-IR(OR=1.758,95%CI:1.083~2.853,P=0.022)、YKL-40(OR=2.016,95%CI:1.237~3.284,P=0.004)、NOX2(OR=2.292,95%CI:1.388~3.786,P=0.001)是MAFLD患者发生肝纤维化的影响因素(P<0.05)。YKL-40、NOX2单独预测MAFLD患者肝纤维化的曲线下面积(AUC)分别为0.833、0.838,YKL-40联合NOX2预测MAFLD患者肝纤维化的AUC为0.922,优于单一指标(Z_(二者联合-YKL-40)=2.268,P=0.023、Z_(二者联合-NOX2)=1.999,P=0.046)。结论 YKL-40、NOX2在MAFLD患者血清中水平增加,且与肝纤维化相关,YKL-40联合NOX2可作为预测肝纤维化的生物标志物。

鸡矢藤提取物对酵母膏和氧嗪酸钾致小鼠高尿酸血症的影响

目的探讨鸡矢藤提取物(EPS)对酵母膏和氧嗪酸钾致小鼠高尿酸血症的影响及可能的作用机制。方法采用酵母膏和氧嗪酸钾造成小鼠高尿酸血症模型,观察EPS对模型小鼠血清尿酸水平及体重和肾功能的影响,并进一步观察其对模型小鼠黄嘌呤氧化酶和腺苷脱氨酶的抑制作用。结果EPS(6.3、3.15、1.57g/kg,ig,qd×14d)在显著降低高尿酸血症小鼠血清尿酸水平的同时,对模型小鼠体重和肾功能均无明显影响;EPS(6.3、3.15、1.57g/kg,ig,qd×14d)可显著抑制高尿酸血症小鼠肝脏黄嘌呤氧化酶的活性,EPS(6.3g/kg)对模型小鼠血清腺苷脱氨酶的活性也具有一定的抑制作用。结论EPS可显著降低酵母膏和氧嗪酸钾致高尿酸血症小鼠的血清尿酸水平,其机制可能与抑制黄嘌呤氧化酶和腺苷脱氨酶活性有关。

新烟碱类杀虫剂吡虫啉和噻虫嗪的代谢研究进展

对新烟碱类杀虫剂吡虫啉和噻虫嗪的化学结构特点及代谢研究进展进行了综述,重点对其在哺乳动物、植物和昆虫体内的代谢途径及相关的生物代谢酶进行了阐述。吡虫啉和噻虫嗪在环境中可被动物、植物、微生物及昆虫所代谢,与其生物代谢相关的酶主要是微粒体细胞色素P450同工酶和醛氧化酶,其中,P450同工酶可催化吡虫啉和噻虫嗪发生羟基化、去饱和、脱烷基、硝基还原等代谢反应,而醛氧化酶主要催化其硝基部分的还原。吡虫啉和噻虫嗪经过代谢后其生物活性通常有所降低,但也有部分代谢产物的活性反而升高,增加了其对昆虫的毒性以及对非靶标生物的风险。明确吡虫啉和噻虫嗪的代谢途径、代谢产物及其生物活性,对于了解新烟碱类杀虫剂的代谢机理,以及安全有效地使用该类杀虫剂具有重要意义。

葡萄糖氧化酶对黄羽肉鸡生产性能和养分代谢的影响

本试验研究葡糖糖氧化酶对快大黄羽肉鸡生产性能和养分代谢的影响,选择600只0日龄雏鸡分为A、B、C、D 4个处理,每个处理5个重复,每个重复30只,分别在基础日粮中添加0、250、350、380g/t葡萄糖氧化酶制剂,测定35、70日龄的生产性能和45日龄的养分代谢率。结果表明,35日龄时,黄羽肉鸡的生产性能不受葡萄糖氧化酶制剂添加的影响;葡萄糖氧化酶制剂对36～70日龄黄羽肉鸡的日增重和料重比有显著影响(P<0.05),D组与B、C组在日增重和料重比上有显著影响(P<0.05);添加葡萄糖氧化酶制剂对45日龄黄羽肉鸡的干物质、有机物质、粗蛋白质、粗脂肪的消化代谢有显著影响(P<0.05)。因此,葡萄糖氧化酶对36～70日龄黄羽肉鸡的日增重、料重比和养分代谢率有显著影响,且在本试验条件下,添加380g/t葡萄糖氧化酶制剂最适宜。

松油烯-4-醇对粘虫几种代谢酶及酚氧化酶的影响

【目的】探讨杀虫植物砂地柏Sabina vulgaris精油中主要杀虫成分松油烯-4-醇的作用机理。【方法】以点滴法处理粘虫5龄幼虫后,测定兴奋期、痉挛期、麻痹期及复苏期等4个中毒阶段试虫体内4种代谢酶及酚氧化酶(PPO)的活性。【结果】松油烯-4-醇仅在麻痹期对酸性磷酸酯酶(ACP)具有一定的抑制作用,而在其它时期均可明显激活ACP及碱性磷酸酯酶(AKP);对谷胱甘肽S转移酶(GSTs)则表现出先抑制后恢复的趋势;可显著抑制细胞色素P450O-脱甲基活性,各中毒阶段酶抑制率分别为26.27%、46.03%、80.24%和90.22%;离体和活体条件下,均可显著抑制PPO活性。【结论】松油烯-4-醇对粘虫代谢酶系细胞色素P450、GSTs及PPO的抑制与其毒杀活性有关,而中毒试虫的复苏可能与GSTs活性的恢复有关。该化合物可开发为新型农药或增效剂,在害虫抗性治理中具有潜在的应用价值。

苦杏仁甙对脑缺血能量代谢中细胞色素氧化酶的影响

将大鼠鼠脑右额颞叶，快速冰冻切片进行细胞色素无化酶孵育染色，染色切片通过显微电视图像测量系统观察，数据经微机处理，结果表明苦杏仁甙有明显提高脑缺血状态下细胞色素氧化酶活性作用。

合成冰片对大鼠肝CYP450酶含量及CYP3A1 mRNA表达的影响

[目的]研究冰片对大鼠肝脏细胞色素氧化酶(cytochrom e P450,CYP450)含量及其亚型CYP3A1m RNA表达的影响。[方法W]istar大鼠合成冰片(设0.3gk/g和0.03gk/g剂量组,1次d/,连续7d)灌胃,以溶媒羧甲基纤维素纳(CM C-Na)和苯巴比妥钠为对照组,钙沉积法提取肝微粒体,紫外分光光度法测定CYP450含量,实时定量RT-PCR法检测肝脏CYP3A1m RNA的表达。[结果]0.3gk/g合成冰片口服可诱导大鼠肝脏CYP450酶含量增高(P<0.05),CYP3A1m RNA表达上调(P<0.05)。[结论]高剂量合成冰片口服可能影响肝脏药物代谢。

植物抗寒基因工程研究

低温伤害严重影响植物的生存和分布,有关植物抗寒的分子生物学研究成为近10年的研究热点之一。文章综述了几种植物抗寒基因的研究途径:抗冻蛋白基因的特性与功能研究、与抗寒相关的脂肪酸代谢途径和抗氧化酶基因工程的研究概况,并探讨了今后的研究方向。