中粮中宏生物：提高缺氧耐受力,精神焕发好身体
某大学生物工程学院《生物化学》考试试卷(1809)
某大学生物工程学院《生物化学》课程试卷（含答案）__________学年第___学期考试类型：（闭卷）考试考试时间：90 分钟年级专业_____________学号_____________ 姓名_____________1、判断题（100分，每题5分）1. 从低等的单细胞生物到高等的人类，能量的释放、储存和利用的主要形式均是ATP。
答案：正确解析：2. 由色氨酸脱羧、羟化形成的5′羟色胺是一种新的抗抑郁症药物。
（）答案：正确解析：3. 真核生物细胞核中也发现了由RNA和蛋白质组成的RNase P，但是其RNA部分不具有催化活性。
（）答案：正确解析：4. 鞘磷脂的代谢过程主要与细胞质膜的流动有关，与细胞生物活性分子的生成调节无关。
（）答案：错误解析：5. 体内嘌呤核苷酸和嘧啶核苷酸的从头合成场所主要是肝脏组织。
（）答案：正确解析：6. mRNA的选择性拼接可以改变外显子的连接次序。
（）答案：错误解析：外显子连接次序不会改变。
7. 糖原合成酶和糖原磷酸化酶磷酸化后活性都升高。
（）答案：错误8. 氨是有毒物质，必须在肾脏中合成尿素后排出体外。
（）答案：错误解析：9. 有些蛋白质的内含肽是断裂的，需要经过反式拼接才能得到有功能的蛋白质。
（）答案：正确解析：10. dTMP合成的直接前体物质是TDP。
（）答案：错误解析：dTMP合成的直接前体是dUMP。
细胞内脱氧核苷酸的合成是在核苷二磷酸的水平上进行的。
11. 脂肪酸的从头合成中，将糖代谢生成的乙酰辅酶A从线粒体内转移到胞液中的化合物是苹果酸。
（）答案：错误12. 核糖体上每一段肽键的形成除在氨基酸活化中用去两个高能磷酸键外，还需要消耗两个高能磷酸键。
（）答案：正确解析：13. 基因工程使用的Ⅱ类核酸限制性内切酶不仅具有内切核酸酶的活性，而且有甲基化酶的活性。
（）答案：错误解析：Ⅱ类核酸限制性内切酶没有甲基化酶的活性。
14. 每种氨基酸只能有一种特定的tRNA与之对应。
国家食品药品监督管理局
国食健字G20100036
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2010年1月22日
33
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广赛牌益生菌粉
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34
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诺金康牌纳豆胶囊
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上海诺金科生物科技有限公司
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12
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多佰之牌多佰之咀嚼片
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辅助改善记忆
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13
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维尔健牌枸芪五味子胶囊
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国食健字G20100038
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2010年1月22日
35
产品名称：
盛坤牌芪贞胶囊
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36
产品名称：
郁健牌百合酸枣胶囊
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改善睡眠
申报单位：
王洪彪（身份证号：210121197504152453）
申报单位：
江西益康药业有限公司
批准文号：
国食健字G20100023
银杏叶提取物改善了肝细胞中由于高胰岛素处理引起的葡萄糖不耐受
Ginkgo Biloba Extract (GBE) Enhances Glucose Tolerance in Hyperinsulinism-induced Hepatic CellsZaiqing Yang, Tao Xia, Li Gan, Xiaodong Chen, Lei ZhouCollege of Life Science and Technology, Huazhong Agricultural University, Wuhan city, Hubeiprovince, 430070, P.R.China yangzq@AbstractGinkgo biloba, an herbal medication, is capable of dropping glucose, fat and lipid peroxide and preventing atherosclerosis and complications in diabetic patients. In our studies, we tested the hypothesis that ginkgo biloba extract (GBE) prevents glucose intolerance induced by hyperinsulinismin hepatocytes. We investigated the effects of GBE on glucose ingestion, glucokinase activity and mRNA levels of key genes in glucose metabolism and insulin signaling pathway. To better show its efficacy, we included a control group that was treated with rosiglitazone, a kind of thiazolidinediones (TZDs). The data showed that GBE repressed glucose ingestion in normal status, whereas it dramatically improved glucose tolerance in insulin resistance status. Moreover, by analyzing gene expression, we suggested that GBE chiefly exerted its effects by stimulating IRS-2 transcription. It should be noted that, not like rosiglitazone, GBE didn’t stimulate overmuch glucose uptake in improving glucose tolerance. It is said that GBE treatment could avoid drug-induced obesity. The data suggested that GBE had potential efficacy to prevent insulin resistance induced by hyperinsulinism. Keywords: antidiabetic drugs, diabetes prevention, insulin resistance, liver, rosiglitazone Abbreviations: Glucose-6-P, glucose-6-phosphate; GK, glucokinase; G-6-Pase, glucose-6-phosphatase; IRS, insulin receptor substrate; GLUT, glucose transporter; PPAR, peroxisome proliferator-activated receptor; SREBP, sterol regulatory element-binding protein.1 INTRODUCTIONGinkgo biloba, an herb, has been used as traditional Chinese medicine for thousands of years. Ginkgo biloba extract (GBE) is being widely studied and applied for its beneficial properties in treatment or prevention of human diseases. Ginkgo biloba trees mainly distribute in China, France, and USA, producing a mass of dried leaves each year to meet the commercial demand of market [1]. GBE has been reported to drop glucose, fat and lipid peroxide and prevent atherosclerosis in animal model and human. To our knowledge, no systematic study illustrates the molecular mechanism of its efficacyon improving insulin sensitivity and enhancing glucose tolerance in insulin resistance model.In previous studies, GBE was found to have anti-inflammatory [2] and stimulate skin microcirculation [3]. And it was used as a therapeutic agent for some cardiovascular and neurological disorders. People also found it could attenuate the negative effects of some drugs [4, 5]. Recently, accumulating in vitro and in vivo evidence demonstrated that it had potential efficacy in lipid metabolism, glucose metabolism and diabetes mellitus. Saponara showed that GBE inhibited cAMP phosphodiesterase in rat adipose tissue [6]. Mario illustrated that the biflavones of ginkgo biloba stimulated lipolysis in fully differentiated 3T3-L1 adipocytes [7]. Boveris obtained the same results as Mario and further showed GBE inhibited lipid peroxidation [8]. By investigating diabetic rodent model, Nian hong et al. indicated that GBE dropped the after-dinner blood-glucose, decreased the contents ofThis work was supported by the High Education Doctorial Subject Research Program (No: 20010504003), the grants from the General Program (No: 30170674) and Key Program of NationalTC, TG and LDL, promoted SOD activity and relieved the damage of pancreatic islet [9]. Moreover, Li et al. found GBE could prevent and treat atherosclerosis by decreasing serum lipids levels, suppressing inflammatory response and protecting endothelial cells [10]. As we know, oxidation-modified LDL plays an important role in the pathogenesis of artherosclerosis with type II diabetes melllitus. GBE was also capable of inhibiting the oxidation of LDL [11, 12]. In addition, early detection of pathologic function of the retina plays very crucial role in monitoring of visual complications in diabetic patients. Researchers showed GBE prevented diabetic retinopathy and they thought it was a good adjuvant to patient with long lasting diabetes mellitus [13]. All data suggested that GBE was of value in diabetic therapy.Liver is an important organ for glucose metabolism and energy homeostasis. And hepatic insulin resistance is an important component in the development of type II diabetes mellitus. In this process, PPARs, GLUT, G6Pase, IRS and SREBPs play crucial roles. GLUT2 is the primary glucose-transporter isoform in liver and plays a key role in glucose homeostasis by mediating bidirectional transport of glucose [14]. PPARs and SREBPs are characterized well transcription factors. PPARγ was deemed the main isoform in adipocytes before, but now people found it might also mediate lipid metabolism and energy homeostasis by changing its expression in liver [15]. SREBP1c is crucial for the regulation of lipogenic gene. And recent studies also found that it was interrelated with insulin action [16]. G6Pase as the last enzyme in hepatic glucogenesis, is an important determinant of hepatic glucose fluxes. Moreover, IRS-2 was main isoform in liver. It compensated for the lack of IRS-1 in IRS-1-/- model [17]. So hepatic insulin signaling was mediated mainly through IRS-2, rather than IRS-1 [18].In this study, we tested the hypothesis that GBE involves in modulation of insulin action and enhances glucose tolerance. To better interpret its molecular mechanism, we assayed above gene expressions and glucokinase activity.2 MATERIALS and METHODS2.1 Materials.The powder form of GBE was purchased from Greensky Biological Tech Co., Ltd. (Hangzhou, China). The GBE contained 24% flavonoids, 6% terpenes and less than 1 ppm of ginkgolic acid. The composition of the flavonoids and terpenes in GBE was similar to that of EGb 761 used in European countries. TRIzol was obtained from Sangon Co., Ltd. (Shanghai, China). Mammalian Cell Protein Extraction kit was purchased from Shenergy Biocolor BioScience & Technology Co., Ltd. (Shanghai, China). Glucose Assay Kit was obtained from Shenergy-diasys Diagnostic Technology Co., Ltd. (Shanghai, China).2.2 Cell culture and treatment.L-02 cell line was derived from normal adult liver [19]. They were grown in DMEM supplemented with 10% fetal bovine serum at 5% CO2 and 37°C. For the relevant experiments, the density of cells was about 5×105 cells/well in 24-well culture plates for RNA extraction or 5 × 106 cells/dish in 60-mm Petri dishes for metabolite concentration assay. There were two group cells in experiments, namely A and B. A mimicked normal physiological status and included NC, NRT and NGT. All cells were treated with 10nM insulin. NC stood for Normal Control (NC); NRT was given 10µM rosiglitazone that was a kind of TZDs and stood for Normal Rosiglitazone Treatment (NRT); NGT was given 10mg/l GBE and stood for Normal GBE Treatment (NGT). B mimicked insulin resistance status by hyperinsulinaemic and hyperglycaemic treatment in vitro[20, 21].There were three kinds of B,designated AC, ART, AGT. AC, ART and AGT were given 100nM insulin and AC stood for Abnormal Control (AC). ART was given 10µM rosiglitazone and stood for Abnormal Rosiglitazone Treatment (ART). AGT was given GBE and stood for Abnormal GBE Treatment (AGT). All treatments are listed in table 1.Table 1. The description of cell treatment. + indicates that groups include relevant agents.Insulin(10nM) +++Insulin(100nM) +++ Rosiglitazone ++GBE ++2.3 RNA isolation.Total RNAs were isolated from L-02 cells using TRIzol after culturing the cells for 36h. All of the RNA samples were treated with Dnase I to digest the genomic DNA and stored at -80°C.2.4 Semi-quantitative RT-PCR.Semi-quantitative RT-PCR with glyseraldehyde- 3-phosphate dehydrogenase (GAPDH) as an internal control was performed to determine the levels of PPARγ, IRS-2, GLUT2, SREBP1c and G6Pase mRNA in L-02 cells. A 4μl RNA sample was reverse transcribed with oligo(dT)18. cDNA (2μl) was used for PCR amplification with 1U Taq DNA polymerase. The PCR products were run on a 1% agarose gel containing ethidium bromide and viewed under UV light. All primers are listed in table 2. Preliminary experiments were carried out with various amounts of PCR cycles to determine the linear range of amplification for all of the studied genes. The results for the expression of studied gene mRNAs are always presented relative to the expression of GAPDH.Table 2. The primers use for semi-quantitative RT-PCR.Gene name Size (bp) Forward and Reverse primer (5′-3′) accession numberPPARγ 195 F: TCTCCAGTGATATCGACCAGC BT007281R: TTTTATCTTCTCCCATCATTAAGGIRS-2 383 F: CACCTCCCCACGACAGTTGC NM_003749R: GGTGGGACAAGAAGTCAATGCTGGLUT2 398 F: TTTTCAGACGGCTGGTATCAGC J03810R: CACAGAAGTCCGCAATGTACTGGSREBP1c 248 F: CACCGTTTCTTCGTGGATGG BC057388R: CCCGCAGCATCAGAACAGCG6Pase 244 F: CGACCTACAGATTTCGGTGCTTG NM_000151R: AGATAAAATCCGATGGCGAAGCGAPDH 452 F: ACCACAGTCCATGCCATCAC BC083511R: TCCACCACCCTGTTGCTGTA2.5 Protein isolation and concentration assay.Proteins were isolated using the Mammalian Cell Protein Extraction kit. Protein concentrations were determined by Bradford assay [22].2.6 Glucose concentration assay.The glucose concentration in medium was assayed using the Glucose Assay Kit. Absorbance was assayed at 340nm using BECKMAN COULTER DU 800 UV/Visible spectrophotometer. All sample concentrations were normalized by each protein amount.2.7 Glucokinase assay.Enzymatic activity was assayed as described previously [23], using NAD as coenzyme and Glucose-6-phosphate dehydrogenase as coupling enzyme. The assay buffer contained 100mM triethanolamine hydrochloride (Tris-HCL, pH 7.8), 5mM MgCl2, 5mM ATP, 150mM KCl, 2mM dithiothreitol, 0.2% bovine serum albumin, 1mM NAD, and 1unit/ml of G6PDH. Correction for low hexokinase activity was applied by subtracting the activity measured at 0.5mM glucose from the activity measured at 100mM glucose. Absorbance was measured at 340nm using BECKMAN COULTER DU 800 UV/Visible spectrophotometer. Enzymatic activity was expressed in milliunits per mg of protein.2.8 Statistical analysis.Results are expressed as means ± S.E. of 3experiments. The comparison of different groups was carried out using Student’s t test. The significance level chosen was P < 0.05.3 RESULTS3.1 In normal status, GBE suppressed glucose ingestion and glucokinase activity.All cells were cultured in DMEM. NC was treated with 10nM insulin; NRT was treated with 10nM insulin and rosiglitazone; NGT was treated with 10nM insulin and GBE (as described in Materials and Methods). The glucose uptake and glucokinase activity were determined at 0h, 18h and 36h, respectively. The data indicated that GBE inhibited glucose uptake (36% reduction, p<0.05, 18h; 9% reduction, 36h) (Fig. 1A) and glucokinase activity (no effect, 18h; 5% reduction, 36h) (Fig. 1B) compared with control (NC). The trend was impaired with time. The decline of GBE concentration was a possible explanation for this phenomenon. Contrary to GBE, rosiglitazone stimulated glucose uptake (20% induction, 18h; 44% induction, p<0.01, 36h) (Fig. 1A) and glucokinase activity (1.8-fold induction, p<0.01, 18h; 27% induction, p<0.05, 36h) (Fig. 1B) compared with control (NC). The results suggested that in normal status, GBE decreased the risk of obesity by suppressing overmuch glucose ingestion.Fig. 1 In normal status, the effects of GBE and rosiglitazone on glucose ingestion and glucokinase activity. After plating, L-02 cells were cultured for 36h as described in Materials and Methods. After 0, 18, and 36h glucose ingestion (A) and GK activity (B) were determined. Results are the mean ± S.E. from values obtained from three independent cultures. A, ∗ (p < 0.05), ∗∗ (p < 0.01) indicates that glucose ingestion was greater or lower in treatment cells than in control cells (NC). B, ∗ (p < 0.05), ∗∗(p < 0.01) indicates that GK activity was greater or lower in treatment cells than in control cells (NC).3.2 In normal status, GBE increased mRNA levels of PPARγ, IRS-2 and G6Pase.To further understand the mechanism that GBE regulated glucose ingestion, the mRNA levels of PPARγ, G6Pase, GLUT2, SREBP1c and IRS-2 genes were measured. All cells were treated as described in Materials and Methods. After 36h, cell RNAs were isolated. The results from semi-quantitative RT-PCR (Fig. 2A) demonstrated that GBE stimulated expressions of PPARγ (30% induction; p<0.05), IRS-2 (69% induction; p<0.05) and G6Pase (1.2-fold induction; p<0.01) observably (Fig. 2B). PPARγ involved in insulin signaling pathway and could regulate insulin sensitivity. The increase of its expression would make cells be sensitive to insulin. IRS-2 was a crucial molecular in intracellular insulin signal transduction. It was able to elevate intracellular insulin sensitivity by enhancing its expression. The increases of PPARγ and IRS-2 indicated that GBE was able to enhance insulin sensitivity. As a result, cells would increase glucose ingestion. G6Pase as a key enzyme catalyzed the last step reaction in hepatic glucose synthesis. Its increase might lead to augment glucose output in liver. It was interesting, that GBE might enhance glucose ingestion and output at one time. The data suggested that GBE quickened cellular metabolic rate. Different to GBE, rosiglitazoneFig. 2 In normal status, the effects of GBE and rosiglitazone on gene expression. After plating, hepatocytes were cultured for 36h as described in Materials and Methods. After 36h, total RNA was extracted and analyzed for the expressions of PPARγ, IRS-2, GLUT2, SREBP1c and G6Pase (A). The quantification of blots for these gene expressions, obtained in 3 independent cultures is shown (B). GAPDH was used as an internal control to normalize the expression levels of these genes. ∗ (p < 0.05), ∗∗ (p < 0.01) indicates that expression level of gene was greater or lower in treatment cells than in control cells (NC).3.3 In insulin resistance status, GBE improved glucose ingestion and glucokinase activity.All cells were cultured in DMEM. NC was treated with 10nM insulin; AC was treated with 100nM insulin; ART was treated with 100nM insulin and rosiglitazone; AGT was treated with 100nM insulin and GBE (as described in Materials and Methods). The glucose uptake and glucokinase activity were determined at 0h, 18h and 36h, respectively. The results showed that 100nM insulin inhibited glucose uptake absolutely (Fig. 3A). The data indicated that GBE stimulated glucose ingestion dramatically (Fig. 3A). It suggested that GBE had potential efficacy in preventing insulin resistance. In addition, GBE enhanced glucokinase activity, but it was not significance. It meant glucokinase did not play a key role in GBE treatment. Rosiglitazone had the similar efficacy with GBE’s. It stimulated markedly glucose uptake (Fig. 3A) and glucokinase activity (Fig. 3B), too. But in this process, rosiglitazone made cells ingest overmuch glucose.Fig. 3 In insulin resistance status, the effects of GBE and rosiglitazone on glucose ingestion and glucokinase activity. After plating, L-02 cells were cultured for 36h as described in Materials and Methods. After 0, 18, and 36h glucose ingestion (A) and GK activity (B) were determined. Results are the mean ± S.E. from values obtained from three independent cultures. A, ∗ (p < 0.05), ∗∗ (p < 0.01) indicates that glucose ingestion was greater or lower in treatment cells than in control cells (NC); # (p < 0.05), ## (p < 0.01) indicates that glucose ingestion was greater or lower in treatment cells than in control cells (AC). B, ∗ (p < 0.05), ∗∗ (p < 0.01) indicates that GK activity was greater or lower in treatment cells than in control cells (NC); # (p < 0.05), ## (p < 0.01) indicates that GK activity was greater or lower in treatment cells than in control cells (AC).3.4 In insulin resistance status, GBE increased expressions of IRS-2 and GLUT2 and decreased SREBP1c expressions.To further understand the mechanism that GBE improved glucose tolerance, the mRNA levels of PPARγ, G6Pase, GLUT2, SREBP1c and IRS-2 genes were measured. All cells were treated as described in Materials and Methods. After 36h, cell RNAs were isolated. The results from semi-quantitative RT-PCR (Fig. 4A) demonstrated that GBE enhanced expressions of IRS-2 (1.5-fold induction; p<0.01) and GLUT2 (0.9-fold induction; p<0.01) and inhibited SREBP1c expression (27% reduction; p<0.05) in hyperinsulinaemic hepatocytes (Fig. 4B). As in normal status, GBE also stimulated IRS-2 expression. It was very important to improve insulin sensitivity. GLUT2 as a main glucose transporter in liver, the increase of its expression was helpful to cell for taking glucose. SREBP1c is crucial transcriptional factor to regulate lipid metabolism. On the one hand, the decrease of its expression would reduce lipid production; on the other hand, considering SREBP directly suppressed IRS-2 expression in transcriptional level, its decline might be a reason for augment of IRS-2 expression. Rosiglitazone had similar effect with GBE on genes expression. Different from GBE, PPARγ had a higher expression level and IRS-2 had a lower expression level in rosiglitazone treatment.Fig. 4 In insulin resistance status, the effects of GBE and rosiglitazone on gene expression. After plating, hepatocytes were cultured for 36h as described in Materials and Methods. After 36h, total RNA was extracted and analyzed for the expressions of PPARγ, IRS-2, GLUT2, SREBP1c and G6Pase (A). The quantification of blots for these gene expressions, obtained in 3 independent cultures is shown (B). GAPDH was used as an internal control to normalize the expression levels of these genes. ∗ (p < 0.05), ∗∗ (p < 0.01) indicates that expression level of gene was greater or lower in treatment cells than in control cells (AC).4 DISCUSSIONThis study proved that GBE had potential efficacy to prevent insulin resistance. And the proper molecular mechanism driving this process was discussed.As we known, TZDs were prevalent drugs used in type II diabetes mellitus therapy. They were thought as PPARγ agonists [24] and improved downstream insulin signaling in type II diabetic patients [25]. On the one hand, they improved glucose tolerance and enhanced insulin sensitivity; on the other hand, TZDs increased weight of patients, too [24, 26]. It is unclear whether gaining weight in this way could do further harm to diabetic patients. But it is well known that obesity is a major risk factor for insulin resistance and type II diabetes mellitus. By contrast, GBE suppressed overmuch glucose ingestion when enhancing glucose tolerance in our experiments. Moreover, although GBE decreased glucose ingestion in normal status, it didn’t induce insulin resistance. Longtime (3 months) ingestingGBE by normal glucose-tolerant individuals caused a significant increase in pancreatic beta-cell insulin response [27]. The effect of GBE on glucose (improved glucose tolerance and inhibited overmuch glucose uptake) made us believe that GBE has a potential role in diabetes therapy.Liver, as a key metabolic organ, is bifunctional in glucose metabolism, namely utilization and production of glucose. And it played a crucial role in regulating energy balance. So, the hepatic insulin resistance was deemed to be chiefly responsible for type II diabetes [28]. In our experiments, GBE improved glucose tolerance in hyperinsulinism-induced hepatocytes. It suggested that GBE prevented insulin resistance in liver. To further explore its signaling pathway, we determined mRNA levels of related genes and glucokinase activity. Our data showed that in normal status, GBE enhanced expressions of PPARγ, IRS-2 and G6Pase; in insulin resistance status, GBE stimulated expressions of IRS-2 and GLUT2, and repressed SREBP1c expression. Interesting, there was a paradoxical result in our data. On the one hand, GBE improved glucose tolerance. On the other hand, GBE also increased G6Pase expression, which was thought a key enzyme in glucose synthesis. Considering glucose ingestion was increased in insulin resistance status, a rational explanation for this result was that GBE enhanced glucose tolerance by accelerating metabolic rate, not by merely ingesting and depositing glucose [29].Glucokinase (GK) is main HKs in liver and plays key role in regulating glucose phosphatization. In our experiment, its activity did not change after GBE treatment. The data suggested that GBE did not exert its effects on glucokinase. It should be noted that IRS-2 expression was improved after GBE treatment both in normal status and insulin resistance status. Since IRS-2 was a crucial element in downstream insulin signaling, its expression was closely relational with insulin signaling transduction. Researchers found that deficiency of IRS-2 caused insulin resistance [30]. So we suggested that GBE exerted its effects mainly on IRS-2 expression. Moreover, our data showed that the increase of IRS-2 was followed by the decrease of SRBEP1c. It indicated there was an inner link between them. The results of Tomohiro supported our supposition. They found SREBP1c directly suppressed IRS-2 transcription in hepatocytes [31]. So we suggested that GBE mainly improved insulin action by enhancing IRS-2 transcription.In summary, our data support the notion that GBE improves glucose tolerance in hyperinsulinism-induced L-02 cells. And the study also provides a base to further explore its signaling pathway.REFERENCES[1] Schmid, W. Ginkgo thrives. Nature 1997; 386: 755.[2] Della Loggia R, Sosa S, Tubaro A, et al. Anti-inflammatory activity of some Ginkgo biloba constituents and of their phospholipid-complexes. Fitoterapia 1996; 67: 257-264.[3] Bombardelli E, Cristoni A, Curri SB. Activity of phospholipid-complex of Ginkgo biloba dimeric flavonoids on the skin microcirculation. Fitoterapia. 1996; 67: 265-273.[4] Kazumasa Shinozuka, Keizo Umegaki, Yoko Kubota, Naoko Tanaka, Hideya Mizuno, Jun Yamauchi, Kazuki Nakamura, Masaru Kunitomo. Feeding of Ginkgo biloba extract (GBE) enhances gene expression of hepatic cytochrome P-450 and attenuates the hypotensive effect of nicardipine in rats. Life Sciences. 2002; 70: 2783-2792.[5] Tomomi Sugiyama, Yoko Kubota, Kazumasa Shinozuka, Shizuo Yamada, Jian Wu, Keizo Umegaki. Ginkgo biloba extract modifies hypoglycemic action of tolbutamide via hepatic cytochrome P450 mediated mechanism inaged rats. Life Sciences. 2004; 75: 1113-1122.[6] Saponara R, Bosisio E. Inhibition of cAMP-phosphodiesterase by biflavones of Ginkgo biloba in rat adipose tissue. Journal of Natural Products 1998; 61: 1386-1387.[7] Mario Dell’Agli, Enrica Bosisio. Biflavones of Ginkgo biloba stimulate lipolysis in 3T3-L1 adipocytes. Planta Med. 2002; 68: 76-79.[8] Boveris, A. D., Galatro, A., Puntarulo, S. Effect of nitric oxide and plant antioxidants on microsomal content of lipid radicals. Biol Res. 2000; 33: 159-165.[9] Nian hong, Song Baohui and Wang Wan. Antioxidative Hress Effect of Ginkgo Biloba Extract to Experimental Diabetes Rats. Journal of Mudanjiang Medical College 2004; 25: 3-6.[10] Li Xin, Liao Xinxue and Liao Xiaoxing. The preventive and therapeutic effect of Ginkgo extract on atherosclerosis. Chin J Emerg Med. 2004; 13: 609-611.[11] Huang Peili, Feng Gaoqian, Zhang Shuhua, Wang Hui. Effect of Ginkgo Biloba L Leaves on Oxidation of Human Low Density Lipoproteins in vitro. Journal of Hygiene Research 2004; 33: 453-454.[12] Ni Haixiang, Luo susheng and Huang qi. Effect of GBE on Plasma Oxidization-modified Low Density Lipoprotein in Patients with Type-2 Diabetes Mellitus. Zhe Jiang Zhong Xi Yi Jie He Za Zhi 2000; 10: 454-456. [13] Bernardczyk-Meller, J., Siwiec-Proscinska, J., Stankiewicz, W., et al. Influence of Eqb 761 on the function of the retina in children and adolescent with long lasting diabetes mellitus--preliminary report. Klin Oczna. 2004; 106: 569-571.[14] Bell GI, Kayano T, Buse JB, et al. Molecular biology of mammalian glucose transporters. Diabetes Care 1990; 13: 198-208.[15] Riaz A. Memon, Laurence H. Tecott, Katsunori Nonogaki, et al. Up-Regulation of Peroxisome Proliferator-Activated Receptors (PPAR-a) and PPAR-g Messenger Ribonucleic Acid Expression in the Liver in Murine Obesity: Troglitazone Induces Expression of PPAR-g-Responsive Adipose Tissue-Specific Genes in the Liver of Obese Diabetic Mice. Endocrinology 2000; 141: 4021-4031.[16] Jay D. Horton, Joseph L. Goldstein, and Michael S. Brown. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J. Clin. Invest. 2002; 109: 1125–1131.[17] Patti Mary-Elizabeth, Sun Xiao-Jian, Bruening Jens C., et al. 4PS/Insulin Receptor Substrate (IRS)-2 Is the Alternative Substrate of the Insulin Receptor in IRS-1-deficient Mice. J. Biol. Chem. 1995; 270: 24670-24673. [18] Kristina I. Rother, Yumi Imai, Matilde Caruso, et al.Evidence that IRS-2 phosphorylation is required for insulin action in hepatocytes. J. Biol. Chem. 1998; 273:17491–17497.[19] Yeh Hsiu-jeng, Chu Ten-ho and Shen Tin-wu. Ultrastructure of Continuously Cultured Adult Human Liver Cell. Acta Biologiac Experimentalis Sinica 1980; 13: 361-364.[20] Garvey, W. T., Olefsky, J. M. and Marshall, S. Insulin Receptor Down-regulation Is Linked to an Insulin-induced Postreceptor Defect in the Glucose Transport System in Rat Adipocytes. J. Clin. Invest. 1985; 76: 22-30.[21] PR Pryor, SC Liu, AE Clark, et al. Chronic insulin effects on insulin signaling and GLUT4 endocytosis are reversed by metformin. Biochem. J. 2000; 348: 83-91.[22] Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976; 72: 248-54.[23] Zhou Jianxin, Zhong Xiaolin, LI Rongfen, et al. Changes of hepatic glucokinase, muscular hexokinase, blood glucose, plasma lactate, and erythrocytic ATP after scalding in rats. Acta Academiae Medicinae Militaris Tertive 1994; 16: 178-180.[24] Hannele Yki-Jarvinen. Thiazolidinediones. N Engl J Med. 2004; 351: 1106-18.[25] Yoshinori Miyazaki, Helen He, Lawrence J. Mandarino, and Ralph A. DeFronzo. Rosiglitazone ImprovesDownstream Insulin Receptor Signaling in Type 2 Diabetic Patients. Diabetes 2003; 52: 1943–1950.[26] YUTAKA MORI, YUICHI MURAKAWA, KAZUHISA OKADA, et al. Effect of Troglitazone on Body Fat Distribution in Type 2 Diabetic Patients. Diabetes Care 1999; 22: 908–912.[27] Kudolo GB. The effect of 3-month ingestion of ginkgo biloba extract on pancreatic beta-cell function in response to glucose loading in normal glucose tolerant individuals. Journal of Clinical Pharmacology 2000; 40: 647-654.[28] Cullen M. Taniguchi, Kohjiro Ueki and C. Ronald Kahn. Complementary roles of IRS-1 and IRS-2 in the hepatic regulation of metabolism. J. Clin. Invest. 2005; 115: 718–727.[29] Kudolo GB. The effect of 3-month ingestion of ginkgo biloba extract (EGb 761) on pancreatic beta-cell function in response to glucose loading in individuals with non-insulin-dependent diabetes mellitus. Journal of Clinical Pharmacology 2001; 41: 600-611.[30] Naoto Kubota, Kazuyuki Tobe, Yasuo Terauchi, et al. Disruption of Insulin Receptor Substrate 2 Causes Type 2 Diabetes Because of Liver Insulin Resistance and Lack of Compensatory β-Cell Hyperplasia. Diabetes 2000; 49: 1880–1889.[31] Tomohiro Ide, Hitoshi Shimano, Naoya Yahagi, et al. SREBPs suppress IRS-2-mediated insulin signaling in the liver. Nat Cell Biol. 2004; 6: 351-357.。
某大学生物工程学院《生物化学》考试试卷(179)
某大学生物工程学院《生物化学》课程试卷（含答案）__________学年第___学期考试类型：（闭卷）考试考试时间：90 分钟年级专业_____________学号_____________ 姓名_____________1、判断题（100分，每题5分）1. 嘌呤碱合成的限速步骤是合成IMP的反应。
（）答案：错误解析：嘌呤碱合成的限速步骤是合成5磷酸核糖胺（PRA）的反应。
2. DNA复制时，冈崎片段的合成需要RNA。
（）[山东大学2016研]答案：正确解析：冈崎片段的合成需要RNA引物。
3. 氨甲蝶呤和四氢叶酸结构相似，可以抑制核苷酸的合成，在临床上作为抗肿瘤药物。
（）答案：正确解析：4. 氨可直接掺入到大多数氨基酸中。
（）答案：错误解析：5. 从丙酮酸形成葡萄糖共消耗6个高能磷酸键。
（）答案：正确解析：6. 若1个氨基酸有3个遗传密码，则这3个遗传密码的前两个核苷酸通常是相同的。
（）答案：正确解析：7. 级联系统是一个信号放大系统。
（）答案：正确解析：8. 低糖、高脂膳食情况下，血中酮体浓度增加。
（）解析：9. dTMP合成的直接前体物质是TDP。
（）答案：错误解析：dTMP合成的直接前体是dUMP。
细胞内脱氧核苷酸的合成是在核苷二磷酸的水平上进行的。
10. 鞘磷脂的代谢过程主要与细胞质膜的流动有关，与细胞生物活性分子的生成调节无关。
（）答案：错误解析：11. 生物体编码20种氨基酸的密码子数共有64个。
（）[山东大学2017研]答案：错误解析：生物体编码20种氨基酸的密码子数为61个，还有三个为终止密码子，不编码任何氨基酸。
12. 苯丙酮酸和酪氨酸代谢缺陷时可导致多种疾病，如苯丙酮酸尿症、白化病和尿黑酸症等。
（）解析：13. 氧化磷酸化的解耦联剂都是质子载体。
（）答案：正确解析：14. 丙酮酸激酶反应几乎不可逆地朝向ATP合成方向进行是磷酸烯醇式丙酮酸转化为丙酮酸高度放能的结果。
（）答案：正确解析：15. 生物固氮作用需要厌氧环境，是因为钼铁蛋白对氧十分敏感。
海红米米糠对慢性应激诱导小鼠抑郁样行为和异常肠道微生物及神经递质的改善作用
海红米米糠对慢性应激诱导小鼠抑郁样行为和异常肠道微生物及神经递质的改善作用李晓红;Rabia Parveen;杨志友;张永平;周鸿凯;刘文超;苏伟明;宋采【期刊名称】《中国粮油学报》【年(卷),期】2022(37)3【摘要】“微生物-肠-脑轴”失常在抑郁症的发病中发挥着重要作用,调节肠道菌群失衡成为最新的治疗方向。
海红米米糠可发挥益生元作用调控肠道微生物。
为探究海红米米糠改善慢性不可预测温和应激(CUMS)诱导的小鼠抑郁样行为的作用。
对照和暴露于CUMS的小鼠接受正常或含5%海红米米糠饮食喂养9周,通过糖水偏好实验和悬尾实验分析小鼠的抑郁样行为,实时荧光定量PCR法检测结肠内容物菌群的数量,HPLC测定前额皮层中单胺类神经递质的含量。
应激使小鼠糖水偏好度、乳杆菌属和双歧杆菌属的数量、去甲肾上腺素(NE)与其代谢产物、五羟色胺(5-HT)与其代谢产物、多巴胺(DA)与其代谢产物的含量都显著下降,悬尾不动时间和梭菌属的数量都显著升高;海红米米糠干预后提高了小鼠的糖水偏好度、乳杆菌属和双歧杆菌属的数量、5-HT与其代谢产物和NE的含量,降低了悬尾不动时间。
海红米米糠改善CUMS诱导的小鼠抑郁样行为可能与改善肠道菌群失衡及神经递质有关。
【总页数】6页(P25-30)【作者】李晓红;Rabia Parveen;杨志友;张永平;周鸿凯;刘文超;苏伟明;宋采【作者单位】广东海洋大学食品科技学院;广东省水产品加工与安全重点实验室;广东海洋大学滨海农业学院;广东海洋大学深圳研究院【正文语种】中文【中图分类】R964【相关文献】1.米邦塔仙人掌果胶对小鼠慢性不可预知温和应激所致抑郁样症状的改善作用2.丁螺环酮和米安色林对梁氏情境应激箱诱导小鼠焦虑和抑郁样行为的影响3.奶粉摄入改善慢性不可预知性应激诱导的小鼠抑郁样行为4.对香豆酸对慢性束缚应激诱导小鼠抑郁样行为的作用5.石斛多糖通过改善肠道屏障功能、调节肠道微生物群、减少氧化应激和炎症反应改善右旋糖酐-硫酸钠诱导的小鼠结肠炎因版权原因，仅展示原文概要，查看原文内容请购买。
复方黄精对小鼠耐缺氧及抗疲劳能力的影响.
复方黄精对小鼠耐缺氧及抗疲劳能力的影响作者：金英子，曲香芝，张红英［摘要］［目的］观察复方黄精对小鼠耐缺氧能力和抗疲劳能力的影响. ［方法］分别灌胃给予4，2g/kg 复方黄精后，采用常压耐缺氧、负重游泳及转棒等实验方法，观察小鼠的缺氧存活时间、负重游泳存活时间及转棒耐力时间. ［结果］复方黄精大剂量组小鼠缺氧存活时间及负重游泳存活时间均明显延长，复方黄精大、小剂量组小鼠的转棒耐力时间亦明显延长. ［结论］复方黄精具有提高小鼠耐缺氧及抗疲劳能力的作用.关键词］耐缺氧;植物，药用;小鼠Effects of the compound Polygonatum on anti-hypoxia capacity and anti-tiredness in miceABSTRACT:OBJECTIVE To study the effects of the compound Polygonatum on anti-hypoxia capacity and anti-tiredness in mice.METHODS The mice were observed by ordinary pressure hypoxia ，loaded swimming and rotational stick to measure the survival time and endurance time after being given2 ，4g/kg compound Polygonatum.RESULTS The survival time under the condition of ordinary pressure hypoxia and the loadling swimming of high dosage group of compound Polygonatum were prolonged ，and the endurance time of rotational stick of low and high dosage groups of compound Polygonatum was prolonged ，respectively.CONCLUSION The compound Polygonatum has antihypoxia cpacity and anti-tiredness effects in mice.Key words:bearing hypoxia;plants ，medicinal;mice复方黄精是由黄精、黄芪、茯苓、枸杞子、鹿茸及当归等组成. 本研究观察了复方黄精对小鼠抗疲劳及耐缺氧能力的影响.1材料1.1实验动物取昆明种小鼠，体重为(20±2) g,雌雄兼用，由延边大学医学部实验动物科提供.1.2药物黄精、黄芪、茯苓、枸杞子、鹿茸及当归等中药均为市售品，临用前用水浸泡2h,加水煎煮3次，收集水煎液，浓缩制备成所需浓度•2方法与结果2.1 复方黄精对小鼠常压耐缺氧能力的影响取健康小鼠30只，雌雄各半，随机分为3 个组，即大、小剂量实验组及对照组，每组各为10只. 每日分别灌胃给予大、小剂量实验组小鼠4，2g/kg 复方黄精，对照组小鼠灌胃给予等量蒸馏水，连续给予14d.末次灌胃给药后1h,将小鼠置于放置20g钠石灰的300mL 广口瓶中，盖紧瓶盖涂以凡士林密闭，记录小鼠死亡时间，即存活时间[1].统计学处理采用t检验，所有数据以均数土标准偏差(x± SD表示.结果示对照组及大、小剂量实验组小鼠的存活时间分别为( 31.50±4. 64)min，(41.90±5.33)min，(36.80±7.67)min; 大剂量实验组小鼠的存活时间明显长于对照组，两组间有显著性差异( P<0.01 ).2.2复方黄精对小鼠抗疲劳能力的影响2.2.1 复方黄精对小鼠负重游泳能力的影响分组、给药及统计学处理方法同2.1 项下方法. 末次灌胃给药1h 后，给小鼠尾部施加10%体重的负荷，放置于水温(26± 1)°C，水深25cm的水缸内，记录小鼠的游泳存活时间，即开始至沉到水底6s 不再游出水面时间 [1] . 结果示对照组及大、小剂量实验组小鼠负重游泳存活时间分别为( 8.40±2.12)min，(17.20±7.17) min，( 13.10 ±8.85) min;大剂量实验组小鼠负重游泳存活时间较对照组明显延长，两组间有显著性差异( P<0.01 ).2.2.2复方黄精对小鼠转棒耐力的影响分组、给药及统计学处理方法同2.1项下方法.末次灌胃给药1h后，将小鼠放置于转速为20r/min的电动转棒上，以1min 内不落降为标准，记录各组小鼠的转棒耐力时间 [1] . 结果示对照组及大、小剂量实验组小鼠转棒耐力时间分别为(3.40±1.24)min，(35.50 ±8.17 ) min，( 28.10 ±10.22 ) min; 大、小剂量实验组小鼠的转棒耐力时间与对照组比较均明显延长，分别有显著性差异( P<0.01).3讨论实验结果表明，复方黄精可明显提高小鼠心脑耐缺氧能力，降低组织耗氧量;4 ，2g/kg 复方黄精可不同程度地提高小鼠抗疲劳能力. 缺氧影响机体各种代谢，特别是机体的氧化供能. 复方黄精具有较好抗缺氧能力，可明显延长小鼠在常压缺氧条件下的存活时间、负重游泳存活时间和转棒的耐力时间. 机体的游泳抗疲劳时间和体能状态，与协调运动能力密切相关[2] . 复方黄精可提高小鼠耐缺氧能力，提高机体的抗应激能力，并具有一定的抗疲劳作用，其机制尚待进一步研究阐明.[参考文献][1]李仪奎•中药药理实验方法学[M\ .上海：上海科学技术出版社，1991.149.[2] 回晶，尚德静，李庆伟. 西藏人参果对小鼠抗疲劳及抗缺氧能力的影响[ J] . 营养学报，2003，25( 2) ： 21 9.。
螺旋藻补充对西部寒旱地区大学生有氧耐力及血液生化指标的影响
螺旋藻补充对西部寒旱地区大学生有氧耐力及血液生化指标的影响唐晓宏;丁斌;颜维宝;赵霞【摘要】就螺旋藻补充前后对西北寒旱地区大学生(河西学院在校大学生)有氧耐力以及血常规某些生化指标变化进行研究,结果显示:螺旋藻有控制和降低体重、延缓运动性疲劳、提高大学生心功能指数的功效,血红蛋白、红细胞计数、细胞压积均有上升,起到了调节生理机能的作用,可提高有氧耐力,是西北寒旱地区大学生良好的营养补剂.【期刊名称】《体育科技》【年(卷),期】2017(038)003【总页数】3页(P23-24,28)【关键词】螺旋藻;西北寒旱地区;大学生;有氧耐力【作者】唐晓宏;丁斌;颜维宝;赵霞【作者单位】河西学院体育学院,甘肃张掖 734000;河西学院体育学院,甘肃张掖734000;河西学院体育学院,甘肃张掖 734000;河西学院体育学院,甘肃张掖734000【正文语种】中文教育部、国家体育总局对我国大专院校的学生体质健康进行调研的结果显示，我国当代大学生身体素质水平均呈继续下降趋势。
为贯彻教育部、国家体育总局就大学生体质健康标准达标测试要求的精神，河西学院从2007年开始对大学生体质健康达标进行跟踪测试，近几年的结果显示与全国大学生体质健康状况相似，体质健康水平显下降趋势，导致了有氧耐力低下。
近期有报道某高校学生进行1000米体质测试后死亡，河西学院学生在进行男子1500米、女子800米测试中也频频出现呕吐、昏厥等不适反应，引起学校及社会对大学生体质健康的担忧。
如何提高大学生的体质健康水平，尤其提高有氧耐力是当今急需解决的问题。
经国内外众多学者研究证实，螺旋藻营养价值丰富，有许多保健功能，尤其是调节免疫和抗疲劳功能，螺旋藻是至今为止世界上最丰富、最全面的天然食物，几乎含有人体所需的全部营养素[1]，对人体体质健康的改善有一定的保健作用。
但有关补充螺旋藻对地处高原寒旱地区大学生体质健康及有氧耐力影响的研究甚少。
处于高原寒旱地区的大学生，生活的环境海拔较高、寒冷、干燥，空气中氧含量相对较低，一定程度上影响到体质健康水平和有氧耐力，本文从高校大学生体质健康状况及有氧耐力“差”入手，研究螺旋藻的补充对高原寒旱地区大学生体质健康、有氧耐力、某些血液生化指标的作用，旨在为提高大学生体质健康水平和有氧耐力寻找新的营养源提供一定的理论科学依据。
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——提高缺氧耐受力
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什么是角鲨烯？ 什么是提高缺氧耐受力？ 为什么要提高缺氧耐受力？ 如何提高缺氧耐受力？
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什么是角鲨烯？
角鲨烯，1916年，日本化学科学家 Tsujimoto在深海鲨鱼肝脏中发现一 种新的淡黄色不饱和烃类化合物[2] ， 是一种天然存在的三萜烯类，是高度 不饱和脂肪族 [1] 。 是人体胆固醇代 谢途径中一个关键的中间产物[2] 。
等营养物质无法彻底分解、氧化 、利用。释放能量减少，机体便 发生各种生理变化，如血压升高 或血脂、血糖升高等。
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什么是提高缺氧耐受力？
提高缺氧耐受力在哪些情况下有所体现？
人体由于环境或机体生理原因导致组织细胞不能充分获得氧气时，缺氧耐受力强具有重要意义。 如：高空、井下、水底、商场、会议室、雾霾等环境，及人体呼吸系统、循环系统出现故障时。
身处高原地区时
密闭的空调房内时
空气环境污染时
获得氧的能力降低时
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为什么要提高缺氧耐受力？
慢性缺 氧
缺氧我们很熟悉，慢性缺氧呢？
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为什么要提高缺氧耐受力？
正常情况1下% 空气的成分
21%
78%
环境中氧气含量21%左右时，机体是相对舒服的。
王元龙·空气和氧气_专题复习的探索与实践 王浩宇·空调房间缺氧环境对人体的影响及补氧方案探讨2018
如何提高缺氧耐受力？
角鲨烯+有氧运动
角鲨烯可以增强细胞内线粒体代谢功能，提高组织细胞在缺氧环境状态下的 耐受能力。通过提高缺氧耐受力，各种营养物质正常代谢和转换，维持内环 境营养平衡。
动力工厂
角鲨烯软胶囊提高缺氧耐受力的研究_邱春媚
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Байду номын сангаас
如何提高缺氧耐受力？
研究表明，角鲨烯具有类似红细胞摄取氧的功能，与氧结合生成活化的氧化 角鲨烯，在血液循环中输送到机体末端细胞后释放氧气，使细胞恢复活力， 提高身体的“自愈”能力。
刘纯友，马美湖等·《角鲨烯及生物活性研究进展》2015 本文图片来自网络
什么是提高缺氧耐受力？
即：提高组织细胞在缺氧状态下的耐受能力。 通过提高缺氧耐受力，增强细 胞内线粒体功能，使各种营养物质正常代谢和转换，维持内环境营养平衡。
线粒体耗氧量占组织细胞所得氧 的80％～90％。不能充分获得氧
线粒体 和利用氧时，糖、脂肪和蛋白质
感提谢高缺聆氧听耐受力，健康生活好身体！
主讲人：姜影
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[1]罗娇依，李刚等·《高效液相色谱法测定保健食品原料和产品中角鲨烯的含量》2019 [2]刘纯友，马美湖等·《角鲨烯及生物活性研究进展》2015
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什么是角鲨烯？
自日本发现角鲨烯以来，研 究者们对角鲨烯展开了大量 的研究，并发现角鲨烯广泛 存在于动植物中，甚至人体 内都可以提炼出角鲨烯，但 深海鲨鱼中角鲨烯含量远远 高于其他提取物。
黄宗锈·角鲨烯对小鼠缺氧耐受力的影响 本文图片来自网络
如何提高缺氧耐受力？
角鲨烯软胶囊
（国食健字G20140687）
本品是以角鲨烯、明胶、甘油、纯化水为主要原料制成的保 健食品，经动物功能试验证明，具有提高缺氧耐受力的保健 功能。 【标志性成分及含量】每100g含：角鲨烯99g 【包装规格】6瓶/盒（0.75g/粒×30粒/瓶） 【保健功能】提高缺氧耐受力 【适宜人群】处于缺氧环境者 【不适宜人群】少年儿童 【食用方法及食用量】每日1次，每次2粒，口服
罗娇依，李刚等·《高效液相色谱法测定保健食品原料和产品中角鲨烯的含量》2019
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什么是角鲨烯？
角鲨烯的应用小科普： 1.角鲨烯在医药工业上可作为药物 缓释剂，可延长药物的半衰期； 2.角鲨烯在化妆品工业上是一种良 好的润肤剂，表现出较好的保湿现 象； 3.角鲨烯在食品工业上作为一种自 由基清除剂，提高食用植物油的稳 定性，延长产品的货架期。