从肿瘤的耐药性角度探讨P53蛋白、P-糖蛋白表达与肿瘤预后关系

目的：研究P53、P－糖蛋白在肿瘤中的表达与肿瘤预后关系。方法：应用经改良的SP免疫组化方法，统计学分析采用X^2检验。结果：P53蛋白阳性率52．63％；P－糖蛋白阳性率为51．32％。P53蛋白和P－糖蛋白阳性表达与肿瘤细胞的分化程度和临床分期无显著性差异（P＞0．05），但两者之间存在密切相关（P＜0．01）。结论：P53基因对P－糖蛋白的阳性表达有关，表明P53蛋白阳性的肿瘤细胞对某些化疗药物具有较低的敏感性，P53蛋白阳性表达和P－糖蛋白阳性表达是病人预后较差的主要原因之一。     

卵巢肿瘤组织中P—糖蛋白的表达及临床意义

目的研究Ｐ－糖蛋白（Ｐ－ｇｐ）在卵巢组织中的表达及其临床意义。方法用免疫组化的方法测定４０例卵巢恶性肿瘤及１０例卵巢良性肿瘤组织中的Ｐ－糖蛋白表达及其与组织学类型和分级，临床分期及术前化疗的关系。结果Ｐ－ｇｐ在良性肿瘤中无阳性表达。在恶性肿瘤中Ｐ－ｇｐ表达阳性率为３７．５０％，Ｐ－ｇｐ表达与组织学类型、临床分期、术前化疗无关。Ｐ－ｇｐ生表达在低分化癌中占５８．３３％，高于高、中分化癌（１４．２８％     

长裙竹荪菌丝体糖蛋白DiGP-2的组成分析和抑瘤作用的研究

目的：探讨长裙竹荪菌体糖蛋白DiGP-2的组成分析和抑瘤作用,方法：长裙竹荪菌丝体糖蛋白DiGP-2用氨基酸自动测定仪测定。结果：DiGP-2含有16种氨基酸,气相层析分析表明DiGP－2的单糖组成半乳糖,葡萄糖和甘露糖,其摩尔比为0．78：2．13：1．00,结论：DiGP－2对小鼠肉瘤S－180具有一定的抑制作用,抑瘤率为36．82％。     

胃液α1酸性糖蛋白测定和胃癌关系的研究

应用ＩＣＳ－Ⅱ型免疫化学自动分析仪测定６７例胃癌和２０１例良性胃疾病胃液中α１酸性糖蛋白和前白蛋白水平，探讨其对胃癌临床诊断的价值以及与胃癌临床病理分期、浸润深度和转移的关系。结果表明，胃癌胃液α１酸性糖蛋白水平显著高于良性胃疾病（Ｐ〈０．０５）；胃液前白蛋白水平相互间无明显差别（Ｐ〉０．０５）。α１酸性糖蛋白诊断界限为１０ｍｇ·Ｌ＾－１。诊断敏感性７９．１０％，特异性８０．６０％，准确性８０．２     

麻黄碱逆转K562/A02细胞多药耐药性的研究

目的：观察非细胞毒性质量浓度的麻黄碱对耐药的白血病细胞株（KS62／A02）多药耐药性的逆转作用，并探讨其逆转机制。方法：用MTT法检测麻黄碱的细胞毒作用；用流式细胞仪检测非细胞毒性浓度的麻黄碱处理后K562／A02细胞膜表面糖蛋白P170表达及功能的变化。结果：麻黄碱对K562／A02有一定的细胞毒作用，其非细胞质量浓度（IC10）为75mg·L^-1，非细胞毒性质量浓度的麻黄碱对K562／A02细胞对阿霉素的耐药性有部分逆转作用（5．67倍），作用于K562／A02细胞后，细胞膜糖蛋白P170的表达从（85．3±5．5）％下调至（34．8±1．2）％，DNR外渗试验显示，细胞内化疗药物的质量浓度明显增加。结论：麻黄碱通过下调K562／A02细胞膜糖蛋白P170的表达，抑制其将化疗药物“泵”出细胞外的功能，提高化疗药物在K562／A02细胞内的有效质量浓度，能部分逆转K562／A02细胞的多药耐药性。     

脑出血患者血小板膜糖蛋白测定及其临床意义

采用流式细胞术，单克隆抗体作分子探针，检测了脑出血患者血小板α－颗粒膜糖蛋白、溶酶体膜糖蛋白和血小板膜糖蛋白的变化，同时观察了血小板的粘附、聚集功能。结果：血小板三种膜糖蛋白阳性表达率在急性期显著增高（Ｐ＜０．０１），恢复期虽较急性期呈下降趋势，但仍高于健康对照组（Ｐ＜０．０５或０．０１）。血小板粘附率和最大聚集率的变化规律与膜糖蛋白相似。提示脑出血患者血小板活化程度也增高，血小板粘附聚集功能也呈活跃态势。说明患者进入恢复期后应根据血小板活化程度和功能状态，可适当给予抗血小板活化治疗。     

环孢菌素A联合干扰素对白血病细胞株的多药耐药逆转的实验研究

目的：观察联合逆转剂对白血病细胞株多药耐药（MDR）的逆转作用，提高化疗的敏感性，方法：用环孢菌素A（CsA)和干扰素－α（INF-α）单独或联合逆转多药耐药细胞株K562／A02对柔红霉素（DNR）的耐药，药敏试验采用MTT法，同时用流式细胞仪检测逆转前后P糖蛋白（PgP)表达的变化及细胞内DNR浓度分布情况。结果：DNR对K562／A02及K562／S细胞的半数细胞抑制剂量（IC50）分别为7．3μg/ml和0．2μg/ml，CsA联合INF－α后明显增强DNR对K562／A02的细胞毒作用，IC60由7．3μg/ml降低到0．7μg/ml，而对K562／S细胞无影响，且逆转后细胞内DNR浓度明显增加，PgP表达无明显变化，结论：CsA和IFN－α联合能使白血病细胞株K562／A02对DNA的敏感性增加，具有逆转多药耐药的作用。     

血清糖蛋白电泳分析在肝病诊断中价值的探讨

为探索血清糖蛋白电泳在肝病诊断中的价值。对200例各种肝病和40例正常人进行了血清糖蛋白电泳分析。结果:肝硬变、慢活肝、慢迁肝α1糖蛋白、α2糖蛋白明显低于正常(P<0．01)。以肝硬化组降低最为显，γ糖蛋白带明显高于正常(P<0．01)。急性肝炎组与正常对照组无显差异。肝癌组：α1糖蛋白、α2糖蛋白明显高于正常(P<0．01)，γ、β糖蛋白带明显低于正常。说明血清糖蛋白电泳是一项简便，易于普及的肝病诊断和鉴别诊断试验．特别是对肝癌和其它肝病的鉴别诊断方面有着重要价值，明显优于目前临床普遍采用的血清蛋白电泳分析。     

双波长分光光度法测定替硝唑葡萄糖注射液中5-羟甲基糠醛的含量

目的：建立替硝唑葡萄糖注射液中5－羟甲基糠醛（5－HMF）的测定方法。方法：用双波长分光光度法，以水为溶剂，在波长为284．0及348.7nm处测定。结果：以A284．0为标示值的5－HMF溶液的ΔA与A284．0成良好的线性相关，平均回收率为100．7％，RSD为1．79％。结论：本方法简便快速，准确可靠。     

生技霉素小组分的研究I．分离纯化和4″—异丁酰螺旋霉素II（生技霉素B2β）的结构鉴定

生技霉素是一组以4″－异戊酰螺旋霉素为主的基因工程杂合抗生素，除了主要组分4″－异戊酰螺旋霉素III、II、I（生技霉素A1、B1、E1）和小组分4″－丁酰／异丁酰螺旋霉素III（生技霉素A2α/A2β）以外，还含有其它4″－酰化螺旋霉素II和少量杂质。采用连续逆流分配法，碱性硅胶柱层析，制备薄层层析和中压柱层析等分离方法，并以薄层层析和HPLC作为检测手段，从生技霉素混合物中分离得到了四个小组分A0、B2、B3和C2，其含量分别为0．5％、3．3％、6．2％和2．6％，其中B2为B2α和B2β两个异构体的混合物。经过UV、IR、SI－MS、GC－MS、^1H-NMR、^13C-NMR、^1H-^1H COSY6等光谱分析，并与生技霉素A1、B1、A2α、A2β等的光谱数据进行比较,确定了生技霉素B2α为4″－丁酰螺旋霉素II，B2β为4″－异丁酰螺旋霉素II，其中4″－异丁酰螺旋霉素II变一个新的基因工程杂合抗生素。     

白头翁糖蛋白对小鼠腹腔巨噬细胞免疫的增强作用

目的 :研究白头翁糖蛋白对巨噬细胞免疫功能的调节作用。方法 :在体外培养的小鼠腹腔巨噬细胞中加入不同浓度白头翁糖蛋白后 ,观察其对巨噬细胞吞噬功能、一氧化氮合成和白介素 1分泌的影响。结果 :白头翁糖蛋白能在体外显著增强小鼠腹腔巨噬细胞吞噬中性红的作用 ,并可诱生巨噬细胞产生一氧化氮 ,对巨噬细胞分泌白介素 1亦有一定的提高作用。结论 :白头翁糖蛋白对小鼠腹腔巨噬细胞有免疫增强作用。     

Inhibition of phenol sulfotransferase (SULT1A1) by quercetin in human adult and foetal livers

1. Quercetin is one of the most abundant flavonoids in edible vegetables, fruit and wine. The aim was to study the type of inhibition of SULT1A1 by quercetin in the human adult and foetal livers. 2. The activity of SULT1A1 was measured with 4 microM 4-nitrophenol and 0.4 microM 3'-phosphoadenosine-5'-phosphosulphate-[(35)S], and its mean (+/-SD) and median were 769 +/- 311 and 740 pmol min(-1) mg(-1), respectively (adult liver, n = 10), and 185 +/- 98 and 201 pmol min(-1) mg(-1), respectively (foetal liver, n = 8, p < 0.0001). 3. In non-inhibited samples, K(m) for SULT1A1 (mean +/- SD) was 0.31 +/- 0.14 microM (adult liver) and 0.49 +/- 0.17 microM (foetal liver, n.s.). V(max) for SULT1A1 (mean +/- SD) was 885 +/- 135 pmol min(-1) mg(-1) (adult liver) and 267 +/- 93 pmol min(-1) mg(-1) (foetal liver, p = 0.007). 4. The IC(50) of quercetin for SULT1A1 was measured in three samples of adult and foetal livers and was 13 +/- 2.1 and 12 +/- 1.4 nM, respectively. 5. The type of inhibition was mixed non-competitive in adult and foetal livers and K(i) was 4.7 +/- 2.5 nM (adult liver) and 4.8 +/- 1.6 nM (foetal liver). 6. In the adult liver, the intrinsic clearance (mean +/- SD) was 3.3 +/- 1.5 ml min(-1) mg(-1) (non-inhibited samples), 0.9 +/- 0.4 ml min(-1) mg(-1) (12.5 nM quercetin) and 0.5 +/- 0.06 ml min(-1) mg(-1) (25 nM quercetin). In the foetal liver, the intrinsic clearance (mean +/- SD) was 0.5 +/- 0.2 ml min(-1) mg(-1) (non-inhibited samples), 0.12 +/- 0.01 ml min(-1) mg(-1) (12.5 nM quercetin) and 0.2 +/- 0.09 ml min(-1) mg(-1) (25 nM quercetin). 7. In conclusion, quercetin is a potent inhibitor of human adult and foetal liver SULT1A1. It reduces the sulphation rate and intrinsic clearance of 4-nitrophenol in both human adult and foetal livers. This suggests that quercetin may inhibit the sulfation rate of those drugs sulphated by SULT1A1. The inhibition of SULT1A1 is complex and not due solely to competition at the catalytic site of SULT1A1.     

(9S)-9-(2-hydroxy-4,4-dimethyl-6-oxo-1-cyclohexen-1-yl)-3,3-dimethyl-2,3,4,9-tetrahydro-1H-xanthen-1-one, a selective and orally active neuropeptide Y Y5 receptor antagonist

(9S)-9-(2-Hydroxy-4,4-dimethyl-6-oxo-1-cyclohexen-1-yl)-3,3-dimethyl-2,3,4,9-tetrahydro-1H-xanthen-1-one ((S)-1) was identified as a selective and orally active neuropeptide Y Y5 receptor antagonist. The structure-activity relationship for this structural class was investigated and showed that limited substitution on the phenyl ring was tolerated and that modification of the 4,4-dimethyl group of the cyclohexenone and the 3,3-dimethyl group of the xanthenone parts slightly improved potency. The plasma concentration-time profile after oral administration of (S)-1 in Sprague-Dawley (SD) rats showed significant in vivo racemization of (S)-1 and that (S)-1 is cleared much more quickly than (R)-1. The duration of (S)-1 in SD rats after oral administration of (RS)-1 racemate was twice as long as that following oral administration of (S)-1. The C max values of (S)-1 after administration of (S)-1 and (RS)-1 were comparable, and the brain to plasma ratio for (S)-1 was 0.34 in SD rats. In our acute D-Trp (34)NPY-induced food intake model, both (S)-1 and (RS)-1 showed potent and dose-dependent efficacy. Therefore, the use of (RS)-1 is suitable for studies that require sustained plasma exposure of (S)-1.     

Curcumin is a potent inhibitor of phenol sulfotransferase (SULT1A1) in human liver and extrahepatic tissues

1. Curcumin has anti-carcinogen effects and is under clinical evaluation as a potential colon cancer chemopreventive agent. The first aim was to see whether curcumin inhibited phenol sulfotransferase (SULT1A1) and, if so, to study the variability of the IC(50) of curcumin for SULT1A1 in 50 human liver samples. For comparative purposes, the inhibition of catechol sulfotransferase (SULT1A3) in five human liver specimens was studied. The second aim was to measure the IC(50) of curcumin against SULT1A1 in five samples of human duodenum, colon, kidney and lung. 2. Curcumin was a potent inhibitor of SULT1A1 in human liver; the mean +/- SD and median of IC(50) were 14.1 +/- 7.3 nM and 12.8 nM, respectively. The IC(50) ranged from 6.2 to 30.6 nM between the 5th and 95th percentiles and the fold of variation was 4.9. The distribution of IC(50) was positively skewed (skewness 1.2) and deviated from normality (p = 0.0004). 3. Curcumin inhibited human SULT1A3, and the inhibition was studied in five liver specimens with an IC(50) of 4324 +/- 1026 nM. This inhibition was greater than the IC(50) of curcumin for SULT1A1 (p < 0.0001). 4. In the extrahepatic tissues, the IC(50) of curcumin for SULT1A1 was 25.9 +/- 4.8 nM (duodenum), 25.4 +/- 6.8 nM (colon), 23.4 +/- 2.2 nM (kidney) and 25.6 +/- 5.6 nM (lung). Inhibition in these tissues is greater than that of curcumin for SULT1A1 in human liver (p < 0.0001). 5. In conclusion, curcumin is a potent inhibitor of SULT1A1 in human liver, duodenum, colon, kidney and lung. The IC(50) of curcumin for SULT1A1 varied 4.9-fold in human liver. The comparison of the present data with those of the literature revealed that the IC(50) of curcumin in the liver and extrahepatic tissues is one order of magnitude lower that the peak serum concentration of curcumin after therapeutic doses of 4 g to humans.     

Quantitation of catechol estrogens and their N-acetylcysteine conjugates in urine of rats and hamsters

A method for the analysis of N-acetylcysteine conjugates of catechol estrogens [catechol estrogen mercapturates (CE SRs)], which are likely to be urinary markers of estrogen-induced tumors, was established in this study. The characteristics of the method that was established were (1) cleanup of urine using the immunoaffinity column of CE SRs, (2) detection of catechol estrogens (CEs) and CE SRs by electrochemical detection, which provided the high specificity, and (3) stability of CE SRs through the cleanup. Using this method, the simultaneous quantitation of 2-hydroxy-17beta-estradiol (2-OHE(2)), 4-hydroxy-17beta-estradiol (4-OHE(2)), 2-hydroxyestrone (2-OHE(1)), 4-hydroxyestrone (4-OHE(1)), 2-hydroxyestrone 1-N-acetylcysteine thioether (2-OHE(1) 1SR), 2-hydroxyestrone 4-N-acetylcysteine thioether (2-OHE(1) 4SR), and 4-hydroxyestrone 2-N-acetylcysteine thioether (4-OHE(1) 2SR) in the range of 1-15 ng was performed. We first demonstrated the presence of CE SRs, 2-OHE(1) 1SR and 2-OHE(1) 4SR, in urine from rats treated intraperitoneally with 17beta-estradiol (E(2)) at a dose of 5 mg/kg. In female rats, the amount of 2-OHE(1) 1SR was several-fold greater than that of 2-OHE(1) 4SR, while the presence of 4-OHE(1) 2SR was not confirmed. The level of CEs and CE SRs in male rats was approximately (1)/(2)-(1)/(20) of that in female rats. The excretion rate following administration of 2-OHE(1) at 2 mg/kg and that following the administration of 4-OHE(1) at 2 mg/kg were different in female rats. In addition, 4-OHE(1) 2SR was present in the urine of male Syrian hamsters treated intraperitoneally with E(2), whereas it was absent in rats.     

Characterization of the endothelin-1-induced regulation of L-type Ca2+ current in rabbit ventricular myocytes

The effects of endothelin-1 (ET-1) on the L-type Ca2+ current (I(Ca)) and the interaction of ET-1 with beta-adrenoceptor stimulation were investigated in rabbit ventricular myocytes by the whole-cell patch-clamp technique. ET-1 (10(-8) M) had a biphasic effect on I(Ca) (direct effect), causing a transient decrease that was followed by a long-lasting increase which is much smaller than the increase induced by isoprenaline (ISO). The effect of ET-1 on I(Ca) was abolished by a selective ET(A) receptor antagonist, FR139317 (10(-6) M). The increase in I(Ca) induced by ET-1 (10(-8) M) was enhanced by a selective ET(B) receptor antagonist, BQ-788 (10(-6) M), as the transient decrease but not the increase in I(Ca) induced by ET-1 (10(-8) M) was suppressed by BQ-788. In the presence of ISO (10(-6) M), ET-1 elicited a more pronounced inhibitory effect: at 10(-9)-10(-7) M ET-1 inhibited the ISO-induced increase in I(Ca) in a concentration-dependent manner (anti-adrenergic effect). The maximum inhibition induced by ET-1 at 10(-7) M was approximately 80% of the ISO-induced response, and the IC50 value for anti-adrenergic effect of ET-1 was 4.2x10(-9) M. The anti-adrenergic effect of ET-1 (10(-8) M) was antagonized by the ET(A) antagonist FR139317 (10(-9)-10(-6) M) in a concentration-dependent manner and was partially inhibited by the ET(B) antagonist BQ-788 (10(-6) M). The anti-adrenergic effect of ET-1 was markedly attenuated by pretreatment of ventricular myocytes with pertussis toxin. The increases in I(Ca) induced by forskolin (10(-6) M), 3-isobutyl-1-methylxanthine (10(-4) M), and 8-bromo-cyclic AMP (3x10(-4) M) were also suppressed by ET-1 (10(-8) M). In summary, ET-1 has a differential effect on I(Ca) in the absence and in the presence of ISO: ET- I has a feeble biphasic action on the baseline I(Ca) and, in addition, it elicits a pronounced anti-adrenergic effect on the ISO-induced increase in I(Ca). Pertussis toxin-sensitive G protein is responsible for the anti-adrenergic effect of ET-1 on I(Ca), but the anti-adrenergic effect of ET-1 may involve also the regulation at the level of signaling process beyond the cyclic AMP generation. Anti-adrenergic effect of ET-1 on I(Ca) is mainly due to activation of ET(A) receptors but ET(B) receptors are also involved partially in the anti-adrenergic effect of ET-1 on I(Ca) in rabbit ventricular myocytes.     

Comparison study of lipo PGE1 preparations

The comparison study was performed with 3 kinds of Lipo PGE(1) (5 microg/ml) preparations (Formulation A, B, and C), which are now used in clinical. Under alkali condition, Lipo PGE(1) (5 microg/ml) preparations in combination with physiological solution containing calcium ion were susceptible to stop dropping because of the formation of aggregates. There was a difference of feasibility to form aggregates among these preparations. The percentage of PGE(1) in the LM (lipid microspheres) was 68.8% (Formulation A) when determined by filtration with the pore size of 0.1 microm, and the respective value (%) of Formulation B and Formulation C was 43.0% and 13.9%. This indicates that the latter formulations were significantly susceptible to leak from the LM. PGE(1) can induce an extensive irritation. The potency of irritation was the most in Formulation C. This seems similar with the result of LM retention of PGE(1). PGE(1) increased the blood flow. Formulation A reached the peak by 2.27 fold, which was significantly higher than Formulation C and PGE(1) alone (PGE(1)-cyclodextrin, PGE(1)-CD). The peak was also significantly higher in Formulation B than that of PGE(1)-CD. The AUC value of blood flow rate showed a significant increase in Formulation A and Formulation B as compared to that of PGE(1)-CD. Drug retention in the LM can be a determinant factor for drug distribution and pharmacological effect. This study indicates that there can be some differences among Lipo PGE(1) preparations, which have the same drug dose.     

Kinetics of intramolecular acyl migration of 1beta-O-acyl glucuronides of (R)- and (S)-2-phenylpropionic acids.

The stereoselective acyl migration of diastereomeric 1beta-O-acyl glucuronides of (R)- and (S)-2-phenylpropionic acid [(R)-1PG and (S)-IPG, respectively] in phosphate buffer (pH 7.4) at 310K was investigated using HPLC. The disappearance of (R)-1PG was faster than that of (S)-1PG according to pseudo first-order kinetics. A kinetic model describing the degradation reactions was constructed. The rate constant for acyl migration from the 1beta-O-isomer to the 2-O-acyl isomer (k12) was about one order magnitude larger than that for hydrolysis from 1beta-O-acyl isomer to aglycone (k10). The k12 of (R)-IPG (0.377 +/- 0.005 h(-1)) was about two times larger than that of (S)-IPG (0.184 +/- 0.003 h(-1)). The results indicated that the stereoselectivity in the degradation of 1PG was apparently governed by the acyl migration from 1-isomer to 2-isomer. The kinetic parameters for acyl migration from 1-isomer to 2-isomer were estimated from temperature-dependent experiments using the transition state theory. The value of the free energy of activation at 310 K for (R)-1PG (99.67 kJ/mol) was smaller than that of (S)-IPG (101.60kJ/mol), suggesting that (R)-IPG showed thermodynamically higher reactivity in acyl migration than (S)-1PG.     

异柠檬酸脱氢酶 1基因突变对替莫唑胺干预下脑胶质瘤 U87细胞凋亡的影响

目的 研究异柠檬酸脱氢酶1(isocitrate dehydrogenase 1,IDH1)基因突变对替莫唑胺干预下脑胶质瘤U87细胞凋亡的影响,以期深入了解其生物学特性及其化疗敏感性.方法 通过DNA重组技术构建携带野生IDH1基因(wIDH1)或突变的IDH1基因(mIDH1)的真核表达载体;通过CCK-8检测三种稳定细胞系的增殖能力和细胞活力;利用流式细胞仪技术检测稳转细胞系细胞凋亡率及替莫唑胺干预后细胞凋亡率的变化;构建裸鼠移植瘤模型,替莫唑胺干预,ELISA技术和蛋白质免疫印迹检测细胞相关凋亡蛋白[半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)、半胱氨酸天冬氨酸蛋白酶-9(Caspase-9)、B淋巴细胞瘤-2相关蛋白(Bax)和B淋巴细胞瘤-2(Bcl-2)]的表达情况;测量肿瘤大小为宽和长度,计算肿瘤大小;统计不同处理组肿瘤形成抑制率和总有效率.结果 wIDH1组(100.37±10.24),对照组(102.45±13.57)和mIDH1组(100.63±12.42)之间细胞增殖差异无统计学意义(P>0.05).mIDH1组U87细胞在CCK-8测定中显示出对替莫唑胺的敏感性,mIDH1组(36.84±3.55)细胞增殖和细胞活力较wIDH1组(98.17±8.54)和对照组(73.26±5.37)低(P<0.05);mIDH1组(62.18±3.47)％细胞的凋亡率高于对照组(33.16±6.54)％和wIDH1组(15.36±2.33)％;蛋白质免疫印迹和酶联免疫吸附测定(ELISA)结果显示,三组不同处理中,mIDH1组在Caspase-3,Caspase-9和Bax中的蛋白表达水平最高,Bcl-2的蛋白表达水平最低(P<0.05),wIDH1的异位过表达诱导Bcl-2蛋白表达水平的上调及Caspase-3,Caspase-9和Bax蛋白水平的下调(P<0.05);与其余两组相比,mIDH1组(220.17±12.15)mm3的肿瘤体积最小(P<0.05).wIDH1组(624.36±33.54)mm3与对照组(601.17±36.18)mm3差异无统计学意义(P>0.05);在替莫唑胺治疗组中,mIDH1组的总有效率为(73.15±8.46)％,wIDH1组的总有效率为(22.16±3.96)％.对照组的结果为(42.25±3.17)％.结论 mIDH1通过上调替莫唑胺后胶质瘤细胞Caspase-3、Caspase-9、Bax表达并下调Bcl-2表达提高胶质瘤细胞凋亡率,增强治疗敏感性.