多囊卵巢综合征模型鼠颗粒细胞凋亡及TRAIL蛋白的表达

目的通过观察卵巢颗粒细胞凋亡及TRAIL(肿瘤坏死因子相关凋亡诱导配体)蛋白的表达情况,探讨颗粒细胞凋亡与PCOS发病的相关性及凋亡调控蛋白TRAIL在PCOS颗粒细胞凋亡中的作用。方法采用硫酸普拉睾酮钠诱导大鼠PCOS模型,3’-末端原位标记法(TUNEL)检测大鼠卵巢颗粒细胞凋亡情况,免疫组化染色及RT-PCR分析检测TRAIL蛋白及TRAIL mRNA在颗粒细胞的表达。结果PCOS组大鼠卵巢窦状卵泡颗粒细胞凋亡发生率及TRAIL蛋白的表达较对照组明显增强(P<0.01,P<0.05),窦前卵泡颗粒细胞凋亡发生率及TRAIL蛋白的表达两组无显著性差异(P>0.05),两组卵巢始基卵泡颗粒细胞未发现凋亡征象及TRAIL蛋白表达。PCOS组大鼠卵巢颗粒细胞TRAIL mRNA的表达较对照组明显增强(P<0.01)。结论PCOS大鼠卵巢窦状卵泡颗粒细胞凋亡明显增强,TRAIL在PCOS大鼠卵巢颗粒细胞凋亡调控中发挥了作用。     

Cd24a和前列腺素代谢相关酶在PCOS小鼠模型卵巢颗粒细胞中表达水平的实验研究

目的:探讨Cd24a分子和前列腺素代谢相关酶在多囊卵巢综合征(polycystic ovary syndrome, PCOS)小鼠模型卵巢颗粒细胞中的表达水平。方法:取20只雌性C57BL/6小鼠,随机分为对照组(正常小鼠)和实验组(应用脱氢表雄酮建立PCOS小鼠模型),每组各10只。对照组小鼠于颈背部连续皮下注射20天芝麻油溶液(0.1 m L/100 g)。实验组应用脱氢表雄酮(6 mg/100 g)联合芝麻油溶液(0.1 m L/100 g)连续颈背部皮下注射20天。经苏木精-伊红染色观察两组小鼠卵巢组织病理学改变。应用实时荧光定量PCR法对小鼠卵巢颗粒细胞中Cd24a分子和前列腺素代谢相关酶m RNA表达量进行检测。结果:实验组体重显著高于对照组(P0.05);实验组小鼠卵巢呈多囊样改变,卵泡中颗粒细胞数量减少,闭锁卵泡增多,闭锁卵泡直径明显大于对照组;实验组Cd24a分子和前列腺素代谢相关酶m RNA表达量较对照组存在显著差异(P0.05)。结论:PCOS小鼠卵巢颗粒细胞中Cd24a分子和前列腺素代谢相关酶表达量异常,提示Cd24a分子可能与PCOS疾病发生相关。     

AnnexinⅠ在PCOS 大鼠颗粒细胞中的表达及意义

目的:探讨膜联蛋白Ⅰ(AnnexinⅠ)在多囊卵巢综合征(PCOS)大鼠卵泡颗粒细胞的表达及生物学意义。方法:采用免疫组织化学方法及灰度值测定AnnexinⅠ在PCOS组和对照组的卵泡颗粒细胞中的表达。结果:AnnexinⅠ在两组中的各级卵泡颗粒细胞中均有表达,PCOS组AnnexinⅠ在窦状卵泡中表达显著高于对照组(P<0.05)。结论:PCOS组AnnexinⅠ在窦状卵泡颗粒细胞的表达上调,且PCOS中窦状卵泡颗粒细胞的凋亡增加,说明AnnexinⅠ参与了卵巢颗粒细胞的凋亡过程,并且发挥了重要作用。     

Annexin I在PCOS大鼠颗粒细胞中的表达及意义

目的：探讨膜联蛋白I（AnnexinI）在多囊卵巢综合征（PCOS）大鼠卵泡颗粒细胞的表达及生物学意义。方法：采用免疫组织化学方法及灰度值测定AnnexinI在PCOS组和对照组的卵泡颗粒细胞中的表达。结果：AnnexinI在两组中的各级卵泡颗粒细胞中均有表达,PCOS组AnnexinI在窦状卵泡中表达显著高于对照组（P〈0．05）。结论：PCOS组AnnexinI在窦状卵泡颗粒细胞的表达上调,且PCOS中窦状卵泡颗粒细胞的凋亡增加,说明AnnexinI参与了卵巢颗粒细胞的凋亡过程,并且发挥了重要作用。     

MiR-296-3p调节多囊卵巢综合征大鼠颗粒细胞凋亡的作用机制

目的：探讨miR-296-3p对多囊卵巢综合征(polycystic ovary syndrome, PCOS)大鼠颗粒细胞凋亡的影响。方法：全自动化学发光免疫分析法检测PCOS大鼠血清雌二醇(estradiol, E2)、孕酮(progesterone, P)、睾酮(testosterone, T)水平;利用苏木素-伊红染色(hematoxylin-eosin staining, HE)检测卵巢病理学改变;TUNEL法检测卵巢细胞凋亡;qPCR检测卵巢miR-296-3p表达水平;将各质粒分别转染卵巢颗粒细胞(ovarian granulosa cells, GCs)后分为miR-NC、miR-296-3p mimic、miR-296-3p inhibitor、miR-296-3p mimic+Vector、miR-296-3p mimic+PRKCA和miR-296-3p mimic+PRKCA+NF-κB组,以未处理的GCs为对照组;Western blot法检测p38、p-p38及NF-κB的表达水平,利用StarBase在线预测和双荧光素酶报告实验验证miR-296-3p与P...     

MUC16 对子宫内膜容受性的影响及其意义

目的:多囊卵巢综合征(Polycystic Ovary Syndrome,PCOS)系由于体内复杂的内分泌和代谢环境影响了子宫内膜稳态,导致子宫内膜容受性下降,造成患者生育力减弱和不良妊娠结局.通过测定多囊卵巢综合征患者子宫内膜与正常生育力妇女增生期、分泌早、中、晚期子宫内膜中MUC16的相对表达量,本文探讨MUC16与PCOS患者子宫内膜容受性下降的关系,为临床上改善PCOS患者子宫内膜容受性,提高PCOS患者的妊娠率,降低流产率提供一条新的可能途径.方法:选择PCOS患者子宫内膜、正常生育力妇女增生期、分泌早、中、晚期子宫内膜各20例,用免疫组化SP法检测MUC16在各组的表达情况.结果:(1)MUC16在月经周期各期均有表达,在分泌中期表达最强.(2)PCOS组MUC16的表达较分泌中期组弱,差异有显著性(P＜0.05).结论:(1)在子宫内膜中的表达呈周期性变化.(2)PCOS患者子宫内膜中MUC16表达异常可能使子宫内膜容受性下降,推测其与胚胎不能正常着床或着床后发育不良、导致流产有关.     

三氯生对原代大鼠卵巢颗粒细胞孕酮分泌影响的实验研究

目的:研究三氯生对原代大鼠卵巢颗粒细胞孕酮(P4)分泌功能的影响。方法:原代大鼠卵巢颗粒细胞培养备用。取备用的卵巢颗粒细胞采用不同浓度的三氯生(0、0.01、0.1、1μM)染毒。24 h后分别采用MTT法检测颗粒细胞的相对活力、酶联免疫法(ELISA法)检测颗粒细胞P4分泌水平、实时荧光定量PCR法(q RT-PCR)及western blot法检测类固醇激素合成急性调节蛋白(St AR)、胆固醇侧链裂解酶(P450scc)以及3β-羟基类固醇脱氢酶(3β-HSD)的基因及蛋白表达水平。结果:三氯生在本研究所采用的浓度范围内对颗粒细胞的活性并没有影响(P0.05);三氯生(0.1、1μM)可抑制颗粒细胞P4的分泌,且呈现剂量依赖性下降(P0.05)。三氯生(0.1、1μM)可使St AR的基因表达水平显著增高、P450scc的基因表达水平下降(P0.05)。1μM三氯生可使St AR及P450scc的蛋白表达水平明显降低(P0.05)。三氯生对3β-HSD的基因及蛋白表达水平皆没有影响(P0.05)。结论:三氯生可抑制原代大鼠卵巢颗粒细胞的P4分泌,对类固醇激素合成关键分子的影响可能是其作用机制之一。     

复方麦芽丸对多囊卵巢综合征模型大鼠LH、FSH表达的影响

本文旨在研究复方麦芽丸(Compound Malt Pill,CMP)对多囊卵巢综合征(polycystic ovarian syndrome,PCOS)大鼠黄体生成素(LH)、促卵泡激素(FSH)表达的影响。通过运用9日龄SD大鼠颈背部皮下注射丙酸睾丸酮建立PCOS模型,造模成功的大鼠随机分为模型组,达英-35组和CMP低、中、高剂量组(n=9),另设正常组(n=10)。各治疗组以相应药物灌胃,正常组及模型组灌以等量的蒸馏水。运用免疫组化、PCR测定卵巢组织LH、FSH的蛋白及mRNA表达。结果显示,模型组中LH的蛋白及mRNA表达较正常组显著升高(P0.01),CMP各剂量组LH蛋白及mRNA表达较模型组显著降低(P0.01),达英-35组LH蛋白表达较模型组显著降低(P0.01),mRNA表达较模型组无显著差异(P0.05);模型组中FSH的蛋白及mRNA表达较正常组显著降低(P0.01),各治疗组FSH蛋白及mRNA表达较模型组显著升高(P0.01),研究结果表明,PCOS模型大鼠LH表达明显升高,FSH表达明显降低;复方麦芽丸对PCOS有治疗作用,可能是通过调节LH、FSH表达水平实现的。     

Visfatin mRNA在PCOS患者网膜脂肪组织中的表达

目的：探讨visfatin基因在多囊卵巢综合征（PCOS）网膜脂肪组织中的表达及相关影响因素。方法：采用半定量RT-PCR方法检测PCOS组（30例）和对照组（25例）网膜脂肪组织visfatin mRNA表达,并测量体重指数、腰臀比、空腹血糖、空腹胰岛素、胰岛素抵抗指数和血清性激素水平。结果：①PCOS组网膜脂肪组织visfatin mRNA表达量高于对照组（P=0.000）。②网膜脂肪组织visfatin mRNA的表达量与BMI、WHR、FINS、HOMA-IR呈正相关（P〈0.05）。③多元逐步回归分析显示,HOMA-IR（P=0.000）和WHR（P=0.005）是影响网膜脂肪组织visfatin mRNA表达的相关因素。结论：网膜脂肪组织visfatin mRNA表达可能与PCOS胰岛素抵抗的发生和肥胖相关。     

多囊卵巢综合征患者肠道菌群和生化免疫分子特征

【目的】比较多囊卵巢综合征(polycysticovariansyndrome,PCOS)患者与健康对照间肠道菌群谱结构特征差异,并探讨多囊卵巢综合征患者差异菌群与生化免疫指标之间的联系。【方法】选取初诊多囊卵巢综合征患者23例和健康女性对照23例,每例患者于初诊时留取粪便标本和血液标本,粪便标本提取DNA进行宏基因组测序,血清用于检测性激素和炎症因子。通过生物信息分析比较多囊卵巢综合征患者与健康对照间肠道菌群谱结构特征差异,以及与相关指标的联系。【结果】发现多囊卵巢综合征患者与健康对照的肠道菌群在门、属、种水平均有明显差异。两组间差异菌种为4个,普通拟杆菌(Bacteroides vulgatus)和弗格森埃希菌(Escherichia fergusonii)在PCOS组中的相对丰度高于对照组,并且这两种菌与PCOS的发病机制密切相关。凸腹真杆菌(Eubacteriumventriosum)和Subdoligranulum unclassified菌的相对丰度低于健康对照组。其中普通拟杆菌、凸腹真杆菌和Subdoligranulum unclassified菌3个菌种彼此间存在相关性,差异菌种与生化免疫指标间也存在相关性。发现布鲁米球菌、棒状戈登菌、脱硫弧菌、凸腹真杆菌、斯特雷沃菌5个菌的组合在PCOS患者早期诊断中具有较好的诊断效能。基因分析发现,鸟苷核苷酸从头生物合成的超途径I基因通路在PCOS人群中富集。【结论】多囊卵巢综合征患者与对照组间的肠道菌群和生化免疫指标均具有差异,并具有一定相关性,为PCOS患者的综合性诊疗提供了方向。     

钙网质蛋白在多囊卵巢综合征大鼠子宫内膜的表达及意义

目的：研究钙网质蛋白（CRT）在PCOS大鼠子宫内膜中的表达及生物学意义。方法：60只雌性SD大鼠随机分为PCOS组和对照组,每组各30只。给模型组24日龄大鼠皮下埋植左旋甲基炔诺酮硅胶棒3mm／只,3d后BID皮下注射人绒毛膜促性腺激素1．5IU。给对照组皮下注射等体积生理盐水。注射9d后观察大鼠卵巢形态学（HE染色）,化学发光法测定性激素水平。结果：模型组大鼠卵巢重量和体积均显著高于对照组（P〈0．01）。模型组大鼠卵巢出现类多囊卵巢综合征的改变。模型组卵巢各级发育期卵泡及黄体少见,卵泡多呈囊性扩张。模型组大鼠血清孕激素、睾酮、空腹胰岛素、空腹血糖水平均显著高于对照组（P〈0．05）;卵泡刺激素（FSH）水平显著低于对照组（P〈0．05）。LH／FSH比值显著高于对照组（P〈0．05）。采用免疫组织化学方法及灰度值测定,定量分析CRT在PCOS组和对照组的子宫内膜中表达。CRT在两组中的子宫内膜中均有表达。PCOS组子宫内膜上皮CRT表达显著低于对照组（P〈0．01）。结论：避孕硅胶棒联合hCG诱导SD大鼠多囊卵巢综合征模型是较好的PCOS模型。CRT与PCOS的发病密切相关．     

MUC16对子宫内膜容受性的影响及其意义

目的：多囊卵巢综合征（Polycystic Ovary Syndrome,PCOS）系由于体内复杂的内分泌和代谢环境影响了子宫内膜稳态,导致子宫内膜容受性下降,造成患者生育力减弱和不良妊娠结局。通过测定多囊卵巢综合征患者子宫内膜与正常生育力妇女增生期、分泌早、中、晚期子宫内膜中MUC16的相对表达量,本文探讨MUC16与PCOS患者子宫内膜容受性下降的关系,为临床上改善PCOS患者子宫内膜容受性,提高PCOS患者的妊娠率,降低流产率提供一条新的可能途径。方法：选择PCOS患者子宫内膜、正常生育力妇女增生期、分泌早、中、晚期子宫内膜各20例,用免疫组化SP法检测MUC16在各组的表达情况。结果：（1）MUC16在月经周期各期均有表达,在分泌中期表达最强。（2）PCOS组MUC16的表达较分泌中期组弱,差异有显著性（P〈0.05）。结论：（1）在子宫内膜中的表达呈周期性变化。（2）PCOS患者子宫内膜中MUC16表达异常可能使子宫内膜容受性下降,推测其与胚胎不能正常着床或着床后发育不良、导致流产有关。     

葡萄糖调节蛋白78在子痫前期中的表达及其意义

目的：探讨葡萄糖调节蛋白78（GRP78）mRNA及蛋白在胎盘组织的表达水平及其与子痫前期的发病关系。方法：选择2010年1月-2010年12月在南京医科大学第一附属医院江苏省人民医院产科住院的子痫前期患者35例（子痫前期组）,以同期正常孕妇35例为对照组。采用RT-PCR技术、蛋白印迹（western-blot）法和免疫组化检测两组孕妇胎盘组织中GRP78的mRNA与蛋白表达水平差异。结果：子痫前期组患者胎盘组织中GRP78mRNA与蛋白表达水平均显著高于相应孕周正常妊娠组。结论：子痫前期能够诱导GRP78表达,CHOP/GADD153表达的增高与子痫前期的发病有关。     

Effects of metformin on the expression of GLUT4 in endometrium of obese women with polycystic ovary syndrome

The objective was to explore the effects of metformin on the expression of endometrial glucose transporter 4 (GLUT4) and analyze the related factors of GLUT4 in patients with polycystic ovary syndrome (PCOS). This study included 20 obese patients with PCOS (PCOS group) and 20 obese patients who had infertility caused by oviducal or pelvic factors but had no PCOS (control group). Follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol-2 (E(2)), testosterone (T), fasting serum glucose (FSG), fasting insulin serum (FINS), homeostasis model assessment-insulin resistance (HOMA-IR), and endometrial GLUT4 expression were determined in the two groups. In PCOS group, patients were given 500 mg of metformin three times per day for 3 mo, and then the parameters above were determined again and compared with that before metformin treatment. The parameters above also were compared between PCOS and control groups. The correlation of GLUT4 with its related factors was analyzed. The levels of T, FINS, and HOMA-IR were higher in PCOS group than in the control group (P < 0.01). The levels of protein and mRNA of endometrial GLUT4 were lower in the PCOS group than in the control group (P < 0.001). The expression of protein and mRNA of endometrial GLUT4 increased after metformin treatment (P < 0.001). HOMA-IR was negatively correlated with GLUT4 expression (P = 0.027). In patients with PCOS, the levels of protein and mRNA of endometrial GLUT4 were lower compared with that in non-PCOS women, and HOMA-IR was strongly associated with endometrial GLUT4 expression. Metformin may up-regulate endometrial GLUT4 expression to improve endometrial IR.     

Altered expression of Bcl-2 and Bax in follicles within dehydroepiandrosterone-induced polycystic ovaries in rats

PCOS (polycystic ovary syndrome) is a heterogeneous disease characterized by hyperandrogenaemia, hirsutism, oligo- or amenorrhea, insulin resistance and anovulation. The aim of the present study was to evaluate if the balance between the ovarian expression of Bax (proapoptotic protein) and Bcl-2 (antiapoptotic protein) is altered in a PCOS model developed in rats by DHEA (dehydroepiandrosterone) administration. In addition, the ovarian morphology and the circulating progesterone levels were evaluated. Histological studies confirmed the presence of follicular cysts, atretic follicles and the absence of corpora lutea in the ovaries from the PCOS group and a significant decrease in circulating progesterone levels. Immunohistochemical studies showed that the expression of Bcl-2 and Bax were mainly localized in granulosa cells of AFs (antral follicles) in both groups. Bax expression was greater in preantral and AFs from PCOS ovarian sections than in the controls. In contrast, intense Bcl-2 immunostaining was observed in the control AFs, while Bcl-2 protein was either absent in PFs (preantral follicles) or weakly expressed in AFs from PCOS rats. These results were partially confirmed by Western studies. Data revealed that the ovarian level of Bcl-2 protein was lower in PCOS than in the control and that there were no differences in Bax ovarian levels between groups. However, Bax/Bcl-2 ratio was significantly higher in PCOS group than in the control group. In conclusion, an increase in ovarian apoptosis through an imbalance among the Bcl-2 family members may be involved in the transformation of growing follicles in cystic follicles in the ovaries from DHEA-induced PCOS rats.     

雾化吸入雷公藤内酯醇对哮喘大鼠气道平滑肌增生及NF-κB、Bcl-2表达的影响

目的：探讨雷公藤内酯醇对哮喘气道重构及核因子-kappaB（NF-κB）、Bcl-2表达的影响。方法：将40只SD大鼠随机分为5组（n=8）：正常对照组（A组）;哮喘4周组（B组）;哮喘6周组（C组）;治疗4周组（D组）;治疗6周组（E组）。测定气道反应性并观察气道壁嗜酸性粒细胞浸润;图像分析软件测定支气管壁厚度、支气管平滑肌厚度及支气管平滑肌细胞核数量;免疫组织化学染色、Western印迹法检测PCNA、NF-κB、Bcl-2蛋白的表达,逆转录聚合酶链式反应（RT-PCR）检测Bcl-2mRNA表达。结果：①B组、C组NF-κB的蛋白表达量显著高于A组（P均〈0.01）,E组上述指标较B组、C组、D组均显著降低（P〈0.01、P〈0.01、P〈0.05）;②B组、C组Bcl-2蛋白及mRNA表达水平显著高于A组（P〈0.01）;E组蛋白表达量较B组、C组、D周组均显著降低（依次为P〈0.05、P〈0.01、P〈0.01）,mRNA表达水平与上述各组比较亦均显著降低（P〈0.01）,E组蛋白及mRNA表达水平与A组相比仍较高（依次为P〈0.05、P〈0.01）;③B组、C组PCNA的蛋白表达量明显高于A组（P〈0.01）;④B组及C组支气管壁厚度、支气管壁平滑肌厚度、支气管壁平滑肌细胞核数量均较A组明显增加（P〈0.01）,而E组上述指标较B组、C组、D组均显著降低（P〈0.01）;⑤B组、C组的气道反应性均高于A组（P均〈0.01）,E组较B组、C组、D组均显著降低（P〈0.01、P〈0.01、P〈0.05）。结论：哮喘气道平滑肌增生与气道平滑肌细胞（ASMCs）凋亡不足相关。NF-κB可能通过抑制ASMCs凋亡,参与哮喘气道高反应性及气道重构过程。雷公藤内酯醇可能通过下调NF-κB而抑制Bcl-2的表达,从而促进ASMCs凋亡、抑制气道平滑肌增生。     

Melatonin alleviates insulin resistance through the PI3K/AKT signaling pathway in ovary granulosa cells of polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a common endocrine gynecological disorder. Insulin resistance (IR) is a major cause of PCOS. Melatonin, a critical endogenous hormone, has beneficial effects on the female reproductive system. This study aims to investigate the molecular effect of melatonin on IR in human ovarian granulosa cells (GCs). Hormone levels of the subjects were determined through clinical examination. The expression levels of insulin receptor substrate (IRS)-1 and glucose transporter (GLUT4) in GCs from PCOS patients and a human granulosa cell line (SVOG) were examined using qRT-PCR and western blot. The IR cell model was established by inducing SVOG cells with palmitic acid (PA). IR was detected in GCs of PCOS patients and SVOG by measuring glucose content and glucose uptake. Cell viability and apoptosis levels were detected by CCK-8 assay and flow cytometry. PI3K/Akt pathway expression in SVOG was assessed by western blot. PCOS patients had higher levels of luteinizing hormone (LH), testosterone, and LH/follicle-stimulating hormone. PA decreased cell viability, promoted apoptosis, and reduced glucose uptake in SVOG cells. IRS-1 and GLUT4 mRNA and protein expression was downregulated, and glucose uptake capacity was reduced in PCOS GCs and SVOG cells. Melatonin significantly upregulated IRS-1 and GLUT4 expression, downregulated p-IRS-1 (Ser307), and improved glucose uptake in PCOS patients' GCs and SVOG cells. PA decreased PI3K and Akt phosphorylation, whereas melatonin increased p-PI3K and p-Akt levels. Melatonin can reduce IR in GCs and PA-induced SVOG cells via the PI3K/Akt signaling pathway, providing more evidence for treating polycystic ovary syndrome.     

Long Non-coding RNA HOXA10-AS Promotes Invasion and Migration of Hepatocellular Carcinoma Cells

Some studies have showed that long non-coding RNA (lncRNA) HOXA10-AS acts as an oncogene and regulates the invasion and metastasis of tumor cells. However, its mechanism in the invasion and migration of hepatocellular carcinoma (HCC) cells is unclear. The purpose of this study was to analyze the expression of HOXA10-AS in HCC tissues and its clinical significance, detect the influence of HOXA10-AS on the invasion and migration of HCC cells, and explore the mechanism of HOXA10-AS in promoting the invasion and migration of HCC cells. The results of quantitative real-time PCR (qRT-PCR) showed that the expression of HOXA10-AS was significantly upregulated in HCC tissues compared with the adjacent non-HCC tissues. Age and gender did not show significant correlation with HOXA10-AS expression, while tumor size, lymphatic metastasis and distant metastasis showed significant correlation with HOXA10-AS expression. Meanwhile, the expression of HOXA10-AS in HCC cells was higher than that in normal liver cells. After interfering with HOXA10-AS in HCC cell lines HepG2 and QGY7701, Transwell invasion and scratch experiments showed that the invasion and migration ability of HOXA10-AS cells in the HOXA10-AS group was significantly lower than that in the control group. Western blotting results showed that the expression levels of vimentin and N-cadherin were significantly lower than those of the control group, while the E-cadherin expression was significantly increased. The TGFβ1/Smads signaling pathway was inhibited after HOXA10-AS interference. In summary, HOXA10-AS promotes the invasion and migration of HCC cells by the TGFβ1/Smads signaling pathway.     

维生素E对老年大鼠卵巢颗粒细胞保护作用机制的探讨

目的：通过观察维生素E（VE）对老年雌性大鼠卵巢凋亡相关蛋白Bcl-2、Bax的影响及对其抗氧化能力的影响,探讨VE延缓卵巢衰老的作用和机制。方法：采用自然衰老雌性大鼠,给予不同剂量外源性VE,用免疫组化方法观察卵巢颗粒细胞凋亡调控蛋白Bcl-2、Bax的表达,用Western Blot法检测卵巢Bcl-2、Bax蛋白含量,用生化法测定血清总超氧化物歧化酶（SOD）活力和丙二醛（MDA）含量。结果：与成年对照组相比,老年对照组Bcl-2表达明显降低、Bax表达明显升高（P〈0．01）,血清中SOD活力下降、MDA含量显著升高（P〈0．01）。与老年对照组相比,VE纽Bcl-2表达升高,Bax表达降低（P〈0．05）,MDA含量显著减少（P〈0．01）。结论：VE可调控凋亡相关蛋白Bcl-2、Bax的表达和对抗自由基对颗粒细胞的损伤,对卵巢颗粒细胞具有一定的保护作用。