血必净对活化诱导T细胞凋亡的调节

目的 观察活化诱导对脾脏T淋巴细胞凋亡、凋亡相关基因mRNA表达及caspase3活性的影响,以及活血化瘀中药的调节作用.方法 提取BALB/c小鼠脾脏T淋巴细胞并培养,以Con A+IL-2诱导T细胞活化凋亡,MTT法检测细胞增殖活性,流式细胞仪检测细胞凋亡率,RT-PCR检测Fas、FasL、Bcl-2、Bax、IL-2 mRNA表达水平,分光光度法测定caspase3酶活性,并观察活血化瘀中药对上述各项指标的影响.结果 活化T淋巴细胞于诱导18h后凋亡率明显增加,于诱导6h时未见FasL、Bax mRNA表达,Fas、Bcl-2 mRNA表达无明显变化;于诱导18 h后Fas、FasL、Bax mRNA表达升高,Bel-2 mRNA表达下降,caspase3活性增高.活血化瘀中药可降低T细胞凋亡,并可分别降低Fas、FasL、Bax mRNA表达,提高Bcl-2 mRNA表达,减轻easpase3酶活性.在活化诱导早期(6 h)促进T淋巴细胞内IL-2 mRNA表达,在晚期(18 h)减少IL-2 mRNA表达.结论 过度活化是脾脏T淋巴细胞异常凋亡的诱发因素,而凋亡的发生与Fas、FasL、Bax、Bcl-2 mRNA表达的改变有关.活血化瘀中药可通过调节IL-2及凋亡相关基因mRNA表达而减轻脾脏T淋巴细胞凋亡,同时可以促进T淋巴细胞的增殖活性.     

Modulation of event-related potentials in normal human subjects by visual divided attention to spatial and color factors

Naturally occurring cell death via apoptosis has been reported in the substantia nigra of rats during development, culminating during the perinatal period. Cellular pathways leading to apoptotic death of developing nigral dopamine neurons remain unknown, although the apoptotic mediator, caspase 3, has been shown to be activated during this process. Our previous results demonstrated the inability of antioxidants to rescue the nigral dopamine neurons that undergo apoptosis during development. In the present study, we investigated using immunohistochemistry the expression of cyclins D1, D3, and E in the substantia nigra during pre- and postnatal development, since their re-expression in postmitotic neurons has been proposed to contribute to developmental apoptosis. We also investigated by Western blot analysis of nigral tissue isolated during the first postnatal week the expression of the anti- and pro-apoptotic proteins, Bcl-2 and Bax, respectively, since altered Bcl-2 expression during developmental apoptosis has been described. During apoptotic death of nigral dopamine neurons in development, we detected a significant increase in the Bax:Bcl-2 ratio, which is consistent with enhanced apoptosis. There were no changes in the expression of the cyclins during the same apoptotic period. These novel findings suggest that nigral dopamine neurons undergo developmental apoptotic death through a Bax:Bcl-2-sensitive pathway that does not involve cyclin mediation.     

Time dependent bladder apoptosis induced by acute bladder outlet obstruction and subsequent emptying is associated with decreased MnSOD expression and Bcl-2/Bax ratio

Ischemia/reperfusion (I/R) injury-induced oxidative stress plays an important role in the functional impairment of the bladder following acute bladder outlet obstruction (BOO) via induction of apoptosis. The purpose of this study was to investigate the time course of the bladder apoptosis, and apoptosis related molecular changes in the early stage of acute BOO. Twelve-week-old male Sprague Dawley rats were divided into control, acute BOO only (I), and acute BOO plus subsequent emptying (I/R) for 30, 60, 120 min, 3 days and 2 weeks. We examined the extent of bladder apoptosis, expression of Mn-superoxide dismutase (Mn-SOD), Bcl-2, Bax, caspase 3 and poly (ADP-ribose) (PAR) in the bladder. Bladder apoptosis was significantly increased in the I/R group at 30, 60, and 120 min following bladder emptying. BOO plus subsequent emptying for 30, 60, 120 min showed significant decrease in MnSOD and Bcl-2 expression, and significant increase in caspase 3, Bax expression, and amounts of PAR. These results indicate that bladder apoptosis, induced by acute BOO and subsequent emptying, is associated with decreased MnSOD expression, increased PARP activity and imbalance in apoptosis pathways.     

Bcl-2/Bax蛋白在生后大鼠卵巢不同发育时期的表达

目的 探讨Bcl-2/Bax与卵泡发育和凋亡的关系. 方法 用免疫组织化学技术和图像分析系统,对95只大鼠生后不同发育时期卵巢中凋亡相关因子Bcl-2/Bax的表达情况进行研究. 结果 0～360 d卵巢各级卵泡中的卵母细胞均呈Bcl-2/Bax阳性染色.正常卵细胞中Bcl-2反应强于Bax,退化卵细胞中Bax的反应强于Bcl-2.Bcl-2/Bax在卵泡细胞中的表达模式有所不同,21d前 Bcl-2为阳性,21～150d之间为Bcl-2阴性;180d以后正常卵泡为阴性,闭锁卵泡为阳性;Bax的表达,180d前全为阴性,180d后的表达同Bcl-2.膜细胞中Bcl-2/Bax的表达与卵泡细胞存在相似之处.Bcl-2/Bax在黄体中的表达只见于180d后. 结论 Bcl-2/Bax对卵细胞的生长、发育、存活和凋亡可能有重要的调节作用,其对卵泡细胞、膜细胞及黄体细胞的存活和凋亡的调节作用不明显.     

丙酸睾酮对大鼠胸腺细胞凋亡及胸腺中Bcl-2、Bax表达的影响

目的探讨丙酸睾酮在大鼠胸腺退化过程中的作用及其对大鼠胸腺中Bcl-2和Bax表达的影响。方法雄性大鼠去势后给予丙酸睾酮皮下注射,分别于注射后第1、4、7天取材,用半薄切片甲苯胺蓝染色检测胸腺细胞凋亡情况,免疫组织化学法检测胸腺组织中Bcl-2和Bax的表达情况,采用t检验进行统计学处理。结果丙酸睾酮处理组大鼠胸腺组织中可发现较多的凋亡细胞和凋亡小体;去势组大鼠胸腺组织中Bcl-2表达量明显高于假手术组（P〈0.001）,丙酸睾酮处理后Bcl-2表达量明显减少（P〈0.001）;而Bax的表达正好相反,去势组大鼠胸腺组织中Bax表达量明显低于假手术组（P〈0.001）,给予丙酸睾酮后Bax表达量明显增加（P〈0.001）;结论丙酸睾酮可诱导大鼠胸腺细胞凋亡,并抑制大鼠胸腺组织中Bcl-2的表达,促进Bax的表达。     

大鼠额叶损伤后细胞凋亡及Bax与Bcl-2蛋白的表达变化

本研究目的为探讨大鼠额叶锐器损伤后细胞凋亡的变化规律及调控机制。通过电镜、TUNEL法及免疫组织化学染色方法检测细胞凋亡和Bax、Bcl2蛋白的表达变化,结果发现凋亡细胞在损伤后3h即可发现,24h达到高峰;伤后3hBax和Bcl2表达明显升高,Bax表达12h达到高峰,而Bcl2表达6h即达到高峰;伤后Bax/Bcl2比值上调,24h达到高峰,随后逐渐下降。结果表明大鼠额叶锐器伤后存在细胞凋亡,凋亡细胞数量的变化与伤后时程有关,Bax/Bcl2比值是决定细胞凋亡的重要因素。     

老龄大鼠脑缺血再灌注神经细胞凋亡、Bcl-2、Bax表达与caspase-3活性变化

目的：研究老年与青年急性局灶性脑缺血及再灌注(I/R)后细胞凋亡、Bcl-2、Bax表达与caspase-3活性变化的异同。方法： 采用线栓法建立急性局灶性脑I/R模型，检测青年与老龄大鼠脑缺血3 h及I/R 3 h、6 h、12 h、24 h、 72 h后脑梗死面积、神经细胞凋亡、Bcl-2、Bax表达及caspase-3活性。结果： 老龄大鼠脑缺血3 h和I/R 12 h脑梗死面积较青年大鼠增大。随着I/R时间延长，细胞凋亡明显增加，老龄大鼠出现的早、持续时间长。青年大鼠随着I/R时间的延长Bcl-2表达明显增强，老龄大鼠不明显。老龄大鼠I/R Bax表达早于青年大鼠，其表达增强及持续时间较长。老龄大鼠I/R caspase-3的激活早于青年大鼠。结论： 老龄大鼠I/R脑组织损伤严重，神经细胞凋亡显著，其机制与Bax表达增加、casspase-3活性增高及其持续时间长有关。     

Effect of acrylamide on BEAS-2B normal human lung cells: Cytotoxic,oxidative, apoptotic and morphometric analysis

Due to the broad toxic relevance of acrylamide, many measures have been taken since the 1900s. These measures increased day by day when acrylamide was discovered in foods in 2002, and its toxic spectrum was found to be wider than expected. Therefore, in some countries, the products with higher acrylamide content were restricted. On the other hand, the effects of acrylamide on the respiratory system cells have yet to be well understood. In this study, we aimed at investigating the effect of acrylamide on lung epithelial BEAS-2B cells. Initially, the cytotoxic effect of acrylamide on BEAS-2B was determined by MTT assay. Then, cellular oxidative stress was measured. Flow cytometry analysis was conducted for Annexin-V and caspase 3/7. Furthermore, Bax, Bcl-2 and Nrf-2 proteins were evaluated by immunocytochemistry. Finally, acrylamide-induced cellular morphological changes were observed under confocal and TEM microscopes. According to MTT results, the IC50 concentration of acrylamide was 2.00 mM. After acrylamide treatment, oxidative stress increased dose-dependently. Annexin V-labelled apoptotic cells and caspase 3/7 activity were higher than untreated cells in acrylamide-treated cells. Immunocytochemical examination revealed a marked decrease in Bcl-2, an increase in Bax and Nrf-2 protein staining upon acrylamide treatment. Furthermore, in confocal and TEM microscopy, apoptotic hallmarks were pronounced. In the present study, acrylamide was suggested to display anti-proliferative activity, decrease viability, induce apoptosis and oxidative stress and cause morphological changes in BEAS-2B cells.     

哮喘豚鼠嗜酸细胞Bcl-2和Bax mRNA表达及意义

目的:观察Bcl-2及Bax mRNA表达与嗜酸粒细胞（Eos）凋亡的关系,探讨其在哮喘发病中的作用。方法:健康豚鼠随机分为正常组、哮喘组,卵蛋白致敏激发制作哮喘模型,检测支气管灌洗液（BALF）中低密度EoS（HEos）及正常密度Eos（NEos）细胞凋亡,原位杂交及RT-PCR法检测Bcl-2及Bax mRNA表达。结果:哮喘组EoS显著高于正常组,以HEos为著（P<0.01）;Eos凋亡率明显低于正常组（P<0.01）。哮喘组不同密度Eos表达Bcl-2 mRNA明显增加,而Eos表达Bax mRNA明显减少。结论:哮喘时Eos存在凋亡抑制,这是哮喘时Eos增多的原因之一,哮喘豚鼠BALF Eos表达Bcl-2增加,表达Bax减少,表明Bcl-2及Bax可通过调节Eos凋亡参与哮喘发病。     

A recombined protein (rSj16) derived from Schistosoma japonicum induces cell cycle arrest and apoptosis of murine myeloid leukemia cells

rSj16, a recombined protein from Schistosoma japonicum, has been identified as an anti-inflammatory molecule. In this study, we demonstrated that rSj16 strongly suppressed the growth of murine myeloid leukemia WEHI-3B JCS cells in a dose- and time-dependent manner. rSj16 induced apoptosis by increasing the proportion of sub-G1 apoptotic cells as well as causing cell cycle arrest at the G0/G1 phase. The expressions of cyclin D1, D2, D3, and E, and Cdk 2, 4, and 6 genes in WEHI-3B JCS cells were significantly down-regulated at 24 h as measured by real-time PCR. Furthermore, apoptosis induced by rSj16 was confirmed by 4,6-diamidino-2-phenylindole nuclear staining assay and annexin V/propidium iodide double staining. A reduction of the mitochondrial membrane potential indicated an active involvement of mitochondria in the apoptosis process. rSj16 treatment induced an increase in the activity of caspase 3, 6, and 9, and expression of pro-apoptotic Bax. Meanwhile, the decreased expression of anti-apoptotic Bcl-2 was observed after rSj16 treatment. Taken together, our results implied that rSj16 can inhibit proliferation by inducing G0/G1 cell cycle arrest and apoptosis of murine myeloid leukemia cells via activation of the caspase-mediated mechanism by regulating the expression of Bcl-2 family.     

苦碟子对恶性黑色素瘤细胞抑制及凋亡蛋白Bcl-2/Bax表达的影响

目的观察不同浓度中药苦碟子对恶性B16黑色素瘤细胞的抑制作用和凋亡蛋白Bcl-2/Bax表达的变化,探讨中药苦碟子抑制B16黑色素瘤细胞生长的可能机制。方法通过细胞培养和MTT实验,检测苦碟子对B16黑色素瘤细胞的生长抑制情况,Western blot测定凋亡蛋白Bcl-2/Bax表达,免疫荧光染色检测Bcl-2/Bax蛋白在不同浓度苦碟子处理的黑色素瘤细胞中的表达。透射电镜观察不同浓度梯度中药苦碟子诱导细胞凋亡,其细胞结构的特征性变化。结果随着苦碟子药物浓度的增加,黑色素瘤细胞活细胞数目逐渐减少,细胞存活率显著下降(<0.05),凋亡抑制蛋白Bcl-2表达水平呈现下降趋势,而促凋亡蛋白Bax呈现上升趋势(<0.05),免疫荧光染色显示Bcl-2表达逐渐减少,Bax表达逐渐增加;电镜下凋亡小体数目不断增加,核固缩逐渐明显,细胞间隙增大,线粒体数目减少。结论中药苦碟子有浓度依赖性抑制黑色素瘤细胞生长,促进细胞凋亡,凋亡蛋白Bcl-2/Bax变化呈线性关系。     

Apoptosis in normal rat embryo tissues during early organogenesis: the possible involvement of Bax and Bcl-2

Apoptosis commonly occurs in a variety of developmental processes in mammals. In this study, we investigated the relationship between apoptosis and the expression of both Bax and Bcl-2 during the early organogenesis period (9.5-11.5 days of gestation) of rat embryos. Apoptotic cells detected by the terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) method were extremely abundant in the foregut diverticulum at 9.5 days of gestation, while they largely disappeared at 10.5 and 11.5 days of gestation, although they were detected in newly formed mid- and hindgut diverticulum at these times. Real-time RT-PCR analysis of whole embryos revealed that the expression of bax mRNA was constant at days 9.5 to 11.5, while the expression of bcl-2 mRNA gradually increased. Immunohistochemical studies of Bax and Bcl-2 expression revealed that these apoptotic cells were exactly positive to Bax in mirror sections, while their expression of Bcl-2 was generally too low to be detected. A disappearance of apoptotic cells was associated with strong Bcl-2 expression in the foregut diverticulum at 10.5 and 11.5 days of gestation. It was similarly observed that apoptotic cells detected in the cardiogenic area at 9.5 days of gestation disappeared with the formation of the primitive heart tube--accompanied by a strong expression of both Bcl-2 and Bax--in the developmental process of the primitive heart. Apoptotic cells were also observed in the primitive brain vesicle, optic vesicle, otic vesicle, and thyroid primordium at 10.5 and 11.5 days of gestation during the developmental process, with a strong expression of Bax. These results indicate that the Bax and Bcl-2 may be important in regulating the induction of embryonic cell apoptosis during early organogenesis.     

Apoptosis in the pattern formation of the ventricular wall during mouse heart organogenesis.

Apoptosis is an important mechanism in organogenesis, but its role in heart development has been poorly characterized. We have here studied apoptosis in the developing ventricular wall of mouse embryonic heart. Developing mice hearts on days 11 to 16 of gestation were studied using in situ end-labeling of degraded DNA (TUNEL), immunocytochemistry of regulatory genes Bcl-2 and Bax, and light and electron microscopy. TUNEL end-labeled apoptotic cells were found in the ventricular wall on days 11 to 16 of gestation. The proportions of apoptotic cells of all cells in the ventricular wall differed between the trabecular and compact regions (P = 0.003) and between the days of gestation (P = 0.0001), the calculated apoptotic index was greater in the compact region at all ages except day 14. Ultrastructural analysis showed typical apoptotic shrinkage, chromatin degradation, and apoptotic bodies in several myoblastic and myocardial endothelial cells which were also positive by DNA end-labeling. Immunocytochemical reaction for the apoptosis checkpoint proteins in the ventricular wall showed clearly more Bcl-2 positive cells than Bax positive cells. The numerical densities of all cells in the compact and trabecular regions remained always higher in the compact region (P = 0.04) despite the fact that apoptosis was present in both areas at the same time. In conclusion, apoptosis takes place in the developing myocardial muscle as well as the myocardial endothelium during ventricular morphogenesis on days 11 through 16 and decreases clearly on day 16. We suggest that apoptosis and its regulatory factors are closely involved in the morphogenesis of the ventricular wall of the mammalian heart.     

芹菜素对人肺癌A549细胞凋亡及相关蛋白Bax、Bcl-2表达的影响

目的研究芹菜素对人肺癌 A549细胞增殖抑制和凋亡诱导作用与 Bax、Bcl-2蛋白表达的影响。方法10~80μmol/L 不同浓度芹菜素作用 A549细胞,采用 MTT 法检测芹菜素对 A549细胞增殖抑制作用;Hoechst 33258细胞核染色法观察芹菜素诱导细胞凋亡形态学的变化;流式细胞仪 AnnexinV- FITC/PI 双染色法检测细胞凋亡率;Western blot 法检测凋亡相关蛋白 Bax 和 Bcl-2表达的变化。结果 MTT 法显示,芹菜素对 A549细胞有显著的增殖抑制作用（P <0.01）,且具浓度和时间依赖性;荧光显微镜下观察到芹菜素处理组细胞出现典型的凋亡形态学改变：细胞核固缩、染色质凝集和核碎片化等;流式细胞仪分析结果显示,芹菜素呈浓度依赖性诱导 A549细胞凋亡;Western blot结果显示,促凋亡蛋白 Bax 随着芹菜素浓度升高表达增加,抗凋亡蛋白 Bcl-2随着芹菜素浓度升高表达减少。结论芹菜素具有抑制人肺癌 A549细胞增殖,诱导其凋亡的作用,其机制可能与上调 Bax 蛋白表达和下调 Bcl-2蛋白表达有关。     

Expression of Bcl-2 family members and presence of Epstein-Barr virus in the regulation of cell growth and death in classical Hodgkin's lymphoma

AIMS: To examine the expression of the Bcl-2 family of proteins (Bcl-2, Bcl-x, Bcl-xL and Bax) in classical Hodgkin's lymphoma (cHL) and to correlate the expression of these proteins with proliferation, apoptosis and the presence of Epstein-Barr virus (EBV). METHODS AND RESULTS: Expression of the Bcl-2 family of proteins was detected by immunohistochemistry, proliferation was determined by Ki67 labelling and apoptosis by TUNEL in-situ hybridization. EBV was detected by Epstein-Barr virus early RNA (EBER) in-situ hybridization. Expression of Bcl-2, Bcl-x, Bcl-xL and Bax was detected in the Hodgkin/Reed-Sternberg (H/RS) cells in 43.7% (27/62), 87.5% (56/64), 67.2% (41/61) and 74.6% (47/63) of the cHL cases, respectively. EBER was detected in 53% (35/66) of the cases, whereas Ki67 was observed in 86.7% (52/60) of the cases. Apoptotic H/RS cells were observed infrequently, and only 43.2% (11/26) of the cases showed an apoptotic index of > or = 10% in the H/RS cells. A statistically significant inverse relationship was observed between the expression of Bcl-2 and the presence of EBV (P = 0.003). Bcl-xL showed an inverse correlation with apoptosis in the H/RS cells (P = 0.004). CONCLUSIONS: The higher Bcl-xL expression (67.2%) compared with Bcl-2 expression (43.5%) observed in cHL as well as the statistically significant inverse relationship between Bcl-xL and apoptosis suggests that Bcl-xL plays an important role in the survival of H/RS cells. Expression of Bax may be neutralized by other anti-apoptotic members of the family such as Bcl-2 and/or Bcl-xL.     

C5b-9 terminal complement complex assembly on apoptotic cells in human arterial wall with atherosclerosis

Apoptosis plays an important role in atherosclerosis. The factors regulating this process are not well defined. We examined the relation of apoptotic cells with the terminal complement complex C5b-9 in human atherosclerotic lesions. The extent of apoptosis was determined using TdT dUTP nick-end labeling (TUNEL) and immunohistochemistry of apoptosis regulators caspase-3, caspase-9, Bax, and Bcl-2. C5b-9 was localized by immunohistochemistry and immunoelectron microscopy. The apoptotic index was higher in fibrous plaques when compared with intimal fatty streaks and intimal thickenings. Bax expression was present in TUNEL+ apoptotic cells, and Bcl-2 was rarely present in the atherosclerotic wall. Active caspase 9 and caspase 3 deposits were present in the same areas, suggesting an involvement of the mitochondrial pathway. C5b-9 deposits colocalized with TUNEL+ cells, and the percent of double-positive cells was 2% in fatty streaks, 12% in intimal thickenings, and 35% in fibrous plaques. Colocalization of apoptotic cells with C5b-9 was also confirmed by immunoelectron microscopy. In conclusion, some apoptotic cells carry C5b-9 deposits, suggesting that complement might be activated by apoptotic cells and involved in the promotion of apoptosis, contributing to the progression of atherosclerotic lesions.     

CO and bilirubin inhibit doxorubicin-induced cardiac cell death

The clinical utility of anthracycline anticancer agents, especially doxorubicin (DOX), is limited by progressive toxic cardiomyopathy linked to cardiomyocyte apoptosis. This study examined the protective effects of CO and bilirubin on DOX-induced cardiomyocyte toxicity. In vitro, DOX significantly decreased the viability of H9c2 cells and increased apoptotic features, such as changes in nuclear morphology and caspase protease activation. CO and bilirubin significantly inhibited DOX-induced cell death and caspase-3 activation, which may be explained by increased Bcl-2 expression and inhibition of Bax expression. CO and bilirubin up-regulated the heme oxygenase-1 (HO-1), which was required for the protective effect of CO, and a single bilirubin treatment increased DOX-induced apoptosis in H9c2 cells. The inhibition of HO-1 with ZnPP resulted in a striking increase in apoptosis in the CO, bilirubin, and DOX-treated cells. Furthermore, HO-1 overexpression increased resistance against DOX-induced cytotoxicity in H9c2 cells. In conclusion, CO and bilirubin can inhibit DOX-induced apoptosis in H9c2 cardiomyocytes. These findings imply that the therapeutic index of anthracycline cancer chemotherapeutics can be improved by protecting against cardiomyocyte death.     

Taxol对宫颈癌U14细胞增殖、凋亡及α2,6-SA和ST6Gal mRNA表达的影响

目的:研究泰素(Taxol)对小鼠宫颈癌U14细胞株增殖、凋亡以及α2,6-唾液酸(SA)和α2,6-唾液酸转移酶(ST6Gal)mRNA表达的影响,为进一步探讨宫颈癌Taxol化疗机制提供新思路。方法:Taxol处理U14细胞后,MTT检测Taxol对U14细胞的IC_(50)值。流式细胞术检测细胞α2,6-SA、细胞凋亡相关因子(Bcl-2、Bax、caspase8和caspase 3)、凋亡率和细胞周期改变。qPCR检测ST6Gal1和ST6Gal2 mRNA的表达。结果:与对照组相比,Taxol对U14细胞有明显的抑制作用,减弱α2,6-SA荧光强度,上调Bax表达,下调Bcl-2表达,降低Bcl-2/Bax比值,并增强caspase 8和caspase 3活性;Taxol处理显著增加U14细胞凋亡率及S期细胞和G2/M期细胞比率,此外还下调ST6Gal1 mRNA表达。结论:α2,6-SA和ST6Gal可能参与了Taxol对U14细胞细胞周期和凋亡调控的多重作用。     

黄芪总黄酮对高糖下牛视网膜血管周细胞凋亡及凋亡基因表达的影响

目的探讨不同浓度黄芪总黄酮对高糖下原代培养的牛视网膜血管周细胞凋亡及凋亡基因表达的影响。方法以在体外培养3代近融合的牛视网膜血管周细胞为对象，分别在对照组（5．5mmol／L葡萄糖）、高糖模型组（25mmol／L）、干预组（在高糖组基础上分别加入0．5、1．0、2．0mg／ml黄芪总黄酮）中孵育6d，采用TUNEL法检测周细胞的凋亡率；RT—PCR测定Bcl-2、Bax基因的表达。结果（1）高糖下血管周细胞出现明显凋亡现象，高糖组血管周细胞凋亡率与对照组有显著差异（P〈0．01）。（2）高糖组诱导凋亡调节基因Bax表达增加，Bcl-2表达下降，与对照组有显著差异（P〈0．01）。（3）黄芪总黄酮各组血管周细胞凋亡率明显低于高糖组（P〈0．01），凋亡调节基因Bax表达下降，Bcl-2表达增加。在TFA各干预组之间，1．0mg／ml组与0．5mg／ml相比凋亡率低，Bax表达下降，Bcl-2表达增加（P〈0．01），但1．0mg／ml与2．0mg／ml组间凋亡率及凋亡基因表达无明显差异（P〉0．05）。结论黄芪总黄酮可能通过促使凋亡调节基因Bax表达下降，Bcl-2表达增加，抑制高糖诱导的牛视网膜微血管周细胞凋亡。