Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Proteins after Ischemia-reperfusion in Rats

In order to study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia/reperfusion （I/R） in vitro and the expression of Bcl-2 and Bax proteins, isolated rat hearts were perfused in a Langendorff model. Twenty-four rats were randomly divided into 3 groups （n=8 in each group）： control group was perfused for 120 min. In the I/R group, after 30 min stabilization the injury was induced by 30 min global ischemia followed by 60 min reperfusion. Ethyl pyruvate （EP） group was set up with the same protocol as I/R group except that it was supplied with 2 mmol/L EP 15 rain before ischemia and throughout reperfusion. Myocardial malonaldehyde （MDA） content was measured. Myocardial apoptotic index （AI） was tested by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） method. The expression of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax in cardiac myocytes was detected by immunohistochemistry. As compared with control group, the content of MDA, myocardial AI and the expression of Bcl-2, Bax proteins were increased significantly in I/R group, but the content of MDA, myocardial AI and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was up-regulated in EP group （P〈0.05）. These results demonstrate that EP could inhibit apoptosis of cardiac myocytes possibly via alleviating oxidative stress, up-regulating Bcl-2 and down-regulating Bax proteins.

Influence of Tanshinone lla on heat shock protein 70,Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury

Tanshinone lla is an effective monomer component of Danshen, which is a traditional Chinese medicine for activating blood circulation to dissipate blood stasis. Tanshinone Ila can effectively improve brain tissue ischemia/hypoxia injury. The present study established a rat model of spinal cord ischemia/reperfusion injury and intraperitoneally injected Tanshinone lla, 0.5 hour prior to model establishment. Results showed that Tanshinone Ila promoted heat shock protein 70 and Bcl-2 protein expression, but inhibited Bax protein expression in the injured spinal cord after ischemia/reperfusion injury. Furthermore, Nissl staining indicated a reduction in nerve cell apoptosis and fewer pathological lesions in the presence of Tanshinone Ila, compared with positive control Danshen injection.

Effects of L-Tetrahydropalmatine on the Expressions of bcl-2 and bax in Rat after Acute Global Cerebral Ischemia and Reperfusion

To investigate the effects of L-Tetrahydropalmatine (L-THP) on the expressions of bcl-2, bax and neuronal apoptosis after cerebral ischemia and reperfusion, 60 Wistars rats were randomly divided into 3 groups: sham-operation group (group S, n = 20), ischemic-reperfusion group treated with saline (group I, n=20) and ischemia-reperfusion group treated with L-THP (group T, n=20) .The rat model of global cerebral ischemia and reperfusion was induced by Pulsinelli's four-vessel occlusion method. The expression of bcl-2 and bax mRNA was detected by in situ hybridization and reverse transcriptional polymerase chain reaction (RT-PCR). The number of apoptotic neurons was examined by terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) method. Compared with group S, the expression of bcl-2 and bax mRNA in group I was increased significantly (P<0.01), and the number of apoptotic neurons increased either (P< 0.01). After L-THP treatment, the expression of bcl-2 mRNA was up-regulated (P<0.01) and that of bax mRNA was down-regulated (P<0.01); the number of apoptotic neurons was decreased (P<0.01). Our results indicated that bcl-2 may suppress apoptosis and bax promote apoptosis after cerebral ischemia and reperfusion. L-THP could ameliorate cerebral ischemia and reperfusion damage by reducing the apoptosis through regulating bcl-2 and bax.

THE EXPRESSION AND CLINICAL VALUE OF APOPTOSIS CONTROL GENE Bcl-2 AND Bax IN BREAST CANCER

Objective: To study the expression and clinical value of apoptosis control gene bcl-2 and bax in breast cancer. Methods: Protein bax and bcl-2 in 41 breast cancers obtained from operations in our hospital in 1996 were detected using ABC immunohistochemical stain assay and compared with 10 cases with normal breast tissues. Results: The positive rate of bax in normal breast tissue was 90% and in breast cancer was 59%, with a significant statistical difference between them (P<0.05), but there was no statistical difference in bcl-2 protein expression. Among the 41 breast cancer, the group with lymph node metastasis (21 cases) had obviously low bax expression (43%) and high bcl-2 expression (76%), showing significant difference to the group without lymph node metastasis (P<0.05). Conclusion: The antiapoptosis function of bcl-2 was stronger than bax in breast cancer. Protein bax and bcl-2 assay may be useful in understanding the biological behaviors of breast cancer.

鼠急性全脑缺血再灌注后葛根素对海马CA1区Bcl-2、Bax表达的影响

目的 观察全脑缺血再灌注后葛根素对神经细胞凋亡相关基因Bcl 2、Bax表达的影响。方法 采用免疫组织化学法、原位末端标记法检测大鼠全脑缺血再灌注不同时间内海马CA1区Bcl 2和Bax蛋白表达水平及凋亡细胞数的变化。结果 ①脑缺血再灌注后 ,海马CA1区Bcl 2蛋白的表达随再灌注时间不同而变化 ,缺血 10min后再灌注 6h达高峰 ;葛根素治疗组Bcl 2蛋白的表达于相应的时间点明显增加 ;②Bax蛋白表达在再灌注 2 4h达高峰 ,葛根素治疗组Bax蛋白表达在相应时间点则下降 ;③神经细胞凋亡数随再灌注时间延长而增加 ,葛根素可减少神经细胞凋亡数。结论 在全脑缺血再灌注后细胞凋亡中 ,Bcl 2、Bax发挥重要作用 ;葛根素通过上调Bcl 2蛋白的表达 。

脑缺血再灌注后神经元和内皮细胞凋亡与Bcl-2和Bax表达的时相关系

目的 探讨大鼠局灶性脑缺血再灌注后受损伤的神经细胞和血管内皮细胞凋亡 ,以及Bcl 2和Bax蛋白表达与再灌注时间的关系。 方法 应用原位末端标记 (TUNEL)技术和免疫组织化学方法 ,分别观察脑缺血再灌注 2h、6h、12h、2 4h、2d、3d、7d、14d和 2 1d等不同时间点神经细胞和血管内皮细胞凋亡数及Bcl 2和Bax蛋白的表达。 结果 1.脑缺血周围区 ,再灌注 2h神经细胞和内皮细胞凋亡开始明显增多 ,12～ 2 4h达高峰 ,之后逐渐减少 ,7～ 14d降至假手术组水平 ;血管内皮细胞凋亡迟于神经元凋亡约 12h。 2 .Bcl 2蛋白表达于缺血再灌注 2h开始逐渐增强 ,12～ 2 4h达高峰 ,之后逐渐下降 ,至 7～ 14d接近假手术组水平 ;3.Bax蛋白表达于缺血再灌注 6h开始逐步增高 ,2 4～ 4 8h达高峰 ,之后逐渐下降 ,至 14d与假手术组已无显著性差异。 4 .Bcl 2表达与细胞凋亡的时相变化基本一致 ,Bax表达时相迟于细胞凋亡。 结论 细胞凋亡是脑缺血再灌注损伤细胞死亡的形式之一 ,血管内皮细胞凋亡迟于神经细胞凋亡 ,Bcl 2和Bax参与细胞凋亡的调节。

心脑舒通胶囊对高脂血症大鼠心肌梗死后心肌细胞凋亡及Bax、Bcl-2蛋白表达的影响

目的观察心脑舒通胶囊(主要起效成分为蒺藜总皂苷)对高脂血症大鼠心肌梗死(MI)后心肌细胞凋亡及Bax、Bcl-2蛋白表达的影响,探讨蒺藜皂苷抗高脂大鼠MI后心室重构的作用机制。方法利用高脂血症心肌梗死复合模型,采用TUNEL和免疫组化SP法,观察蒺藜总皂苷对MI后大鼠心肌细胞凋亡、以及Bax、Bcl-2蛋白表达的影响。结果(1)蒺藜总皂苷可减轻MI后心肌细胞损伤和心室重构的程度;(2)与高脂心梗组相比,蒺藜总皂苷大剂量、辛伐他汀均降低MI后心肌细胞凋亡指数,并能下调Bax蛋白表达(P<0．05),各治疗组之间作用比较,差异无显著性(P>0．05)。结论蒺藜总皂苷可通过调控Bax／Bcl-2蛋白表达比值,而抑制心肌细胞凋亡,可能是其抗MI后心室重构的作用机制之一。

双歧杆菌脂磷壁酸对衰老小鼠胸腺细胞凋亡及Bcl-2和Bax蛋白表达的影响

目的研究双歧杆菌表面分子脂磷壁酸(LTA)对衰老小鼠胸腺细胞凋亡及Bcl-2、Bax蛋白表达的影响,探讨双歧杆菌抗衰老的分子机制。方法选择30只小鼠,将其随机分为衰老模型组、LTA治疗组和青年对照组,前两组用D-半乳糖建立衰老小鼠模型,LTA治疗组用双歧杆菌LTA治疗。用原位末端标记法检测胸腺细胞凋亡,用免疫组化法检测胸腺Bcl-2、Bax的表达,并计算Bax/Bcl-2的比值。结果与青年对照组相比,衰老模型组胸腺细胞凋亡指数显著升高,Bcl-2蛋白表达量显著降低,Bax蛋白表达量显著升高,Bcl-2/Bax比值显著降低,差异均有统计学意义(P<0.01)。LTA治疗组上述指标与青年对照组比较,差异无统计学意义(P>0.05)。结论双歧杆菌LTA能延缓胸腺细胞凋亡,使Bcl-2/Bax比值优化,具有抗衰老作用。

前脑缺血再灌注后海马神经元Bcl-2和Bax蛋白的表达及刺五加皂甙的影响

目的 :观察前脑缺血再灌注后海马区神经元Bcl -2、Bax的表达及刺五加皂甙对其表达的影响。方法 :SD大鼠随机分为假手术组 (SAM)、缺血再灌注组 (IR)及刺五加皂甙治疗组 (ASS) ,并根据再灌注不同时间分为五个亚组 ,缺血时间均为 2 0分钟。分别于再灌注 3、6、12、2 4、48小时后取脑组织标本。采用免疫组化检测大鼠脑海马的Bcl -2、Bax蛋白表达水平。结果 :Bcl-2蛋白表达 :假手术组呈阴性表达 ,缺血再灌注组再灌注后 6小时可在CA3区检测到Bcl-2阳性神经元 ,2 4小时达峰值 ,48小时逐渐下降。刺五加皂甙组表达时间及部位同缺血再灌注组 ,与缺血再灌注组对应时间点相比都有显著性增高。Bax蛋白表达 :假手术组海马区呈阴性表达 ,缺血再灌注 12小时在海马CA1区开始表达 ,48小时达峰值 ,刺五加皂甙组表达时间及部位同缺血再灌注组 ,与缺血再灌注组对应时间点相比 ,都有显著性减少。结论 :刺五加皂甙可通过增加Bcl-2表达 ,抑制Bax表达 ,从而抑制脑缺血再灌注时神经细胞凋亡 。

活血化瘀汤对大鼠视网膜急性损伤后Bcl-2和Bax蛋白表达的影响

目的观察大鼠视网膜急性损伤后Bcl-2和Bax蛋白表达的变化及活血化瘀汤干预的结果。方法随机将65只大鼠分为3组:对照组(A组)、加压组(B组)、加压+活血化瘀汤组(C组)。用免疫组化法检测3组大鼠视网膜急性损伤后不同时间点Bcl-2和Bax蛋白的表达。结果A组视网膜神经节细胞层可见一定量的Bcl-2和Bax蛋白表达;B组Bcl-2蛋白表达在2 h开始升高,36 h达峰值,72 h恢复正常,12 h到48 h各时间点与A组的差异有统计学意义(P<0.01);Bax蛋白表达的变化与Bcl-2相近,不同的是达峰值在24 h。C组12 h至48 h与B组相应时间点比较,Bcl-2蛋白表达的差异有统计学意义(P<0.05),Bax蛋白表达与B组的差异无统计学意义(P>0.05)。结论急性视网膜损伤后Bcl-2、Bax蛋白表达均升高,活血化瘀汤上调了Bcl-2蛋白表达,未影响Bax蛋白表达。

脾虚模型小鼠肾脏中Bcl-2、Bax和Fas蛋白表达研究

目的:采用灌胃法诱导SD清洁级小鼠脾虚动物模型,造模完成后检测小鼠肾脏中Bcl-2、Fas和Bax蛋白表达的改变,并探讨其意义。方法:采用大承气汤诱导小鼠脾虚模型,H.E染色后光镜下观察肾脏局部形态,SP法检测Bcl-2、Fas和Bax蛋白在肾脏细胞中的表达。结果:脾虚组小鼠肾小球部位出现炎症,肾近曲小管和远曲小管部位出现凝固性坏死;肾脏细胞中Bax和Fas蛋白的表达率升高(P<0.05),Bcl-2表达降低(P<0.05)。结论:脾虚会引发肾脏发生病理变化,同时会使Bax和Fas蛋白的表达升高,Bcl-2蛋白的表达下降,增加了肾脏细胞发生凋亡的机率。

透骨草提取物对人结肠癌SWⅢ-C细胞增殖及Bcl-2、Bax蛋白表达的影响

目的：观察透骨草提取物对人结肠癌SWⅢ-C细胞增殖的影响,探讨透骨革提取物对SWⅢ-C细胞增殖影响的分子机制.方法：MTT法检测透骨草提取物对SWⅢ-C细胞增殖的影响,荧光显微镜观察透骨草提取物对SWⅢ-C细胞形态的影响,免疫组化方法检测SWⅢ-C细胞Bcl-2和Bax蛋白的表达。结果：6.25～100μg/mL透骨草提取物处理的SWⅢ-C细胞增殖抑制率与对照组相比显著增加（P＜0.05）,而且随透骨草浓度的增加,抑制率逐渐增加。透骨萆提取物对SWⅢ-C细胞的半数抑制浓度（IC50）为38.36μg/mL。荧光显微镜下可见,38.36μg/mL透骨革提取物处理的SWⅢ-C细胞,体积缩小,细胞核固缩、呈新月状且边集.38.36μg/mL透骨草提取物处理的SWⅢ-C细胞Bcl-2蛋白表达显著低于对照组（P＜0.05）,而Bax蛋白表达明显高于对照组（P＜0.05）。结论：透骨苹提取物可以抑制人结肠癌SWⅢ-C细胞增殖,诱导SWⅢ-C细胞凋亡,其机制可能与下调Bcl-2蛋白表达、上调Bax蛋白表达有关。

乌司他丁对脊髓损伤后大鼠凋亡因子Bcl-2和Bax表达的影响

目的观察乌司他丁对脊髓损伤(SCI)后凋亡因子Bcl-2和Bax表达的影响。方法雌性SD大鼠64只,参照Allen’s WD法,制成中度SCI模型,随机分为乌司他丁组和对照组,分别测定大鼠SCI后3和7 d BBB评分及用免疫组化法检测脊髓组织Bcl-2和Bax表达。结果乌司他丁组在术后3和7 d的BBB评分均比对照组高,两组比较差异有显著性;免疫组化结果乌司他丁组Bcl-2阳性细胞数明显多于对照组(P<0.05);乌司他丁组Bax阳性细胞数则明显低于对照组(P<0.05)。结论乌司他丁能促进Bcl-2蛋白表达增多,抑制Bax蛋白表达。

扶正抑瘤颗粒对H_(22)瘤细胞bax、bcl-2及caspase-3蛋白表达的影响

目的观察扶正抑瘤颗粒对H22瘤细胞bax、bcl-2及caspase-3蛋白表达的影响。方法采用免疫组织化学方法检测瘤组织切片中bax、bcl-2及caspase-3的蛋白表达。结果扶正抑瘤颗粒各治疗组bax及caspase-3的IOD值均高于模型组,与模型组比较有显著性差异(P<0.05);扶正抑瘤颗粒各治疗组bcl-2的IOD值均低于模型组,与模型组比较有显著性差异(P<0.05)。结论通过促进bax及caspase-3的蛋白表达、抑制bcl-2基因的蛋白表达来诱导H22瘤细胞凋亡,进而发挥抑瘤效应。

克林霉素对穿通支原体诱导小鼠膀胱移行细胞癌Bcl-2、Bax蛋白表达的影响

目的:探讨克林霉素对穿通支原体(Mycoplsama penetrans,Mpe)诱导免疫缺陷小鼠膀胱移行细胞癌凋亡相关蛋白表达的影响。方法:50只ICR免疫抑制小鼠,分克林霉素干预试验组(n=20只)上行感染0.1 ml Mpe(6×108-9/ml),连续3天,同时肌肉注射克林霉素(25 mg/kg.d),连续保护4天;Mpe非干预对照组(n=20)上行感染相同菌量Mpe,连续3天;NS对照组(n=10)上行感染相同剂量的NS,连续3天。各组在8、18周分批宰杀,取8周小鼠血清Mpe再培养,观察8周、18周小鼠膀胱超微结构的形态学改变,同时用免疫组化检测凋亡相关蛋白Bcl-2及Bax表达的变化。结果:克林霉素干预组较非干预组Mpe菌落显著减少。光镜和电镜结果显示克林霉素干预组小鼠的膀胱组织超微结构未见多核仁等分裂相。免疫组化显示克林霉素干预组较非干预组小鼠膀胱移行上皮细胞凋亡相关蛋白Bcl-2表达显著降低(P<0.05),Bcl-2/Bax比值降低。结论:克林霉素可降低膀胱移行上皮细胞Bcl-2的表达,此结果提示克林霉素对穿通支原体诱导小鼠膀胱移行上皮细胞癌具有一定干预作用。

小檗碱在调控Bcl-2/Bax信号通路诱导细胞凋亡应用效果与研究进展

小檗碱主要是从黄连根茎中提取的天然活性成分,与多个细胞内靶标相互作用,具有抗氧化、抗炎、抗菌等多种广泛的药理活性。细胞凋亡作为一种重要的细胞死亡方式,在生物体的发育、免疫系统的调节、肿瘤抑制以及组织修复等方面扮演着重要的角色。既往研究初步证实,小檗碱能够通过调控细胞凋亡起到治疗神经系统、心血管系统、消化系统以及免疫系统等相关疾病的作用,主要体现在其影响细胞凋亡相关蛋白表达及信号通路的转导上,尤其是Bcl-2/Bax信号通路。Bcl-2/Bax作为细胞凋亡通路中的重要调节者,在神经、心血管、消化以及免疫系统疾病的发生和发展中发挥重要作用,然而,小檗碱在这些疾病中如何调控细胞凋亡的机制仍有待进一步研究。相关研究证实小檗碱在阿尔茨海默病、帕金森、亨廷顿病等疾病中可调控Bcl-2/Bax信号通路诱导的细胞凋亡起到神经系统保护作用;其在阿霉素或缺氧诱导心脏损伤、心肌缺血/再灌注损伤、以及心肌梗死后心力衰竭等疾病中可调控Bcl-2/Bax信号通路诱导的细胞凋亡发挥对心血管系统的保护作用;其在幽门螺杆菌诱导胃损伤、慢性萎缩性胃炎、脓毒症并发肠损伤以及放射性肠炎等疾病中均可调控Bcl-2/Bax信号通路诱导的细胞凋亡发挥对胃肠道系统的保护作用;其在类风湿关节炎、结直肠癌、宫颈癌以及三阴性乳腺癌等疾病中均可调控Bcl-2/Bax信号通路诱导的细胞凋亡,发挥对免疫系统的保护作用。文章从Bcl-2/Bax信号通路角度对小檗碱介导细胞凋亡的作用机理进行系统综述,以期为小檗碱在疾病临床治疗中的应用提供科学依据。

Effect of Bak Foong Pills on the expression of β-amyloid in rat retina with optic nerve transection

AIM:To investigate the effect of Bak Foong Pills(BFP) on the expression of β-amyloid(Aβ) in rats retina with optic nerve transaction,and its roles and possible mechanisms in protecting optic nerve damage.· METHODS:Seventy-two healthy,Sprague-Dawley,adult rats were randomly assigned to three groups:negative control group(control group),optic nerve transection group(model group) and BFP treatment group(BFP group,100μg/mL) followed by establishing optic nerve transection model.The expression of Aβ was measured at 48 hours by Western-blotting.Moreover,the expressions of Bcl-2,Bax and Caspase-3 mRNA were evaluated at 48 hours by reverse transcriptase polymerase chain reaction(RT-PCR).RESULTS:There were significant differences among the control,model and BFP groups in the expression of Aβ(all P <0.01).Aβ expression was significantly higher in the model and BFP groups than that in the control group(P < 0.01),with a more significant reduction in the BFP group than that in the model group(P <0.01).Moreover,there were also significant differences among the three groups in the expressions of Bcl-2/Bax(Bcl-2:anti-apoptotic;Bax:proapoptotic) and Caspase-3 mRNA(proapoptotic)(all P<0.01).Bcl-2/Bax ratio was significantly lower and Caspase-3 mRNA expression was significantly higher in the model and BFP groups than those in the control group(P <0.01),with a significant growing of Bcl-2/Bax and reduction of Caspase-3 in the BFP group than those in the model group(P<0.01).· CONCLUSION:BFP can down-regulate Aβ expression in retina and may inhibit apoptosis and protect optic nerve by enhancing Bcl-2/Bax ratio and inhibiting Caspase-3 pathway.

Influence of Moxibustion Serum on the Expression of Fas bcl-2 mRNA and Protein of EL-4 Lymphoma Cells

Objective： To observe the influence of moxibustion serum of mice on the expression of Fas, bcl-2 mRNA and protein of EL-4 lymphoma cells in vitro. Method： The EL-4 lymphoma cells were cultivated for 24 h in the moxibustion serum of mice. The expression of Fas and bcl-2 mRNA of EL-4 lymphoma cells were detected by in-situ hybridization method, and the protein expression of Fas and bcl-2 were observed by the immuocytochemistry method. Results： The expression of bcl-2 mRNA and protein decreased , and the expression of Fas mRNA and protein increased significantly in EL-4 cells, which were cultivated in the moxibustion serum compared those cultivated in normal mice serum （P〈0.05）. Conclusion： Moxibustion serum could down-regulate the bcl-2 mRNA and protein and up-regulate the Fas mRNA and protein of EL-4 cells.

CIK细胞对MGC-803胃癌细胞株的诱导凋亡作用

目的 研究多种细胞因子诱导的杀伤细胞(CYtokine-inducedkillcells,CIK)对MGC -80 3胃癌细胞株的诱导凋亡作用,并探讨其作用机制。方法 应用(TdT -mediateddUTPnickendla beling)TUNEL法检测CIK细胞诱导凋亡的情况;通过免疫细胞化学法测定Bcl- 2、Bax的阳性表达率,深入研究CIK细胞对MGC - 80 3胃癌细胞株凋亡相关基因蛋白表达的影响。结果 TUNEL法检测对照组成不染或均匀淡蓝色,实验组凋亡细胞缩小,核或核周成深蓝色。CIK实验组5～1 4小时凋亡率上调,1 4～2 4小时凋亡率下降。CIK实验组凋亡率与对照组相比有显著性差异(P <0 .0 1 )。免疫细胞化学结果表明:Bcl- 2蛋白随作用时间延长表达均下降,Bax蛋白表达上调,与对照组相比均有显著性差异(P <0 .0 1 )。结论 CIK细胞对MGC - 80 3胃癌细胞早期诱导凋亡,晚期诱导肿瘤细胞坏死。其作用机制之一可能是通过上调Bax,下调Bcl- 2的蛋白表达实现的。

人退变椎间盘组织细胞凋亡相关基因表达的初步研究

目的探讨细胞凋亡与腰椎间盘退变的发生机制。方法一步法抽提6例退变及6例正常椎间盘组织的总RNA,分别用cy3,cy5荧光标记,获得两组椎间盘cDNA的探针,与cDNA表达谱芯片杂交,扫描芯片荧光信号图像,对所获得的凋亡相关基因进行生物信息学分析。采用原位末端标记法(TUNEL)和免疫组化方法,检测12例人退变椎间盘及10例正常椎间盘组织的细胞凋亡状态及凋亡相关基因Bcl-2、Bax蛋白的表达。结果在4096条基因中,与细胞凋亡相关类蛋白为10条,其中Bax蛋白相关基因表达增高,Bcl-2蛋白相关基因表达降低。正常组TUNEL检测凋亡指数(AI)为(24.897±3.620),Bcl-2阳性细胞百分率为(31.440±4.150)%,Bax阳性细胞百分率为(29.372±2.588)%,阳性颗粒平均光密度值分别为(0.183±0.010)、(0.203±0.012)和(0.169±0.005);退变组AI为(49.232±3.440),Bcl-2阳性细胞百分率为(18.239±2.470)%,Bax阳性细胞百分率为(52.349±3.764)%,阳性颗粒平均光密度值分别为(0.152±0.003)、(0.310±0.008)和(0.262±0.014),两组间的AI均值、Bcl-2、Bax蛋白表达均有显著性差异(P<0.05)。结论细胞凋亡在椎间盘退变的进程中发挥重要作用,凋亡相关基因Bcl-2和Bax参与了髓核细胞凋亡的发生和发展过程。