大豆异黄酮对雌性大鼠内分泌功能的影响

目的动物实验观察大豆异黄酮对雌性大鼠内分泌功能的影响。方法12周龄雌性大鼠42只随机分配为三组：低剂量组每日灌胃大豆异黄酮40mg·kg^-1·d^-1,高剂量组每日灌胃大豆异黄酮80mg·kg^-1·d^-1,对照组灌胃0．9％氯化钠注射液。14d后颈静脉取血,采用化学发光法分别测定促卵泡生成素（FSH）、促黄体生成素（LH）、雌二醇（E2）和孕酮（P）四项指标。结果大豆异黄酮低剂量组、高剂量组和对照组三组FSH分别为（0．13±0．02）mIu／ml、（0．12±0．02）mIu／ml、（0．15±0．02）mIu／ml,LH分别为（0．17±0．03）mlu／ml、（O．15±0．04）mIu／ml、（0．18±0．05）mIu／ml,三组相比较差异无统计学意义（P〉0．05）;三组E2分别为（0．09±0．03）nmol／L、（0．03±0．03）nmol／L、（0．12±O．04）nmol／L;P分别为（1．43±0．27）ng／ml、（2．82±0．37）-s／ml、（0．67±0．56）ng／ml。三组相比较大豆异黄酮组的E2活性明显降低（P〈0．01）,尤其高剂量组的降低更为显著。大豆异黄酮组的P水平较对照组明显升高（P〈0．01）,而高剂量组P的升高更为显著。结论大豆异黄酮对大鼠的垂体激素无明显影响,不同剂量的大豆异黄酮可能通过雌激素活性和抗雌激素活性而影响雌性大鼠卵巢激素的分泌调节。     

毛蕊异黄酮对免疫性肝损伤的保护作用

目的: 研究毛蕊异黄酮对急性免疫性肝损伤小鼠肝脏的保护作用及机制。方法: 毛蕊异黄酮(4, 2, 1 mg·kg^-1)连续10 d预防性给药后,采用刀豆蛋白A(ConA)诱导小鼠急性免疫性肝损伤,12 h后摘眼球取血,比色法测定小鼠血清中丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)活性;处死小鼠分离肝脏、脾脏并称重,计算肝脾指数;制备肝脏匀浆比色法测定超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;HE染色观察肝脏病理组织学变化并进行病理分级;免疫组化法检测肝组织雌激素受体(ER)定位并进行半定量分析。结果: 毛蕊异黄酮可明显减轻由ConA所致的病理损伤,降低免疫性肝损伤肝脏的肝脾指数、ALT、AST活性及MDA含量,升高SOD活性,增加ER的表达。结论: 毛蕊异黄酮对ConA致急性免疫性肝损伤小鼠肝脏具有保护作用,可能与其抗氧化自由基作用及促进肝脏ER表达增强雌激素样作用有关。     

三羟异黄酮对大鼠缺血性脑损伤神经组织的保护作用

目的探讨植物性雌激素三羟异黄酮（GST）对局灶性永久性脑缺血成年雄性大鼠大脑皮层神经组织的保护作用。方法实验分为假手术组、缺血组、GST组和溶剂对照组,采用HE染色、甲苯胺蓝染色和电子显微镜观察的方法,研究颈内动脉注射GST应急治疗对雄性大鼠局灶性永久性脑缺血模型中大脑皮层神经组织神经元,突触和血-脑脊液屏障的保护作用。结果GST组与缺血组比较,神经元、突触和血-脑脊液屏障的损伤均明显减轻。结论GST应急治疗对缺血性脑损伤的神经组织具有明显的保护作用。     

大豆异黄酮对糖尿病大鼠肾脏的保护作用及其机制

目的探讨大豆异黄酮(SI)对糖尿病大鼠肾脏保护作用及其机制。方法建立链脲佐菌素诱导的糖尿病大鼠模型,将模型大鼠随机分为糖尿病组(DM组)、大豆异黄酮低[40 mg/(kg·d),SI1组]、中[120mg/(kg·d),SI2组]、高[360 mg/(kg·d),SI3组]及正常对照组(NC组)。8周末检测大鼠血糖、24 h尿蛋白、肾指数、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、血清肌酐(SCr)、血尿素氮(BUN)水平;Western blot检测肾组织nephrin表达。结果 SI3组尿蛋白(0.88±0.15)mg·d-1、肾指数(4.16±0.36)mg·g-1与DM组尿蛋白(1.26±0.45)mg·d-1、肾指数(6.13±0.76)mg·g-1比较明显降低(P<0.05);SI2组TC(2.07±0.52)mmol·L-1、TG(0.99±0.07)mmol·L-1、LDL-C(0.75±0.03)mmol·L-1和BUN(13.37±5.393)mmol·L-1与DM组TC(2.75±0.47)mmol·L-1、TG(1.36±0.35)mmol·L-1、LDL-C(0.83±0.01)mmol·L-1、BUN(24.32±6.31)mmol·L-1比较亦有明显降低(P<0.05);Western blot结果显示DM组nephrin蛋白表达较NC组显著降低(P<0.05),但SI使nephrin蛋白表达增加(P<0.05),且呈剂量依赖性。结论 SI保护糖尿病大鼠肾脏的机制可能部分与增加nephrin表达有关。     

葛花异黄酮对大鼠缺血性脑卒中的保护作用

目的 研究葛花异黄酮对大鼠脑缺血再灌注脑组织损伤的保护作用及机制。方法 将Wistar大鼠随机分为假手术组、模型组、实验组和阳性组。假手术组只分离双侧颈总动脉不进行结扎缺血;模型组、实验组和阳性组进行结扎缺血;实验组提前7天预防性灌胃给药160 mg·kg^-1葛花异黄酮;阳性组提前7天预防性灌胃给药10 mg·kg^-1依达拉奉。用脑缺血-再灌注模型对葛花异黄酮抗缺血性脑卒中活性进行评价,测定脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、髓过氧化物酶(MPO)、乳酸脱氢酶(LDH)活性,并通过蛋白质印迹法检测血红素氧化酶1(HO-1)、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)蛋白表达,从抗氧化应激与凋亡方面探讨葛花异黄酮对大鼠缺血性脑卒中的保护作用。结果 假手术组、模型组、实验组和阳性组的神经功能评分分别为0、(8.30±1.09)、(5.40±2.11)、(7.20±2.01)分;脑组织含水量分别为(78.50±3.60)%、(85.40±2.60)%、(77.50±2.40)%、(79.30±2.25)%;脑梗死...     

宁神合剂对实验性更年期雌性大鼠性激素的影响

目的　探索复方宁神合剂对实验性更年期雌性大鼠生殖内分泌系统的影响。方法　通过大鼠去卵巢手术制作更年期造模,以更年安为对照,宁神合剂分大、中、小剂量组,观察各组大鼠促卵泡激素(FSH)、促黄体生成激素(LH)、雌二醇(E2 )的变化。结果　宁神合剂各组E2 含量与模型对照组比较,P均<0. 0 5 ;更年安组大鼠FSH、LH、E2 含量与宁神合剂各组相当(P >0 . 0 5 )。结论　宁神合剂具有提高去卵巢大鼠E2 的水平,可能是其作用机制之一。     

葛根异黄酮对MPP~+诱导的PC12细胞凋亡的保护作用

目的探讨葛根异黄酮(Total isoflavones from puerarialobata,TIP)对甲基-苯基-吡啶离子(1-methyl-4-phenylpyr-idinium,MPP+)诱导的PC12细胞凋亡的保护作用及其机制。方法用不同浓度TIP预处理体外培养的PC12细胞后,加入MPP+诱导多巴胺能神经损伤模型,用MTT法检测PC12细胞活力,采用实时定量RT-PCR检测Bcl-2和BaxmRNA的表达水平。结果MPP+处理48~96 h,细胞活力较空白对照组降低,阴性对照组Bax 2-ΔΔCt升高,而Bcl-22-ΔΔCt降低,差异具有统计学意义(P<0.05)。与阴性对照组比较,葛根异黄酮组Bax 2-ΔΔCt降低,而Bcl-2 2-ΔΔCt升高,差异具有统计学意义(P<0.05)。结论葛根异黄酮对MPP+诱导的PC12细胞凋亡具有抑制作用,下调Bax和上调Bcl-2 mRNA表达可能是其作用的机制之一。     

脉冲电磁场对体外成骨细胞的作用及影响

体外培养成骨细胞给予适当强度和频率的脉冲电磁场作用,可以促进成骨细胞的增殖、分化和钙盐分泌,改变细胞内钙离子的浓度,诱导细胞膜表面的生长因子的分泌,促进成骨细胞的成骨作用。进而加速骨折的愈合速度,为骨组织工程的发展起到了推动的作用。     

三羟异黄酮对大鼠肠缺血再灌注损伤的保护作用

目的:探讨三羟异黄酮对肠缺血再灌注损伤的保护作用及其机制。方法:24只雄性Wistar大鼠,随机分为3组,每组8只:假手术组、肠缺血再灌注损伤(模型)组和三羟异黄酮组。模型组大鼠肠系膜上动脉被夹闭1 h,然后开放2 h。三羟异黄酮组大鼠在肠缺血前5 min,静脉注射三羟异黄酮1.0 mg.kg-1。假手术组仅暴露肠系膜上动脉。再灌注2 h处死动物取肠标本,观察肠组织病理学变化,测定肠组织湿/干重比(W/D)、髓过氧化物酶(MPO)活性和血浆D-乳酸含量,检测肠组织细胞间粘附分子1(ICAM-1)蛋白表达水平。结果:与假手术组比较,模型组、三羟异黄酮组肠损伤严重,W/D、MPO活性、血浆D-乳酸含量和ICAM-1表达升高(P<0.05或0.01);与模型组比较,三羟异黄酮组肠损伤明显减轻,W/D、MPO活性、血浆D-乳酸含量和ICAM-1表达降低(P<0.05或0.01)。病理学结果显示假手术组肠组织结构正常,模型组损伤严重,三羟异黄酮组轻度损伤。结论:三羟异黄酮对肠缺血再灌注损伤具有保护作用,其机制可能与其下调ICAM-1的表达而抑制中性粒细胞在肠组织的聚集、激活有关。     

葛花异黄酮对急性心肌梗死小鼠心肌的保护作用

目的通过小鼠急性心肌梗死模型观察葛花异黄酮对缺血心肌的影响,并探讨其作用机制。方法开胸结扎左冠状动脉前降支建立小鼠急性心肌梗死模型,以丹参注射液为阳性对照,观察葛花总黄酮低、高剂量组对心肌梗死面积、血清心肌酶、血清SOD和MDA含量的影响;并通过RT-PCR的方法,检测葛花总黄酮对缺血心肌β-肾上腺受体激酶1(β-adrenergic receptor kinase,β-ARK1)表达的影响。结果葛花总黄酮可明显缩小小鼠心肌梗死面积,降低血清心肌酶和MDA含量,下调心肌β-ARK1 mRNA的表达,并随着剂量的增加其作用加强。结论葛花总黄酮对急性心肌梗死小鼠心肌有明显的保护作用,其作用机制与其抗氧化损伤及下调心肌β-ARK1mRNA的表达有关。     

低频脉冲电磁场治疗骨质疏松症患者的疗效观察

目的 观察低频脉冲电磁场对原发性骨质疏松症的疗效.方法 用低频脉冲电磁场治疗30例骨质疏松症患者,观察患者骨痛的缓解情况、血清骨钙素、β-Ⅰ型胶原羧基前肽水平、骨密度变化情况.结果 患者骨痛缓解率达到57.7%,治疗前后血清骨钙素、β-Ⅰ型胶原羧基前肽水平、骨密度均有显著性差异.结论 低频脉冲电磁场能有效缓解骨质疏松患者的骨痛症状,提高骨密度,是治疗原发性骨质疏松症的有效方法之一.     

脉冲电磁场物理干预治疗Ⅱ型骨质疏松症疗效研究

目的观察脉冲电磁场治疗对Ⅱ型骨质疏松患者的疗效。方法对比分析70例Ⅱ型骨质疏松患者经脉冲电磁场治疗前后骨密度变化及腰背疼痛改善的情况。结果治疗3个疗程后,72.86%患者疼痛消失,22.86%疼痛改善,4.28%疼痛无改善,总有效率为95.72%;经脉冲电磁场治疗3个疗程完成后2～6个月复查骨密度,有31例患者骨密度值明显增加(P<0.05);39例患者骨密度值无升高。结论脉冲电磁场治疗Ⅱ型骨质疏松具有较好的疗效。     

Reproductive and teratologic effects of electromagnetic fields

The reproductive risks of electromagnetic fields (EMF) were evaluated based on an extensive review of the scientific literature pertaining to human epidemiologic studies, secular trend data, in vivo animal studies and in vitro studies, and biologic plausibility. The epidemiologic studies involving the reproductive effects of EMF exposures to human populations have included populations exposed to: (1) video display terminals (VDTs), and (2) power lines and household appliances. The clinical use of diagnostic MRI (magnetic resonance imaging) has been increasing, but there are few reports or studies of pregnant women or individuals of reproductive age who have been exposed to MRI, and whose reproductive performance has been evaluated. The population that has been studied most frequently are women exposed to VDTs, but their EMF exposures are extremely low and frequently are at the level of the ambient EMF in a house or office. The results of epidemiologic studies involving VDTs are generally negataive for the reproductive effects that have been studied. Based on the number of studies, the exposure levels, and the fairly consistent results, it can be argued that VDT epidemiologic studies should no longer be given priority. There have been fewer studies concerned with the reproductive risks of power lines, electric substations, and home appliances. In some publications, positive findings for reproductive risks were reported, but the more consistent findings indicate that EMF, even at these higher exposures, do not generate a measurable increase in reproductive failures in the human population. When compared to other fields of human epidemiology, it is obvious that these studies have many difficulties. Exposures are rarely determined. Studies frequently involve small sample sizes and the investigators rarely have a combined expertise in EMF physics, engineering, and reproductive biology. Because of the allegation that there may be particular windows of frequency, wave shape, and intensity that may be deleterious, it is impossible to disregard low frequency EMF exposures as having no deleterious reproductive effects. Yet the epidemiologic data that are available would point in that direction. Secular trend data analysis of birth defect incidence data indicate that increasing generation of electric power during this century is not associated with a concomitant rise in the incidence of birth defects. There are over 70 EMF research projects dealing with animal and in vitro studies that are concerned with some aspect of reproduction and growth. Unfortunately, a large proportion of the embryology studies utilized the chick embryo and evaluated the presence or absence of teratogenesis after 48 to 52 hours of development. The chick embryo studies were of little assistance to the epidemiologist or clinician in determining whether EMF exposure represents a hazard to the human embryo, and the results were, in any case, inconsistent. Embryo culture or cell culture studies are also of little assistance in determining the human risk of EMF. In vitro or in vivo studies in nonhuman species can be used to study mechanisms and the effects that have been suggested by human investigations. Only well designed whole-animal teratology studies are appropriate when the epidemiologists and clinical teratologists are uncertain about the environmental risks. Other aspects of reproductive failure such as abortion, infertility, stillbirth, and prematurity cannot be addressed by in vitro or culture experiments. In fact, it is very difficult to design and interpret nonprimate in vivo studies. Biologic plausability for teratogenesis can be supported if an agent such as EMF can be demonstrated to be cytotoxic or mutagenic. The studies dealing with mutagenesis, cell death, and cell proliferation using in vitro systems do not indicate that EMF have the potential for deleteriously affecting proliferating and differentiating embryonic cells at the exposures to which populations are usually exposed. Of course, there is no environmental agent that has no effect, deleterious or not, at very high exposures. While there does not appear to be measurable risk of reproductive failure and birth defects from EMF exposures in humans, a modest program of investigation is warranted epidemiologically and in the laboratory to answer some of the issues that have been raised that need clarification. It does not appear that the risk of EMF exposure is significant and, therefore, although preparing conducted research in the area of EMF risks is appropriate, it does not necessitate a massive expenditure of resources.     

Evaluation of testicular degeneration induced by low-frequency electromagnetic fields

The population exposure to electromagnetic fields (EMF) has been growing in recent decades. The generation, distribution and use of electric energy can generate low-frequency electromagnetic fields. The present study investigates the effects of EMF (60 Hz and 1 mT) on spermatogenesis of rats during different periods of maturation. Wistar rats were exposed to EMF from day 13 of gestation to postnatal day 21 or 90 in three daily applications of 30 min. Plasma testosterone concentration was not changed by EMF exposure; however, histopathological and histomorphometrical analyses of the testes showed testicular degeneration in a subset of animals exposed to EMF. The magnitude of the degenerative process varied between those individuals affected, indicating different individual sensitivity to EMF. The main alterations observed through transmission electron microscopy were highly electron-dense mitochondria with loss of their organization and cristae. Exposure to 60 Hz and 1 mT EMF can disturb spermatogenesis and may produce subfertility or infertility.     

大豆异黄酮对去卵巢大鼠血液生化指标的影响

目的研究大豆异黄酮对去卵巢大鼠血液生化指标的影响。方法将4月龄雌性SD大鼠摘除卵巢，按体重分成6组，分别给予不同剂量的大豆异黄酮或／和钙粉。连续灌胃饲养二个半月后，断头处死，收集血样并测定生化指标，采集右股骨、右胫骨、子宫并称重。结果大豆异黄酮对大鼠体重和子宫重量均有影响，可抑制去卵巢大鼠的代偿性增重和促进子宫的生长。大豆异黄酮对去卵巢大鼠血清钙、磷和骨钙素的影响不大，碱性磷酸酶活性稍有降低，血清雌二醇和降钙素水平稍有提高，但这些实验给药组与模型B组的的大多未达到显著水平。结论大豆异黄酮对去卵巢大鼠血液生化指标有一定的调节作用，所起的作用类似于弱雌激素活性，大豆异黄酮与钙剂联合使用时调节作用更明显。     

脉冲电磁场对大鼠坐骨神经损伤的作用研究

目的探讨脉冲电磁场对坐骨神经损伤的作用。方法采用大鼠坐骨神经损伤动物模型,将48只SD大鼠随机分成治疗组、夹伤组、对照组,每组16只,根据实验动物的手术时间和处死取材时间的不同,组内再随机分为术后1,3,7,14d共4个时相观察点,各4只大鼠。夹伤组夹伤右侧坐骨神经,予以空白电磁场治疗(磁场强度为0);治疗组夹伤右侧坐骨神经,予以脉冲电磁场治疗;对照组不给予任何干预,保持同样饲养条件至实验结束。以坐骨神经功能指数(SFI)评定功能状况,HE染色观察组织学改变。结果治疗组SFI值与损伤组相比差异无统计学意义(P>0.05)。HE染色光镜下观察,治疗组神经变性程度较损伤组严重。结论脉冲电磁场对神经损伤早期功能的恢复无明显作用,能加速损伤早期远侧神经段的Wallerian变性进程。     

Estrogenic effect of soy isoflavones on mammary gland morphogenesis and gene expression profile.

We examined the effect of 17beta-estradiol (E2) and soy isoflavones' exposure on morphogenesis and global gene expression in the murine mammary gland. Three exposure regimens were applied: isoflavones added to the diet throughout either the lactational period (via the dams) or the postweaning period and E2 administered orally during the lactational period. Whole mounts of mammary glands were evaluated both in juvenile and adult animals with respect to branching morphogenesis and terminal end bud (TEB) formation. At postnatal day (PND) 28, we observed a significant increase in branching morphogenesis in all treated groups with the most pronounced effect after E2 exposure. For the E2-treated animals there was also a significant increase in TEB formation. At PNDs 42-43 the postweaning isoflavone and the E2 groups showed a transient reduction in the number of TEBs. A similar response after isoflavone and E2 exposure was further substantiated by changes in gene expression, since the same groups of genes were up- and downregulated, particularly in the E2 and postweaning isoflavone regimen. All changes in gene expression correlated with changes in the cellular composition of the gland, i.e., more and larger TEBs and ducts. The results suggest an estrogenic response of physiological doses of isoflavones on mammary gland development at both the morphological and molecular level, which resembled that induced by puberty.     

碳酸钙维生素D3及鲑鱼降钙素联合脉冲电磁场治疗老年女性骨质疏松症的临床观察

目的 观察碳酸钙维生素D3及鲑鱼降钙素联合脉冲电磁场治疗老年女性骨质疏松症的疗效.方法 老年女性原发性骨质疏松症96例,随机分为对照组和观察组,每组48例.对照组给予口服碳酸钙维生素D3(每天1片)及降钙素鼻喷剂(每天喷两次,每次120 IU)治疗12个月,观察组在对照组治疗的基础上加用脉冲电磁场治疗8周.治疗前及治疗后第1、2、4、8周分别测定患者视觉模拟疼痛评分(VAS),治疗前及治疗后1年对患者进行腰椎骨密度(BMD)测量.结果 观察组和对照组在治疗前及治疗后1、2、4、8周,VAS评分分别为:(6.7±2.1),(2.6±0.9),(1.8±0.5),(1.4±0.3),(1.1±0.2)和(6.6±2.0),(4.5±1.3),(4.0±1.1),(3.2±1.0),(2.7±0.8).治疗后两组患者的疼痛均能获得减轻,而且治疗时间越长,疼痛减轻越明显,但观察组比对照组疼痛缓解得更快(P＜0.01).治疗前观察组和对照组的腰椎BMD分别为:(0.737±0.083)和(0.739±0.083),治疗后1年则分别为(0.793 ±0.082)和(0.791 ±0.081),观察组与对照组比较,BMD差别无统计学意义(P＞0.05),而各组治疗前后比较,BMD升高均具有统计学意义(P＜0.01).结论 碳酸钙维生素D3及鲑鱼降钙素治疗老年女性骨质疏松症疗效确切,联合短疗程脉冲电磁场治疗对缓解疼痛具有协同作用,但对治疗后1年的腰椎骨密度的增加似乎无影响.     

红车轴草异黄酮对维甲酸致小鼠骨质疏松的预防作用

目的研究红车轴草异黄酮对维甲酸致小鼠骨质疏松的预防作用,并探讨其主要作用机制。方法维甲酸(90mg.kg-1)致小鼠骨质疏松模型,红车轴草异黄酮(50、100、200mg·kg-1)灌胃给药,实验过程监测体重,2周后以比色法测定血清钙、磷含量和碱性磷酸酶(ALP)、抗酒石酸酸性磷酸酶(TRAP)活性,竞争放射免疫法测定血清中骨钙素(BGP)和雌二醇(E2)含量,取股骨进行骨组织形态学观察。结果维甲酸可引起高转换型骨质疏松,红车轴草异黄酮可升高E2值,降低P、ALP、TRAP、BGP水平。结论红车轴草异黄酮对维甲酸致小鼠骨质疏松有一定的预防作用,其机制可能与其减缓雌激素水平降低,抑制骨高转换有关。     

牛磺酸对高原缺氧大鼠小肠黏膜上皮细胞损伤的保护作用

目的探讨高原缺氧对大鼠小肠黏膜上皮细胞形态结构及超微结构的影响以及牛磺酸的防护作用。方法动物经基础饲料或添加牛磺酸饲料喂养7d后，利用低压舱分别模拟4500m及5500m海拔高度，分别在高原缺氧处理后第2、24、72h剪取大鼠小肠组织，利用光镜及透射电镜观察小肠黏膜上皮细胞形态结构及超微结构的变化。结果高原缺氧可造成小肠黏膜上皮细胞水肿、出血、肠绒毛排列紊乱、大量脱落、坏死，超微结构观察可见线粒体肿胀、内质网扩张、细胞结构紊乱等细胞损伤，而牛磺酸干预可明显减轻损伤。结论高原缺氧可造成严重的小肠黏膜损伤，而牛磺酸具有一定的防护作用。