Anti-tumor effect of bufalin on the orthotopic transplantation tumor model of human hepatocellular carcinoma in nude mice

Objective: To investigate anti-tumor effect of bufalin on the orthotopic transplantation tumor model of human hepatocellular carcinoma in nude mice. Methods: BEL-7402 cells of human hepatocellular carcinoma were inoculated to form subcutaneous tumors in nude mice by subcutaneous injection. Then the subcutaneous tumors were implanted into the liver of nude mice, and the orthotopic transplantation tumor models of human hepatocellular carcinoma were established. Seventy-five models were randomized into 5 groups ( n = 15) . Bufalin was injected intraperitoneally into the 3 groups at dose of 1.5,1 and 0.5 mg/kg for day 15 - 24, respectively. NS group were injected equal volume saline as above and adriamycin were injected intraperitoneally into ADM group at dose of 8.0 mg/kg for day 15. Ten mice in each group were killed at day 25 and detected on morphological and ultrastructural changes in myocardium, brain, liver, kidney and tumor tissues by pathology and electron microscope. The survival time in each group     

Mobilization efficiency of granulocyte colony-stimulating factor and stem cell factor to bone marrow mononuclear cells and mechanisms

The mobilization efficiency of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) to bone marrow mononuclear cells (MNCs) in mice was observed, and the changes of CXCL12/CXCR4 signal were detected in order to find out the mobilization mechanism of stem cells. Kunming mice were randomly divided into two groups. The mice in treatment group were subjected to subcutaneous injection of G-CSF at a dose of 100 μg/kg and SCF at a dose of 25 μg/kg every day for 5 days, and those in control grou...     

Establishment of an Infected Necrotizing Pancreatitis Model by Retrograde Pancreatic Duct Injection of Sodium Taurocholate and E. coli in Rats

A stable and reliable infected necrotizing pancreatitis （INP） model in rats was established in order to study the pathophysiological mechanism and pathological development role of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium taurocholate in combination with different concentrations of E. coli （10^3, 10^4, 10^5/mE, respectively） into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancreatic tissue. The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. coli into the pancreatic duct and the positive rate of germ cultivation in group B was 0. The INP model was established in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h survival-rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 10^4/mL E. coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might be that the hemorrhage and necrosis of pancreatic tissue induced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs. Meanwhile, the necrotic pancreatic tissue provides a good p     

An Experimental Study of the Protective Effects of Chinese Medicine Compound Eye-Patch on Asthenopia

Objective:To observe the therapeutic efficacy and the mechanism of Chinese medicine eye-patch with invigorating blood circulation and detoxification on asthenopia.Methods:A total of 180 rabbits were subjected to three tests,namely the skin microcirculation,the microvascular regeneration in the skin and the skin temperature change,with 60 rabbits for each test.The rabbits in each test were randomly and equally divided into three groups: the normal control group was treated with physiological saline on naked back once per day,the low dose group was treated with the eye-patch on naked back for 15 min once per day,while the high dose group was treated for three times per day.Forty Hartley guinea pigs were randomly and equally divided into four groups for the muscle tone test:the normal control group was treated with physiological saline on naked back,the model group was treated without any medication,the low dose group was treated with the eye-patch on naked back for 10 min once per day, while the high dose group was treated for three times per day.All treatments were continued for 14 days until the termination of the test.The microcirculatory blood flow was observed by using a video-microscopy system.The histological sections were used to detect the microvascular regeneration by observing the expression of factorⅧ. The temperature changes on the skin surface were measured by using infrared thermometer,and the muscle tone was tested by the electromyography.Results:In compare with the normal or the model group,the improvement in the skin microcirculation and the blood vascular regeneration,and the decreasing in the muscle tone in low dose and high dose groups were statistically significant with confident level at P<0.05.Conclusions:The eye-patch with invigorating blood circulation and detoxification has great enhancement in blood vascular regeneration and skin microcirculation,and great improvement in the indexes for muscle tone.The study explains certain therapeutic efficacy and mechanism of the eye-patch and shows that it could reduce the symptoms for patients with asthenopia.     

Role of DOR-β-arrestinl-Bcl2 Signal Transduction Pathway and Intervention Effects of Oxymatrine in Ulcerative Colitis

This study was aimed to investigate the role of the delta-opioid receptor （DOR）-β-arrestinl-Bcl-2 signal transduction pathway in the pathogenesis of ulcerative colitis （UC） and the intervention effects of oxymatrine on UC. Forty Sprague-Dawley rats were divided into nor- mal group, model group, oxymatrine-treated group and mesalazine-treated group （n=10 each） at ran- dom. The rat UC model was established by intra-colonic injection of trinitrobenzene sulfonic acid in the model group and two treatment groups. The rats in oxymatrine-treated group were subjected to intramuscular injection of oxymatrine [63 mg/（kg·day）] for 15 days, and those in mesalazine-treated group given mesalazine solution [0.5 g/（kg·day）] by gastric lavage for the same days. Animals in normal group and model group were administered 3 mL water by gastric lavage for 15 days. On the 16th day, after fasting for 24 h, the rats were sacrificed for the removal of colon tissues. The expres- sion levels of DOR, β-arrestinl and Bcl-2 were determined in colon tissues by immunohistochemistry and real-time quantitative polymerase chain reaction （RT-PCR）, respectively. It was found that the expression levels of DOR, [3-arrestinl and Bcl-2 protein and mRNA were significantly increased in the model group as compared with the other groups （P〈0.05）. They were conspicuously decreased in both mesalazine-treated and oxymatrine-treated groups in contrast to the model group （P〈0.05）. No statistically significant difference was noted in these indices between mesalazine- and oxyma- trine-treated groups （P〉0.05）. This study indicated that the DOR-β-arrestinl-Bcl-2 signal transduc- tion pathway may participate in the pathogenesis of UC. Moreover, oxymatrine can attenuate the de- velopment of UC by regulating the DOR-β-arrestin 1-Bcl-2 signal transduction pathway.     

Effects of Panax Notoginseng Saponins on Homing of C-kit~+ Bone Mesenchymal Stem Cells to the Infarction Heart in Rats

Objective:To investigate the effects of panax notoginseng saponins(PNS) on homing of C-kit+ bone mesenchymal stem cells(BMSCs) to the infarction heart.Methods:The acute myocardial infraction(AMI) model was established in 140 Wistar rats,105 model rats survived after operation,and the model rats were randomly divided into five groups,21 rats in each group:Western medicine group mobilized by subcutaneous injection of human granuloctye colony stimulating factor(G-CSF) 50 μg·kg-1·d-1;sham operation group and a model group treated by subcutaneous injection of normal saline 50 μg·kg-1·d-1;Chinese medicine group mobilized by intraperitoneal injection of Xuesaitong(血塞通)(ingredients of PNS) 150 mg·kg-1·d-1;integrative medicine group mobilized by subcutaneous injection of G-CSF 50 μg·kg-1·d-1 and intraperitoneal injection of Xuesaitong 150 mg·kg-1·d-1.Except for the sham-operated group,each group was divided into three sub-groups by three time points of 1 d,7 d and 14 d.G-CSF was injected once a day for 7 d.Xuesaitong was injected once a day until the rats were killed.The flow cytometry was used for detection of C-kit + cells in the peripheral blood in different time points,and immunohistochemical method was used for detection of the changes of C-kit + cell and Ki-67+ cell numbers in the marginal zone of AMI.Results:Twenty-four hours after the operation,C-kit + cells had a slight increase in the model group compared with the sham operation group(P>0.05).The peripheral blood C-kit+ cells in the integrative group increased significantly compared with the other groups on 7 d and 14 d(all P<0.05).Meanwhile the expression of C-kit + cells and Ki-67+ cells in the marginal zone of AMI in the integrative group increased significantly compared with the Chinese medicine group,the western medicine group and the model group on 1 d,7 d and 14 d(all P<0.05),and the cells in the integrative group decreased significantly on 14 d compared with that on 7 d(P<0.05).Conclusion:PNS can cooperate with G-CSF to mobilize C-kit+ BMSCs from the marrow into the peripheral blood and promote them "homing" to the infarction heart.     

Effect of Qingre Buyi Decoction (清热补益汤) on Nitric Oxide and Histomorphology of Intestinal Mucosa in Rats with Radiation Enteritis

Objective: To explore the mechanism of Qingre Buyi Decoction (清热补益汤,QBD) in prevention and treatment of radiation enteritis in rats. Methods: Forty-eight Wistar rats were randomly divided into four groups, the TCM group, the WM group, the model group and the control group, 12 in each group. Rats in the former three groups were given orally with QBD, norfloxacin and normal saline once a day for 7 successive days, after being irradiated with X-ray at single dose of 10 Gy for modeling of radiation enteritis, while rats in the control group were untreated. Animals were sacrificed at the end of the medication. NO concentration, mean height and number of villi per centimeter in their small intestinal mu-cosa were measured. Results: The intestinal NO concentration was significantly lower in the TCM and WM groups than that in the model group(P<0.05), while the number of villi was significantly more and the height higher in the former two groups than those in the model group (P<0.01 for both), but no signif     

Effect of Combination of Bushen Jianpi Recipe (补肾健脾方) and Erythropoietin on Serum Tumor Necrosis Factor a in Patients with Anemia

Objective: To study the effect of treatment of renal anemia by combination of Bushen Jianpi Recipe (补贤健脾方, BJR, a Chinese experienced recipe for supplementing Shen and supporting Pi) and low dosage erythropoietin (EPO), and the influence of treatment on change of serum tumor necrosis factor α (TNF-α) so as to explore the possible mechanism of integrative Chinese and Western medicine (ICWM) in treating renal anemia. Methods: Patients with renal anemia were randomly divided into two groups, the ICWM group and the control group, supporting treatment such as dialysis, supplementing of ferrous, foliac acid and vitamin B12, was given to both groups. Additionally, to the ICWM group, 50 IU/kg of EPO subcutaneous injection for twice every week, and oral intake of BJR, one dose per day taken in two parts, were given, and to the control group, EPO alone, 50IU/kg by subcutaneous injecting, 3 times perweek, was given. The therapeutic course for two groups was 3 months. Blood levels of hemoglobin (Hb), hematoc     

祛痹镇痛方对胶原蛋白诱导的关节炎大鼠滑液基因表达的作用

Objective: To investigate the effect of the Chinese medical formula Qubi Zhentong Recipe (祛痹镇痛方, QZR) on the synovial gene expression pro?le in collagen-induced arthritis (CIA) rats. Methods: Ten rats were randomly chosen from 60 rats as the control group, and the other 50 rats were used for the CIA models. The CIA model group was constructed by bovine injection of type Ⅱ collagen through the rats'' neck and tail. Twenty rats were randomly chosen from 34 successful CIA models and randomly assigned into two groups: the model group (n=10) and the QZR group (n=10). The QZR group was fed intragastrically with QZR 22.9 g/(kg?d) (10 times the clinical adult dose), and the CIA model group was given the same dose of normal saline. Both model and QZR groups were administered treatment once a day. Total RNA was collected from the knee joint synovium after 30 days. The change in gene expression pro?le was analyzed by a whole gene chip. Results: A total of 76 genes showed a difference in expression between CIA model group and the control group; 35 genes were down-regulated and 41 were up-regulated. A total of 67 genes showed a difference in expression between the model group and the QZR group; 48 genes were down-regulated and 19 were up-regulated. Conclusions: QZR may affect CIA by stimulating multiple genes and targets, which are related to oncogenes, apoptosis, metabolism, the immune system, ion channels, and transport proteins.     

Effect of Wuziyanzong Pill on sperm quality and calcium ion content in oligoasthenospermia rats

OBJECTIVE:To study the effect of Wuziyanzong treatment on the sperm quality and content of calcium ions(Ca 2+) in oligoasthenospermia rats.METHODS:A model of oligoasthenospermia was induced in 50 Sprague Dawley rats by treatment with tripterygium glycosides at 30 mg/kg per day for 8 weeks.They were divided randomly into a model group,a positive group(Huangjingzanyu capsule,3.01 g/kg),and low,medium and high dose Wuziyanzong treatment groups(2.30,4.60,9.20 g/kg crude drug respectively) with 10 in each group.Another 10 rats were used as a control group.The rats in the control and model groups were administered distilled water,while the rats in the remaining groups were administered Wuziyanzong for 30 d.The epididymides were removed,spermatozoa recovered and the sperm density and viability were measured.The spermatozoa were purified and the contents of Ca 2+ in the cytoplasm and mitochondria were detected by flow cytometry and atomic absorption spectrometry,respectively.RESULTS:After 8 weeks of treatment with tripterygium glycosides,the sperm density,sperm activity and the Ca 2 + content of spermatozoa in the model rats were all significantly decreased compared with the control group(all P<0.05).After 30 d treatment,the sperm density and activity improved and the Ca 2 + content of sperm were increased significantly in the medium and high dose Wuziyanzong treatment groups in comparison with the model group(all P<0.05).CONCLUSION:The Wuziyanzong treatment increased sperm density,improved sperm viability and enhanced the content of Ca 2+ in the sperm cytoplasm and mitochondria in this rat model of oligoasthenospermia.     

The antagonism of cholecystokinin octapeptide-8 to the peroxynitrite oxidation on a diabetic cataractal rat model

Background Cataracts is considered be formed because of an abnormal glucose metabolic pathway or oxidative stress. We explored the damaging role of ONOO^- and antagonism of cholecystokinin octapeptide-8 （CCK-8） in diabetic cataractal rat lenses. Methods A diabetic cataractal animal model was established by peritoneal injection of streptozotocine （STZ）. Thirty-six normal SD rats were taken as control group; seventy-two were given STZ （45 mg/kg） and then divided into STZ group and CCK-8 group （peritoneal injection CCK-8）. STZ induced diabetic rats were treated with CCK-8 for 60 days. Lenses were examined with slit lamp at 20, 40 and 60 days. Immunofluorescent staining and Western blot analysis were used for determining nitrotyrosine （NT, a marker for ONOO-）. RT-PCR and gene array analysis were used for determining the expression of inducible nitric oxide synthetase mRNA （iNOS mRNA） in lens epithelium （LEC）. Results STZ group rats developed lens opacity by 20 days that reached a high level by 60 days after STZ injection. CCK-8 group rats delayed the cataract formation. There was no distinct expression of NT and iNOS mRNA in control group. In STZ group, there were distinct expression of NT and upregulation of iNOS mRNA; however, CCK-8 group showed weak expression of NT and downregulation of iNOS mRNA. Conclusions NT, which may be a new form of oxidative stress, was expressed in diabetic rat LEC although CCK-8 could reverse NT damage in LEC. The results suggested that CCK-8 might be a useful therapeutic agent against diabetic cataract. The antagonizing mechanism of CCK-8 may be related to direct antagonism of ONOO^- as well as its inhibition of the expression of iNOS mRNA for production of NO and therefore decrease in the formation of ONOO^-.     

补锌对白内障大鼠晶状体NO和NOS的影响

目的 :探讨补锌对白内障大鼠晶状体中一氧化氮 (NO)和一氧化氮合酶 (NOS)的影响。方法 :用亚硒酸钠复制大鼠白内障模型 ,治疗组双眼点 0 4 %葡萄糖酸锌 (C12 H2 2 OM14 Zn)眼药水 ,对照组与模型组双眼不点任何眼药水。 10wk后观察各组实验大鼠晶状体的变化并测定晶状体中NO含量及NOS活性。结果 :白内障模型大鼠与对照组比较 ,晶状体NO含量和NOS活性差异均无显著意义 (P >0 0 5 ) ;治疗组晶状体NO含量和NOS活性与模型组和对照组比较 ,其差异无显著意义 (P >0 0 5 )。结论 :白内障大鼠眼内补锌对晶状体中NO含量和NOS活性没有明显影响     

大鼠急性肺损伤时iNOS mRNA和eNOS mRNA表达的时相变化

目的 :观察内毒素性急性肺损伤时肺组织中一氧化氮 (NO)和一氧化氮合酶mRNA的时相变化 ,并探讨其相互关系。方法 :用内毒素 (LPS)复制急性肺损伤模型 ,分别测定 0 .5 ,1,2 ,3,4h各组肺组织NO和丙二醛 (MDA)的含量 ;用原位杂交方法检测各组大鼠肺组织中诱导型一氧化氮合酶mRNA(iNOSmRNA)和内皮型一氧化氮合酶mRNA(eNOSmRNA)的表达水平。结果 :大鼠给予LPS后 ,①肺组织MDA含量随时间延长而逐渐增加 ,不同时点的均值互有差异 (P <0 .0 5 ) ,并且均显著高于正常对照组 (P <0 .0 5 ) ;②各时点肺组织NO含量和iNOSmRNA表达量均显著大于正常对照组 (P <0 .0 5 ) ,并且均在 2h时达到高峰 ,以后呈下降趋势。二者的变化呈显著正相关 (P <0 .0 1) ;③ 2h前 (含 2h)肺组织MDA含量随iNOSmRNA表达增加所致的NO产量增多而增加 ,2h后二者变化趋势相反 ;④各时点肺组织eNOSmRNA表达量与正常对照组比差异均无显著性。结论 :内毒素性急性肺损伤时 ,肺组织iNOSmRNA大量表达 ,导致内源性NO爆发式产生 ,从而介导肺损伤。NO产量在静注内毒素后 2h达到高峰 ,以后呈下降趋势。     

白藜芦醇对糖尿病白内障大鼠正沉默信息调节因子2相关酶1基因表达的影响

目的  探讨白藜芦醇对糖尿病白内障大鼠晶状体正沉默信息调节因子2相关酶1（SIRT1）基因表达的影响。方法  80只Wistar大鼠随机分为4组：正常对照组、糖尿病模型组及白藜芦醇低剂量组及白藜芦醇高剂量组。糖尿病模型组、白藜芦醇低剂量组及白藜芦醇高剂量组一次性腹腔注射链脲菌素（STZ）（60 mg/kg）制备糖尿病大鼠模型。成模后低剂量组每日20 mg/kg,高剂量组每日100 mg/kg予白藜芦醇灌胃。裂隙灯显微镜照相机记录各组晶状体变化。12周实验结束时测定各组大鼠晶状体丙二醛（MDA）、超氧化物岐化酶（SOD）、谷胱甘肽过氧化酶含量。逆转录-聚合酶链反应（RT-PCR）检测各组大鼠晶状体SIRT1、肿瘤抑制因子P53、叉头转录因子1、核转录因子κB（NF-κB）表达情况。结果  糖尿病模型组大鼠晶状体均发生不同程度混浊,甚至完全混浊,形成白内障。白内障糖尿病大鼠晶状体MDA（7.96±0.51）nmol/mg·prot较正常对照组（4.21±0.27）nmol/mg·prot升高（P <0.01）,糖尿病白内障大鼠晶状体SOD、谷胱甘肽过氧化酶[（31.92±5.03）和（7.43±1.53）u/mg·prot]较正常对照组[（61.86±6.17）和（13.61±2.27）u/mg·prot]降低（P <0.01）。高剂量白藜芦醇组大鼠晶状体MDA（4.64±0.42）nmol/mg·prot较白内障糖尿病大鼠晶状体（7.96±0.51）nmol/mg·prot降低（P <0.01）。高剂量白藜芦醇组大鼠晶状体SOD、谷胱甘肽过氧化酶[（52.41±6.54）和（12.76±1.72）u/mg·prot]较白内障糖尿病大鼠晶状体SOD、谷胱甘肽过氧化酶[（31.92±5.03）和（7.43±1.53）u/mg·prot]增高（P <0.01）。白内障糖尿病大鼠晶状体SIRT1 mRNA表达（0.187±0.034）较正常对照组大鼠（0.523±0.089）降低（P < 0.01）。高剂量白藜芦醇组大鼠晶状体SIRT1 mRNA表达（0.497±0.072）较白内障糖尿病大鼠晶状体（0.187±0.034）增强（P <0.01）。白内障糖尿病大鼠晶状体P53、叉头转录因子1、NF-κB mRNA表达（0.816±0.153）、（1.269±0.231）、（0.896±0.029）较正常对照组（0.592±0.104）、（0.674±0.112）、（0.495±0.008）增强（P <0.01）。高剂量白藜芦醇组糖尿病大鼠晶状体P53、叉头转录因子1、NF-κB mRNA表达（0.609±0.107）、（0.713±0.121）、（0.397±0.018）较白内障糖尿病大鼠（0.816±0.153）、（1.269±0.231）、（0.896±0.029）降低（P <0.01）。结论  白藜芦醇可能通过调节SIRT1表达,进一步调节下游基因P53、叉头转录因子1、NF-κB的表达,抑制和延缓晶状体上皮细胞凋亡,延缓糖尿病大鼠白内障的发生发展。

     

酪酪肽对实验性重症急性胰腺炎大鼠的作用

目的:通过检测血清一氧化氮(NO),诱导型一氧化氮合成酶(iNOS)及超氧化物歧化酶(SOD)水平,研究酪酪肽(PYY)对重症急性胰腺炎大鼠的作用。方法:健康雄性SD大鼠40只,体重250～300g。随机分成胰腺炎组(20只)和治疗组(20只)两组,实验前大鼠禁食12h,自由饮水。两组大鼠均分3次腹腔内注射6%l-精氨酸溶液(3×1.5mg/g),中间间隔1h。治疗组大鼠在第1次腹腔内注射精氨酸后立即皮下注射酪酪肽(0.8pmol/g体重),此后每间隔4h皮下注射1次,共注射10次。将实验大鼠分别在造模后48h作血清NO,iNOS及SOD测定。结果:酪酪肽治疗组血清NO及iNOS明显低于重症急性胰腺炎组,而血清SOD明显高于重症急性胰腺炎组。结论:酪酪肽对重症急性胰腺炎的保护治疗作用可能与降低血清NO含量,抑制iNOS活性,提高SOD活性有关。     

注射用心肌肽对幼鼠离体心脏缺血 再灌注能量代谢的影响

目的：探讨注射用心肌肽对幼鼠离体心脏缺血再灌注能量代谢的影响及机制。方法：50只SD幼鼠,随机分为5组（n=10）,正常对照组：心脏灌流20 min稳定后,再持续灌注150 min;正常+注射用心肌肽组：同正常对照组,但在灌流液中加入注射用心肌肽50 mg/L;模型对照组：心脏灌流20 min稳定后,停搏液停搏（缺血）90 min,再恢复正常灌流（再灌注）60 min,建立心肌缺血再灌注损伤模型,灌流用K-H缓冲液,停搏用ST.Thomas’II停搏液;注射用心肌肽1组(CMP1组)：停搏液加入注射用心肌肽100 mg/L;CMP2组：灌流液加入注射用心肌肽50 mg/L及停搏液加入注射用心肌肽100 mg/L）。监测不同组离体灌流心脏心率(HR）、收缩力(△T)及最大收缩速度(+dT/dtmax)和最大舒张速度(-dT/dtmax)、冠状动脉流量(CF)、复搏时间,透射电镜观察缺血再灌注损伤模型组中幼鼠心肌组织超微结构改变。进一步检测3个缺血再灌注损伤组冠状动脉流出液中肌酸激酶同工酶（CK-MB）含量的变化,心肌组织能量及氧化抗氧化代谢指标、丙二醛、NO的含量,检测心肌组织NOS、醛糖还原酶的活性,实时荧光定量PCR相对定量检测心肌组织iNOS,eNOS和Akr1b4 mRNA表达。结果：正常对照组离体心脏长时间灌流后心功能无明显变化,注射用心肌肽对正常心脏心功能无明显影响。与模型对照组比较,两个用药组心搏功能下降轻微,冠状动脉流量较好。电镜观察可见模型对照组心肌肌原纤维断裂,线粒体肿胀,而用药组心肌组织结构较完整,线粒体未见明显肿胀变性。再灌注后,模型对照组CK-MB增加。与模型对照组比较, 两个用药组的CK-MB含量低,Na+-K+ ATP酶、Ca2+-Mg2+ ATP酶、心肌总ATP酶活性相对较高,超氧化物歧化酶活性也增高,丙二醛、NO含量低,心肌组织NOS、醛糖还原酶的活性下降,iNOS,Akr1b4 mRNA表达下调,其中CMP2组改变更为明显（P＜0.01或P＜0.05）。此外eNOS mRNA表达在CMP2组升高（P＜0.05）,而在CMP1组中变化无统计学意义（P>0.05）。结论： 注射用心肌肽可改善缺血心脏再灌注后的能量代谢,增加冠状动脉流量,提高心功能,对幼鼠未成熟心肌缺血再灌注损伤具有保护作用,灌流液及停搏液均加入注射用心肌肽对未成熟心肌缺血再灌注损伤的保护作用效果更佳。其作用机制可能与抑制心肌细胞iNOS, Akr1b4 mRNA表达,减少NO生成,抑制醛糖还原酶的活性有关。     

白芍总苷对NAFLD模型大鼠肝脏保护作用的抗氧化机制

目的研究白芍总苷对非酒精性脂肪肝(NAFLD)模型大鼠肝脏保护作用的抗氧化机制。方法SD大鼠54只,随机分为正常对照组(12只)和模型组(42只)。正常组给予普通饲料,模型组给予高脂饮食结合饮10%果糖水,饲养6周时,分别随机抽取2只大鼠,取肝脏做HE染色,观察肝细胞病理组织变化。模型组根据体质量随机分为模型对照组、二甲双胍组(200 mg·kg-1)、白芍总苷高、低剂量组(200、100 mg·kg-1)。连续灌胃给药4周后,测定大鼠血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、谷胱甘肽巯基转移酶(GST)活性和肝脏指数;测定大鼠血清和肝脏组织超氧化物歧化酶(SOD)、氧化亚氮合成酶(NOS)和谷胱甘肽过氧化物酶(GSH-PX)活性、丙二醛(MDA)和氧化亚氮(NO)含量的变化;测定大鼠血清果糖胺(FMN)和晚期糖基化终末产物(AGEs)水平。结果与正常对照组比较,模型组大鼠ALT、AST和GST活性以及肝脏指数增高(P<0.01);SOD和GSH-PX活性降低(P<0.01),NOS活性增高(P<0.01),MDA、NO、FMN和AGEs含量升高(P<0.01)。药物治疗4周后,明显降低ALT、AST和GST活性以及肝脏指数(P<0.01,P<0.05),提高SOD和GSH-PX活性(P<0.01,P<0.05),并降低NOS活性(P<0.01,P<0.05)以及MDA、NO、FMN和AGEs含量(P<0.01或P<0.05)。结论白芍总苷具有保肝作用,其作用机制可能与增强抗氧化能力有关。     

FS-1272滴眼液对体外大鼠白内障晶状体的影响

[目的]观察FS-1272滴眼液对硒性白内障的防治作用.[方法]采用离体晶状体培养方法,观察FS-1272滴眼液对亚硒酸钠性白内障大鼠晶状体混浊程度、晶体中超氧化物歧化酶(SOD)、谷胱苷肽1过氧化酶(GSH-PX)、过氧化氢酶(CAT)活性,丙二醛(MDA)、可溶性蛋白(WSP)和不溶性蛋白(WIP)含量的影响.[结果]FS-1272滴眼液高、中剂量组晶状体混浊度明显低于模型组,SOD、CAT、GSH-Px活性高于模型组,MDA和WIP含量低于模型组.[结论]FS-1272滴眼液可减轻晶体氧化损伤程度,从而起到防治白内障的作用.     

姜黄素对糖尿病脑病大鼠氧化应激及海马iNOS表达的影响

\[摘要\]目的探讨糖尿病脑病与氧化应激和诱导型一氧化氮合酶(iNOS)的关系,及姜黄素治疗的效果和机制。 方法大鼠随机分为正常对照组(CN)、正常姜黄素组(Cur)、糖尿病组(DM)、糖尿病+姜黄素治疗组(DM+Cur),以注射链脲佐菌素建立糖尿病大鼠模型,Cur组和DM+Cur组采用Cur(60 mg·kg-1·d-1)灌胃给药。12周后测定海马组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及丙二醛(MDA)、一氧化氮(NO)含量,RT-PCR和免疫组化方法检测海马iNOS mRNA表达水平及iNOS免疫阳性细胞平均光密度值(MOD)值。 结果与CN组相比,DM组海马组织SOD和CAT活性明显降低(P<0.01),NO和MDA含量明显增加(P<0.01),海马组织iNOS mRNA及蛋白表达较CN组明显增加(P<0.01);与DM组相比,DM+Cur组SOD和CAT活性明显增加(P<0.01),NO和MDA含量明显降低(P<0.01),海马组织iNOS mRNA及MOD值明显降低(P<0.01)。 结论糖尿病脑病与氧化应激水平及海马组织iNOS 表达升高相关;姜黄素可能通过抗氧化活性及下调iNOS表达,而对糖尿病脑病起保护作用。     

缺血-再灌注心肌诱导型一氧化氮合酶基因表达及其活性的变化和卡托普利的影响

目的探讨心肌诱导型一氧化氮合酶（iNOS）mRNA表达及其活性的变化在心肌再灌注损伤中的作用；研究卡托普利对缺血再灌注心肌保护作用的机制。方法采用Langendorff离体鼠心灌流模型；将18只SD大自鼠随机均分为3组：对照组、缺血一再灌组及卡托普利组；观察心肌iNOS mRNA表达及其活性、丙二醛（MDA）含量、过氧化物歧化酶（SOD）活性、肌酸激酶（CK）含量和冠状静脉流出液一氧化氮（NO）的变化。结果缺血再灌注后心肌iNOS mRNA表达显著上调（P〈0．001），iNOS活性增高（P〈0．001）；卡托普利组再灌注30min，心肌iNOS mRNA表达及其活性、心肌MDA含量均低于缺血-再灌组（P〈0．01，P〈0．05），而心肌SOD活性（P〈0．01）和CK含量（P〈0．05）高于缺血-再灌组，再灌注期间冠状静脉流出液NO含量高于缺血-再灌组（P〈0．01）。结论缺血-再灌注心肌iNOS基因表达上调，心肌iNOS活性增高；影响心肌iNOS mRNA表达、调节心肌iNOS活性可能是卡托普利抗心肌脂质过氧化作用的机制之一。