小陷胸汤治疗功能性消化不良的实验研究

[目的]探讨小陷胸汤对功能性消化不良（FD）模型大鼠的作用机制。[方法]采用不规则喂养配合夹尾刺激法建立FD大鼠模型，予以小陷胸汤水煎液灌胃治疗。观测大鼠胃固体排空率，检测胃组织内一氧化氮（NO）及血浆胃动素（MOT）水平，并与空白对照组、模型对照组和多潘力酮组进行比较。[结果]小陷胸汤能明显升高胃排空率（P〈0．05），与多潘力酮等效（P〉0．05）；能显著降低胃组织NO水平，且优于多潘力酮（P〈0．01）；能明显升高血浆MOT水平（P〈0．05），与多潘力酮等效（P〉0．05）。[结论]小陷胸汤能提高FD大鼠胃固体排空率；减轻NO对胃排空的抑制；增强MOT水平，促进胃排空。在降低胃组织NO方面明显优于多潘力酮。     

平胃消导胶囊对功能性消化不良模型大鼠胃电活动和胃肠激素的影响

[目的]观察平胃消导胶囊对情志刺激引起的功能性消化不良（FD）模型大鼠胃电活动和胃肠激素水平的影响,探讨其可能的作用机制。[方法]将实验大鼠随机分为6组：空白对照组,模型组,多潘立酮药物对照组,平胃消导胶囊大、中、小剂量组。除空白对照组外,其余各组用夹尾激怒法复制FD大鼠模型,观察和对比各组大鼠胃窦消化间期综合肌电（IMC）活动,检测血浆胃动素（MOT）和血管活性肠肽（VIP）水平,并以此评价药物疗效。[结果]与模型组相比,平胃消导胶囊治疗组IMC周期缩短（P〈0．05,〈0．01）、Ⅲ相时程延长（P〈0．01）、Ⅲ相发生率增高（P〈0．05,〈0．01）,血浆MOT水平升高（P〈0．05,〈0．01）,VIP水平降低（P〈0．01）。[结论]平胃消导胶囊可增强FD模型大鼠胃电活动,恢复性调节MOT、VIP）水平,表现出良好的整体调节和促进胃排空作用。加大剂量治疗效果更好,是治疗FD疗效确切的中药制剂。     

舒胃汤对功能性消化不良大鼠胃动素及胃窦Cajal间质细胞的影响

[目的]探讨舒胃汤对功能性消化不良( functional dyspepsia,FD)肝郁脾虚证大鼠胃排空、胃动素(Motilin,MOT)、胃窦Cajal间质细胞(interstitial cells of Cajal,ICO的影响.[方法]将60只大鼠随机分为舒胃汤低剂量组(低剂量组)、舒胃汤高剂量组(高剂量组)、木香顺气丸组(中成药组)、莫沙必利组、对照组、模型组,每组10只.采用夹尾刺激方法制造FD模型,造模后第3天各组给予相应药液灌胃,对照组、模型组给予蒸馏水灌胃,持续14d.实验结束后检测胃排空,免疫组化法检测MOT水平,电镜观察胃窦ICC超微结构.[结果]模型组与对照组大鼠比较胃排空延迟,MOT水平明显升高(均P＜0.05).与模型组比较,给药各组大鼠胃排空改善(均P＜0.05);高剂量组和莫沙必利组MOT降低(均P＜0.05);透射电镜观察高剂量组胃窦部ICC与模型组比较结构明显改善,接近对照组.[结论]舒胃汤能够促进胃排空,下调MOT水平,改变胃窦ICC超微结构,恢复胃肠道运动功能可能是舒胃汤治疗FD的作用机制之一.     

疏肝健脾法对功能性消化不良血浆胃动素和生长抑素的影响

[目的]观察中医疏肝健脾法治疗肝郁脾虚型功能性消化不良（FD）的临床疗效及对血浆胃动素（MOT）和生长抑素（SS）水平的影响。[方法]选择确诊为FD患者120例，按2：1比例随机分为2组，治疗组（疏肝健脾方治疗）80例，对照组（莫沙必利治疗）40例，并设正常组40例。采用放射免疫法测定2组患者治疗前、后空腹血浆MOT和SS水平，并与正常组测得值对比。[结果]治疗组临床症状总有效率为92．5％，对照组为90．0％，差异无统计学意义，但前者显效率为85．0%，明显高于对照组的60．0%（P〈0．05）。治疗组MOT及SS治疗前后比较差异均有统计学意义（均P〈0．01）。[结论]中医疏肝健脾法治疗FD患者疗效显著，能升高血浆MOT及降低SS水平，推动胃肠蠕动，促进胃肠道排空，达到改善患者临床症状的目的。     

消渴安糖方颗粒对实验性糖尿病大鼠血浆促胃液素及胃动素水平的影响

[目的]观察消渴安糖方颗粒对实验性糖尿病大鼠血浆促胃液素（GAS）、胃动素（MOT）水平的影响。[方法]用链脲佐菌素（STZ）经腹腔一次性大剂量（60mg／kg）注射制备实验性糖尿病大鼠模型，50只Wistar大鼠随机分为正常对照（A）组、模型（B）组、参芪降糖胶囊（C）组、消渴安糖方颗粒低剂量（D）组、消渴安糖方颗粒高剂量（E）组，每组10只。实验结束后，用放射免疫法测各组血浆GAS、MOT。[结果]C、D、E组大鼠糖尿病症状及体重明显改善；B组的GAS、MOT、胰岛素（INS）及空腹血糖（FPG）水平明显高于A组（P〈0．01），C、D、E组的GAS、MOT、FPG水平明显低于B组（P〈0．05），D、E组的GAS、MOT与C组比较差异有统计学意义（P〈0．05）。[结论]实验性糖尿病大鼠普遍存在GAS、MOT水平的异常增高，消渴安糖方颗粒能显著降低实验性糖尿病大鼠血浆GAS、MOT水平。     

肝胃不和型功能性消化不良大鼠胃动素和P物质的表达及中药情志舒的干预作用

目的：观察肝胃不和型功能消化不良（FD）大鼠胃和十二指肠运动功能、血浆胃动素（MOT）含量和胃肠壁P物质（SP）的表达，探讨肝胃不和型FD的发病机制及中药情志舒治疗肝胃不和型FD的可能机制。方法：将64只大鼠随机分为对照组，模型组，多潘立酮组及情志舒组；应力传感器记录大鼠胃和十二指肠移行性复合运动（MMC）；放免法测定大鼠血浆MOT含量；PAP免疫组化法观察SP在胃窦壁和十二指肠壁的表达情况。结果：与模型组比较，情志舒组MMC周期缩短，Ⅲ相延长，频率加快，幅度高，MMCⅢ相发生率增加，胃和十二指肠协调收缩率显著增加，MMCⅢ相时血浆MOT含量显著增加；胃肠壁SP免疫阳性产物表达也明显增强（P＜0．01，＜0．05）。结论：胃肠MMCⅢ相异常，胃肠协调运动障碍可能是肝胃不和型FD的发病机制之一，肝胃不和型FD大鼠血浆MOT含量的降低和胃肠壁SP表达的降低可能是肝胃不和型FD发病的神经生学基础，情志舒可能增加MMCⅢ相血浆MOT的释放和胃肠壁SP的表达，从而改善胃肠运动功能来治疗肝胃不和型FD。     

莪术对大鼠胃动力及脑肠肽调节作用的实验研究

[目的]探讨莪术对大鼠胃动力作用机制及脑肠肽的调节作用。[方法]40只大鼠随机分成正常对照组、模型组、25%莪术组、50%莪术组和0.1%多潘立酮组,每组8只。正常对照组以外的各组采用不规则进食加稀盐酸饲养制作胃电节律失常模型,并给予相应处理,4周后观察大鼠胃肌电活动异常节律指数和慢波频率变异系数、胃排空率,放免法测定胃窦及空肠组织胃动素（MOT）、血管活性肠肽（VIP）的水平。[结果]与正常对照组比较,模型组肌电活动异常节律指数和慢波频率变异系数明显升高（P〈0.01）,胃排空率下降（P〈0.01）;MOT在胃窦、空肠组织的水平下降,而VIP水平则上升（P〈0.01）。经25%莪术水煎剂治疗后上述各值均恢复或接近正常,与多潘立酮组比较差异无统计学意义（P〉0.05）,与模型组比较差异有统计学意义（P〈0.01）。[结论]25%莪术水煎剂有明显的促胃动力作用,其机制可能与其调节肽能神经的体液,改善胃电节律有关。     

调中颗粒对胃肌间Cajal间质细胞功能及数量的影响

[目的]观察功能性消化不良（FD）大鼠胃肌间Cajal间质细胞（ICC）超微形态结构、分布特点和密度变化,探讨调中颗粒治疗FD的机制。[方法]将40只大鼠随机分为5组,各8只,除正常组外,其余采用夹尾法制备FD模型,胃电图的方法检测造模是否成功,电镜观察胃肌间ICC的超微结构。酪氨酸激酶受体c-kit免疫组化法观察不同药物治疗后胃肌间阳性ICC的分布和水平变化。[结果]模型组大鼠胃电参数低于正常组（P〈0．05）;ICC的超微结构证实ICC与胃平滑肌运动具有密切相关性;调中颗粒能明显升高胃窦ICC水平（P〈0．05）,优于多潘立酮（P〈0．05）。[结论]调中颗粒能通过调节ICC的分布和数量,升高胃窦ICC的表达,促进胃蠕动,改善FD大鼠胃电节律。调中颗粒疗效优于半夏泻心汤和多潘立酮,具有整体调节作用。     

枳实消痞丸不同剂型治疗功能性消化不良的临床研究

[目的]了解功能性消化不良（FD）的临床分型及枳实消痞丸方不同剂型治疗FD的临床疗效。[方法]以西沙必利作为对照，运用枳实消痞丸3种剂型（饮片、合煎冲剂、分煎冲剂）治疗FD患者，并观察该方对患者迷走神经张力、血浆胃动素（MOT）水平及食管收缩功能的影响。[结果]各剂型组总有效率与西沙必利组相比差异无统计学意义（P〉0．05），但不良反应少见；各组药物均能显著减少治疗后各症状出现的百分比。该方能显著提高患者迷走神经张力及血浆MOT水平（P〈0．01，P〈0．05），改善食管收缩功能；其3种剂型间的疗效亦未见显著差别。[结论]枳实消痞丸方能明显改善FD患者的临床症状，提高患者迷走神经张力及血浆MOT水平，改善食管下括约肌收缩功能。     

香砂六君颗粒与丸剂对脾虚胃肠动力及胃肠激素影响的对比观察

[目的]观察香砂六君颗粒和香砂六君丸对脾虚胃病患者胃肠动力和胃肠激素的影响,探讨香砂六君颗粒治疗脾虚胃病的机制。[方法]将患者随机分为香砂六君颗粒（颗粒）组和香砂六君丸（对照）组,分别于治疗前后以B超检测胃半排空时间,以放免法测血浆胃动素（MOT）、生长抑素（SS）和血清促胃液素（GAS）水平,同时观察症状积分情况。[结果]2组分别与治疗前比较,症状积分改善、胃半排空时间缩短（均P〈0．01）,MOT、GAS升高,SS降低（P〈0．01,〈0．05）;颗粒组与对照组比较,症状积分降低（P〈0．01）,胃半排空时间缩短,MOT升高（P〈0．05）,2组间GAS、SS差异无统计学意义。[结论]香砂六君颗粒通过调节胃肠激素水平可明显促进胃排空,减慢小肠蠕动,改善脾虚症状,且优于香砂六君丸。     

调肝理脾方抑制酒精性肝纤维化的实验研究

[目的]探讨调肝理脾方对实验性酒精性肝纤维化大鼠的抑制作用及其机制。[方法]Wistar雄性大鼠以“白酒-吡唑-玉米油”混合液灌胃16周制备酒精性肝纤维化大鼠模型,给药后检测肝功能、肝组织病理学变化、肝组织中转化生长因子-β1（TGF-β1）蛋白表达。[结果]酒精性肝纤维化模型大鼠肝功能显著异常,肝纤维化明显;经4周治疗,与模型组比较,中药组及西药组血清中丙氨酸氨基转移酶、天冬氨酸转氨酶、透明质酸水平均有显著下降（P〈0．01）,且中药组能显著下调大鼠肝组织中TGF-β1蛋白。[结论]调肝理脾方能够有效阻止和逆转酒精性肝纤维化的进程。     

生黄合剂对大鼠心肌缺血再灌注损伤的保护作用

目的观察生黄合剂对大鼠心肌缺血再灌注损伤(MIRI)的保护作用。方法将48只SD大鼠随机分为6组,即空白对照组、模型组、阳性药物组及生黄合剂低、中、高剂量组,每组8只,分别给药7 d后,建立MIRI模型。检测大鼠血清乳酸脱氢酶(LDH)及心肌丙二醛(MDA)和超氧化物歧化酶(SOD)的含量,用TUNEL法检测心肌细胞凋亡情况,并观察心肌组织形态学改变。结果与模型组比较,生黄合剂能降低大鼠LDH及MDA的含量,增加SOD活性,降低心肌细胞凋亡指数,改善心肌组织病理损害。结论生黄合剂对大鼠MIRI具有保护作用,其机制可能为通过抗自由基作用来抑制MIRI诱导的细胞凋亡。     

Ethanol-Induced Intrauterine Growth Retardation: Correlation with Placental Glucose Transfer

Placental transfer of glucose and alanine analogs was studied at term in ethanol-fed and control rats. Ethanol was provided as 30% of the caloric intake throughout gestation. Control groups received isocaloric liquid diet without ethanol by pair-feeding (PF) or ad libitum (AF). On the 22nd day of pregnancy, the rats were injected with a mixture of [3H]2-deoxyglucose and [14C]alpha-aminoisobutyric acid. The ratios of fetal:maternal plasma radioactivities 1 hr later were used to compare placental transfer between the groups. Mean +/- SE body weight of EF fetuses (4.54 +/- 0.07 g) was significantly lower than that of PF (4.88 +/- 0.06 g) or AF (5.17 +/- 0.09 g) fetuses. Maternal ethanol ingestion reduced placental transfer of 2-deoxyglucose and alpha-aminoisobutyric acid by 12% and 35%, respectively. Placental transfer of both analogs was not affected in the PF controls. The weight of EF fetuses correlated (p less than 0.001) with transfer of 2-deoxyglucose to the fetus. This relationship was also found in the control groups. Fetal body weight did not show a strong correlation with alpha-aminoisobutyric acid transfer. Thus, impaired transfer of glucose to the fetus may play a significant role in the growth retardation observed in fetuses of ethanol-fed rats.     

Effect of synbiotics on intestinal microflora and digestive enzyme activities in rats

AIM: To investigate the effect of synbiotics, i.e. probiotics and prebiotics mixture, on the gut microbial ecology and digestive enzyme activities in rats. METHODS: Forty-eight SD rats weighing about 280 g were used in this study. Rats were divided into three groups according to the contents of probiotics and prebiotics mixture in the feed as control, low and high dose groups. The duration of the experiment was 8 wk. RESULTS: Compared with the control group, the fecal Lactobacillus and Bifidobacterium counts were significantly increased and the fecal Coliform organism counts were markedly reduced in the low and high dose groups. Concerning the digestive enzyme activity of jejunum, only lactase activity increased in low dose group. However, significant increase of lipase, lactase, sucrase, and isomaltase activities were observed in high dose group. CONCLUSION: Intake of low and high dosages of probiotics and prebiotics mixture significantly improved the ecosystem of the intestinal tract by increasing the probiotics population and digestive enzyme activities in rats.     

Vascular prostacyclin and Goldblatt hypertensive rats

Vascular prostacyclin production in Goldblatt hypertension was examined in one-kidney, one clip (1K, 1C) and two-kidney, one clip (2K, 1C) rat models. Vasodepressor responses to prostacyclin and nitroprusside correlated well with resting blood pressure in both groups of rats, but when measured as a percentage of resting blood pressure the responses did not differ significantly between hypertensive rats and the normotensive controls within each group. In contrast, the vasodepressor effects of arachidonic acid (1-3 mg/kg, i.v.) were much greater in the 1K, 1C rats than in their normotensive controls, but did not differ significantly between hypertensive 2K, 1C rats and sham-operated controls. The effects of arachidonic acid were virtually abolished by indomethacin (10 mg/kg, i.v.). The metabolism of [14C]-arachidonic acid was also studied in isolated aortae of both one- and two-kidney rats by high pressure liquid chromatography of extracts of the incubation mixture. [14C]-6-oxo-PGF1 alpha was the only prostanoid conversion product recovered from the incubations and significantly more of this metabolite was produced by aortic tissue from 1K, 1C rats than from normotensive controls. There was no difference in [14C]-6-oxo-PGF1 alpha production between 2K, 1C rats and controls. These results demonstrate an enhanced ability of vascular tissue from 1K, 1C hypertensive rats to convert exogenous arachidonate to vasodilator prostacyclin, but this is not evident in the two-kidney model. Although enhanced biosynthetic capacity for prostacyclin in the one-kidney model and spontaneously hypertensive rats does not lessen peripheral vascular resistance, it might reflect a fundamental disturbance in phospholipid metabolism which contributes to increased vascular resistance.     

酸枣仁加锌合剂对睡眠剥夺大鼠下丘脑星形胶质细胞活性的影响

目的 探讨酸枣仁加锌合剂对睡眠剥夺(SD)大鼠下丘脑星形胶质细胞(AS)活性的影响.方法 健康Wist-ar大鼠50只,雌雄各半,按体重随机分为空白组、模型组、阳性药组、低剂量组、高剂量组.各组连续7 d按体重灌服酸枣仁加锌合剂.7 d后除空白组外,其他各组采用水上站立法进入SD状态.随后取大鼠主动脉血采用酶联免疫吸附试验(ELISA)检测胶原纤维蛋白(GFAP),并摘取大鼠下丘脑固定切片,观察AS形态.结果 各组血清GFAP与模型组差异有统计学意义(P<0.05).下丘脑AS银染后,经电镜观察,SD后AS与空白组比较出现明显排列紊乱,细胞体形状不均,增生现象明显.而经灌服酸枣仁加锌合剂的大鼠,其AS形态基本稳定,排列紊乱现象减少,细胞增殖现象不明显.结论 酸枣仁加锌合剂可对抗SD,起到养心安神保护大脑作用,其作用机制与调控AS活性密切相关.     

Does Aspirin Play a Role in Analgesic Nephropathy?

Summary: Using a compound analgesic mixture, it was found that renal pathology could be produced in rats if the analgesic mixture was administered as a concentrated aqueous suspension, but that development of renal pathology was not favored by hot, dry environmental conditions. Determination of whole body total salicylate concentrations in rats and humans receiving various doses of aspirin revealed that twice daily doses of 24, 60 and 125 mg/kg aspirin in the rat were equivalent to human doses of 8, 20 and (approximately) 40 ordinary 325 mg aspirin tablets daily. These doses of aspirin were then employed in a subchronic study of the nephrotoxicity of aspirin in the rat using the experimental design which maximized the nephrotoxic effects of the compound analgesic mixture. Six groups of ten male and ten female rats received aspirin orally at doses of 24, 60 or 125 mg/kg twice a day five days a week for 12 weeks. Two additional groups of ten male and ten female rats received only the vehicle, at a volume equivalent to that received by the high dose group, and served as controls. Four groups (one each, control, low, mid-, and high dose) were denied access to water for 16 hours daily overnight. No pathologic renal changes were observed in any of the rats. These findings are consistent with a growing body of evidence, from both animal and human studies, that aspirin alone does not produce analgesic nephropathy.     

抗脂肪肝中剂对大鼠高脂血症防治的实验研究

目的：探讨抗脂肪肝冲剂对高脂血症大鼠脂质代谢的影响,寻求防治高脂血症的有效药物。方法：采用高脂饮食喂养大鼠,形成高脂血症模型,饲以抗脂肪肝冲剂,观察大鼠血清总胆固醇（TC）及甘油三酯（TG）的含量,结果：抗脂肪肝冲剂能显著降低高脂血症大鼠血清中TC含量（与模型对照组比较P＜0．01）及TG含量（大、中、小剂量组与模型对照组比较P＜0．01,P＜0．05,P＜0．05）。结论：抗脂肪肝冲剂能够降低高脂血症大鼠TC、TG的含量,具有防治高脂血症的作用。     

日本血吸虫表位肽-DNA颗粒性疫苗对小鼠免疫应答的影响

采用已构建的日本血吸虫Sj22.6抗原CTL、Th和B细胞表位肽-DNA颗粒性疫苗(PDDV)及其混合疫苗免疫C57BL/6小鼠。36只小鼠随机均分6组,即18K对照组([K]_(18)-空质粒PDDV)、PBS对照组、C组(C-PDDV)、T组(TPDDV)、B组(B-PDDV)和C-T-B组(C-PDDV、T-PDDV和B-PDDV等量混合),每鼠分别在第0、3和6周麻醉下经尾脊部皮下注射100μl PDDV(含10μg DNA和28μg肽),对照组注射等量的空质粒DNA和[K]_(18)肽或PBS。末次免疫后7d,脱颈处死,制备脾细胞悬液,经日本血吸虫成虫抗原(SWA)刺激后根据~3H标记的胸腺嘧啶核苷(~3H-TdR)检测脾细胞增殖反应,ELISA法检测脾细胞培养上清中γ干扰素(IFN-γ)和白细胞介素-4(IL-4)的含量。ELISA结果显示,T组小鼠脾细胞中IFN-γ的含量[(76.0±11.2)pg/m1],高于PBS[(13.0±2.1)pg/ml]和18K对照组[(14.0±3.2)pg/ml](P<0.01),T组和C-T-B组小鼠脾细胞中IL-4的水平分别为(152.0±21.1)和(8...     

Natural 25,26-dihydroxyvitamin D3 is an epimeric mixture.

Radiolabeled 25,26-dihydroxyvitamin D3 was prepared in vitro by using chicken kidney homogenates and in vivo in rats from [23,24-3H]-25-hydroxyvitamin D3. These compounds were mixed with synthetic (25S)- and (25R)-25,26-dihydroxyvitamin D3, converted to the corresponding (+)-alpha-methoxy-alpha-trifluoromethylphenylacetyl esters, and subjected to high-performance liquid chromatography that separates the derivatized epimers. The radiolabeled 25,26-dihydroxyvitamin D3 derivatives were a 1:1 mixture of the 25S and 25R isomers. Similarly unlabeled 25,26-dihydroxyvitamin D3 isolated from the plasma of rats given large amounts of vitamin D3 was shown to be a 1:1 mixture of the S and R isomers. Therefore, naturally occurring 25,26-dihydroxyvitamin D3 is a mixture of the 25R and 25S isomers and not just the S isomer reported previously.