槟榔对大鼠胃运动及神经递质的影响

[目的]探讨槟榔对大鼠胃排空运动的影响及其机制,为临床应用槟榔提供理论依据。[方法]48只Wistar大鼠随机分为低浓度（25％）槟榔（A）组、高浓度（100％）槟榔（B）组、对照（c）组。分别给大鼠灌服低、高浓度槟榔液、蒸馏水1、6h后,以葡聚糖蓝-2000为胃内标记物,观察大鼠胃肠动力变化;同时用免疫组化染色观察胃窦肌间神经丛P物质（SP）、血管活性肠肽（VIP）的变化;放射免疫分析法测定胃窦、空肠组织匀浆及血浆胃动素（MOT）、SP、VIP水平。[结果]灌服低、高浓度槟榔液1、6h后大鼠胃排空运动明显增强,胃窦肌间神经丛SP明显增加,VIP明显减少（均P〈0．01或〈0．05）;胃窦及空肠组织匀浆MOT、SP明显增加,VIP明显减少（均P〈0．01或〈0．05）;血浆MOT、SP明显增加,VIP明显减少（均P〈0．01或〈0．05）。[结论]槟榔对大鼠胃运动有明显促进作用,其机制可能与胃窦肌间神经丛、胃窦及空肠组织、血浆SP;胃窦及空肠组织、血浆MOT增加及胃窦肌间神经丛、胃窦及空肠组织、血浆VIP减少有关。     

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。     

胃胀舒合剂对功能性消化不良大鼠胃排空及血浆胃肠激素水平的影响

[目的]观察胃胀舒合剂对功能性消化不良（FD）大鼠胃排空和胃肠激素的影响，探讨其可能的作用机制。[方法]采用不规则进食加稀盐酸喂养以及劳倦过度的复合因素制作大鼠FD模型。随机分成胃胀舒合剂高、低剂量（高、低剂量）组、多潘立酮组、正常对照（正常）组、模型对照（模型）组共5组，连续给药14d后，放免法检测血浆胃动素（MOT）和生长抑素（SS）水平，以酚红法观察胃排空。[结果]与正常组相比，模型组胃排空和血浆MOT水平显著降低，SS显著升高（均P〈0．05），与模型组相比，高、低剂量及多潘立酮组胃排空和血浆MOT显著升高，SS显著降低（均P〈0．05）。[结论]胃胀舒合剂具有促进内源性MOT及抑制SS释放和促进胃排空作用，是其治疗FD机制之一。     

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。     

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。     

胃肠激素在肝衰竭大鼠胃肠道动力改变中的影响

[目的]探讨胃肠激素对肝衰竭大鼠胃肠动力障碍的影响。[方法]40只Wistar大鼠随机分为肝衰竭模型组和对照组,采用葡聚糖蓝-2000为胃肠内标记物,观察大鼠胃排空及肠道传输的变化,同时测定大鼠血浆及胃肠组织中胃动素（MTL）、P物质（SP）及生长抑素（SS）的含量。[结果]与对照组比较,肝衰竭模型组大鼠胃排空及小肠动力明显减弱（P〈0.01）,血浆及胃窦、空肠组织中生长抑素的含量明显增加（P〈0.01或P〈0.05）,P物质的含量则显著减少（P〈0.01）,但胃动素的含量无明显变化。[结论]肝衰竭大鼠胃肠功能下降与P物质及生长抑素的变化有关,胃动素在其中可能不起作用。     

加味四逆散对肝硬化大鼠异常胃电图的作用观察

[目的]观察加味四逆散对肝硬化大鼠异常胃电图的作用,并对其机制进行初步探讨。[方法]Wister雄性大鼠48只随机分为正常、模型、西药和中药组,每组12只。除正常组外,其他3组大鼠均给予腹腔注射40%CCl4花生油2.5 ml/kg,每周2次造模,连续造模11周。造模后2周中药组用加味四逆散灌胃治疗,西药组以西沙比利灌胃治疗;正常、模型组则给予等体积0.85%氯化钠灌胃。实验11周末次给药后,检测大鼠胃电图。[结果]模型组慢波节律、主频率、主功率、快波频率明显低于正常组（P〈0.05,〈0.01）,胃电慢波振幅无明显改变;中药组慢波节律、主频率、主功率、快波频率与模型组比较明显增强（P〈0.05,〈0.01）,胃电慢波振幅无明显改变,胃电波接近正常水平,与西药组比较慢波节律及快波频率均有明显差异（P〈0.05,〈0.01）;西药组主频率、快波频率与模型组比较明显增强（P〈0.05）,主功率、慢波节律与模型组比较无统计学意义（P〉0.05）。[结论]加味四逆散能明显改善实验性肝硬化大鼠的胃电波异常,提示有明显促胃动力作用。     

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.     

旋覆代赭汤对胃动力低下大鼠胃窦组织中脑肠肽受体mRNA表达的影响

[目的]观察旋覆代赭汤对胃动力低下大鼠胃窦平滑肌细胞促胃液素受体（GASR）及血管活性肠肽2受体（VIPR2）mRNA表达的影响。[方法]将70只大鼠随机分为正常组和模型组,正常组10只,模型组60只。模型组每只大鼠按10 g/kg体重的甘草煎剂灌胃后,随机分为模型3 d、模型7 d组,旋覆代赭汤低、中、高剂量组及多潘立酮组。多潘立酮组予0.27 mg/ml的多潘立酮混悬液灌胃,旋覆代赭汤低、中、高剂量组分别予浓度为0.369、0.738、1.476 g/ml的旋覆代赭汤灌胃,给药5 d。采用原位杂交法检测大鼠胃窦平滑肌细胞GASR及VIPR2 mR-NA的表达。[结果]一定剂量甘草煎剂可复制大鼠胃动力低下模型,旋覆代赭汤可使胃动力低下大鼠胃窦平滑肌细胞GASR mRNA的阳性细胞平均光密度升高,平均灰度值降低;而VIPR2 mRNA的阳性细胞的平均光密度降低,平均灰度值升高（P〈0.05或〈0.01）。[结论]旋覆代赭汤可通过调节脑肠肽受体在胃窦组织中的表达达到促胃动力的作用。     

胆囊收缩素在胃电节律失常中的作用及其神经病理学机制

目的：探讨胆囊收缩素（CCK）在胃电节律失常中的作用及其神经学机制。方法：在建立胃窦肌间神经丛铺片方法的基础上,用酶组织化学与免疫细胞化学方法,观察胃电节律失常大鼠胃窦肌间神经丛内胆碱能（Ach）神经、一氧化氮合酶（NOS）神经及CCK神经的变化。结果：模型组和CCK组大鼠均出现胃电节律失常,异常节律指数及慢波频率变异系数均显著高于正常组（P＜0．01）;模型组和CCK组NOS神经显著增加,Ach神经含量显著减少（P＜0．01）。结论：外源性及内源性CCK增加,能诱发胃电节律失常。CCK通过激活NOS,产生胃电节律失常。胃窦肌间神经丛神经中CCK及NOS神经含量异常增加,Ach神经减少是发生胃电节律失常的神经病理学机制之一。     

威灵仙对实验性肝纤维化的干预作用

[目的]通过比较肝纤维化模型组、威灵仙组、虎杖组、丹参组、易善复组及正常对照组大鼠肝脏的肝纤维化分期,探讨威灵仙在肝纤维化中的干预作用和意义.[方法]成年雄性SD大鼠120只,随机分为模型组、威灵仙组、虎杖组、丹参组、易善复组和正常对照组共6组,每组20只.通过四氯化碳诱导制备肝纤维化大鼠模型,同时分别用威灵仙、虎杖、丹参及易善复治疗,设立正常对照组,10周后光镜观察肝脏组织学改变,进行肝纤维化分期,使用统计学方法进行分析.[结果]造模结果：10周末随机抽取模型组大鼠2只,经病理检查证实肝纤维化模型造模成功.各组肝纤维化分期：模型组（3.22±0.65）,正常对照组0,威灵仙组（1.20±0.62）,虎杖组（1.32±0.48）,丹参组（1.30±0.57）,易善复组（1.45±0.69）.模型组、威灵仙组、虎杖组、丹参组和易善复组肝纤维化分期均明显高于正常对照组,差异均有统计学意义（P＜0.01）;威灵仙组、虎杖组、丹参组和易善复组肝纤维化分期均明显低于模型组,差异均有统计学意义（P＜0.01）,而威灵仙组、虎杖组、丹参组和易善复组之间肝纤维化分期比较差异无统计学意义（P＞0.05）.[结论]威灵仙能有效干预实验性肝纤维化,且与虎杖、丹参、易善复无明显差异,可为临床上中医药和中西医结合治疗肝纤维化提供新思路和重要理论依据.     

Effects of glutamine supplementation on splenocyte cytokine mRNA expression in rats with septic peritonitis

AIM: To investigate the effects of glutamine (GLN)-enriched diets before and GLN-containing total parenteral nutrition (TPN) after sepsis or both on the secretion of cytokines and their mRNA expression levels in splenocytes of rats with septic peritonitis. METHODS: Rats were assigned to a control group and 4 experimental groups. The control group and experimental groups 1 and 2 were fed a semipurified diet, while experimental groups 3 and 4 had part of the casein replaced by GLN which provided 25% of the total nitrogen. After rats were fed with these diets for 10 d, sepsis was induced by cecal ligation and puncture (CLP), whereas the control group underwent a sham operation, at the same time, an internal jugular vein was cannulated. All rats were maintained on TPN for 3 d. The control group and experimental groups 1 and 3 were infused with conventional TPN, while the TPN in experimental groups 2 and 4 was supplemented with GLN, providing 25% of the total nitrogen in the TPN solution. All rats were kiued 3 d after sham operation or CLP to examine their splenocyte subpopulation distribution and cytokine expression levels. RESULTS: Most cytokines could not be detected in plasma except for IL-10. No difference in plasma IL-10 was observed among the 5 groups. The IL-2, IL-4, IL-10, and TNF-α mRNA expression levels in splenocytes were significantly higher in experimental groups 2 and 4 than in the control group and group 1. The mRNA expression of IFN-γ was significantly higher in the GLN-supplemented groups than in the control group and experimental group 1. The proportion of CD45Ra+ was increased, while those of CD3+ and CD4+ were decreased in experimental group 1 after CLP was performed. There were no differences in spleen CD3+ lymphocyte distributions between the control and GLN-supplemented groups. CONCLUSION: GLN supplementation can maintain T-lymphocyte populations in the spleen and significantly enhance the mRNA expression levels of Th1 and Th2 cytokines and TNF-αin the spleen of rats with septic peritonitis.     

丹参酚酸B山楂黄酮联用对大鼠非酒精性脂肪性肝病相关因素的干预作用

[目的]探讨中药成份复方(丹参酚酸B、山楂黄酮)对大鼠非酒精性脂肪性肝病相关因素的影响.[方法]大鼠被随机分为:①正常对照组,普通鼠饲料喂养;②模型组,高脂饲料喂养;③中药预防组,高脂饲料喂养的同时加每天1次灌服丹参酚酸B(200 mg/kg)和山楂黄酮(40 mg/kg);④中药治疗组,高脂饲料喂养4周后加每天1次灌服丹参酚酸B(200mg/kg)和山楂黄酮(40mg/kg);⑤西药组:高脂饲料喂养4周后加每天1次灌服二甲双胍片(0.5 g/kg).实验共12周.[结果]①12周时中药预防组大鼠血清脂联素含量较模型组显著升高(P＜0.01);②各组大鼠血清游离脂肪酸和肿瘤坏死因子-α含量比较差异无统计学意义;③与模型组相比,6、8、12周时,中药预防组和中药治疗组大鼠肝组织三酰甘油含量明显降低(P＜0.01).[结论]丹参酚酸B和山楂黄酮联用对大鼠非酒精性脂肪性肝病相关因素具有干预作用.     

Effects of fish meal as source of protein on intestinal maltase activity and intestinal and renal leucine aminopeptidase activity of growing rats

The effect of high-protein fish meal on maltase and leucine aminopeptidase (LAPase) activities of the intestinal mucosa as well as the renal LAPase activity was studied. Four groups of female Wistar rats, weighing between 40-60 g, were fed diets with a 4 or 12% protein content of dry matter for 25 days. The protein source was casein for the control groups and fish meal derived from Coryphaenoides rupestris for the test groups. The results show a decrease (p less than 0.005) in intestinal maltase and LAPase activities and renal LAPase activity in animals fed with 12% of fish meal protein compared to those fed with casein, while the rats fed 4% of fish meal protein showed a decrease in intestinal maltase activity and no significant difference in LAPase activity compared with the control group. These results seem to indicate that the intestinal maltase is influenced by the quality and quantity of dietary protein, while the intestinal and renal LAPase activity is only changed by the quality of protein.     

正肝方对大鼠癌前病变肝组织细胞周期蛋白D1及依赖性激酶4的影响

[目的]观察正肝方对黄曲霉毒素B1（AFB1）诱发的大鼠癌前病变肝组织细胞周期蛋白D1（Cyclin D1）、细胞周期蛋白依赖性激酶4（CDK4）的影响。[方法]Wistar大鼠100只随机分为4组：模型、正肝方小剂量、正肝方大剂量组各30只、正常组10只。除正常组外,先后用AFB1和2-乙酰氨基芴（2-AAF）处理各组大鼠造模。正肝方大、小剂量组在造模期间,将正肝方水剂（0.6、0.3 g/ml）按10 ml/kg分别灌胃;模型组用无菌蒸馏水按10 ml/kg灌胃。8周后处死大鼠,肝组织取材。分别采用免疫组化法和RT-PCR法,检测大鼠肝组织中Cyclin D1、CDK4蛋白和mRNA表达。[结果]模型组Cyclin D1、CDK4染色阳性细胞百分率（LI）和表达强度（PU）最高,Cyclin D1、CDK4mRNA表达水平也最高（P〈0.01）。正肝方能降低大鼠癌前病变肝组织Cyclin D1、CDK4蛋白和mRNA的异常高表达（P〈0.01或〈0.05）,且呈现出一定的量效关系。[结论]正肝方能通过下调Cyclin D1、CDK4异常表达,改善细胞周期G1~S期调控点失控,从而减缓肝细胞异常增生。     

2型糖尿病大鼠并发心肌病的研究

目的 在大鼠中复制类似人类2型糖尿病模型,观察并发糖尿病性心肌病的情况.方法 取健康雄性SD大鼠120只,体质量180～220 g,按体质量及血糖值分为4组:(1)糖尿病组:40只,高糖高脂饲料喂养,一次性腹腔注射30 mg/kg链脲佐菌素(STZ)溶液;(2)STZ组:30只,普通饲料喂养,一次性腹腔注射30 mg/kg STZ溶液;(3)高糖高脂饲料组:25只,高糖高脂饲料喂养,一次性腹腔注射等容积柠檬酸盐缓冲液溶液;(4)对照组:25只,普通饲料喂养,一次性腹腔注射等容积柠檬酸盐缓冲液溶液.腹腔注射STZ溶液或柠檬酸盐缓冲液溶液后,观察动物饮水、进食及尿量变化.注射后4、8、12、16周,各组分批抽样检查,称取体质量,取血检测空腹血糖、空腹胰岛素、三酰甘油、总胆固醇;处死动物取心脏称质量,取心肌组织行光镜及透射电镜观察.结果 实验饲料喂养1周,各组大鼠体质量、血糖差异无统计学意义(P>0.05);喂养4周,STZ或柠檬酸盐缓冲液注射前,糖尿病组和高糖高脂饲料组大鼠体质量、空腹胰岛素、胰岛素抵抗指数较对照组和STZ组明显升高(P<0.05);糖尿病组与高糖高脂饲料组相比、STZ组和对照组相比差异均无统计学意义(P>0.05).注射后4个时段,糖尿病组和高糖高脂饲料组大鼠血糖、体质量、心脏质量、血三酰甘油、总胆固醇比同时段的对照组和STZ组增高(P<0.05),糖尿病组大鼠的上述指标较高糖高脂饲料组大鼠增加更显著,差异有统计学意义(P<0.05),STZ组和对照组相比差异无统计学意义(P>0.05).心肌光镜和电镜检查结果显示,糖尿病组大鼠心肌细胞肥厚并出现变性、凋亡等显著病变,间质胶原纤维增生;STZ组大鼠心肌无明显病理改变;高糖高脂饲料组大鼠心肌呈现类似糖尿病大鼠病理改变,但与糖尿病组大鼠相比,改变较不明显.结论 2型糖尿病大鼠成模4周后,心脏发生糖尿病性心肌病的病理改变,表现为心肌细胞肥大、变性,间质纤维组织增生,其发生率为100%.     

异甘草酸镁治疗大鼠非酒精性脂肪性肝炎及其作用机制

目的探讨异甘草酸镁对非酒精性脂肪性肝炎（NASH）的治疗作用及其作用机制。方法雄性SD大鼠50只随机分为5组：正常组（N组）普通饲料喂养;模型Ⅰ组（M1组）和模型Ⅱ组（M2组）高脂饲料喂养;异甘草酸镁治疗组（T1组）和饮食治疗组（T2组）在喂饲高脂饲料12周后改为普通饲料喂养,其中T2组同时给予异甘草酸镁120 mg.kg-1.d-1尾静脉注射。12周末处死N和M1组大鼠;16周末处死M2、T1和T2组大鼠。观察各组大鼠肝脏组织病理学改变,并测定各组大鼠肝功能（血清AST、ALT）、脂代谢（血清TC、TG、HDL、LDL-C）及脂质过氧化（肝匀浆MDA、SOD、GSH）指标。结果 12周末M1组大鼠出现NASH,肝脏的脂肪变性程度和炎症活动度均显著增高,TC、TG、LDL-C、MDA明显升高,HDL、SOD和GSH明显降低（P〈0.05）;16周末,M2组大鼠NASH程度进一步加重,并出现AST和ALT的明显升高（P〈0.05）。和M1、M2组相比,T1组脂肪变性和炎症活动程度明显减轻,肝功能、脂代谢和脂质过氧化各项指标均改善（P〈0.05）;而T2组差异无统计学意义（P〉0.05）。结论异甘草酸镁可能通过抗脂质过氧化、调节血脂代谢、抑制炎症反应等作用减轻NASH大鼠肝脂肪变性和炎症,对NASH有治疗作用。     

<Emphasis Type="Italic">Moringa oleifera</Emphasis> supplemented diet modulates nootropic-related biomolecules in the brain of STZ-induced diabetic rats treated with acarbose

There are strong correlations between diabetes mellitus and cognitive dysfunction. This study sought to investigate the modulatory effects of Moringa oleifera leaf (ML) and seed (MS) inclusive diets on biomolecules [acetylcholinesterase (AChE), butyrylcholinesterase (BChE)] angiotensin-I converting enzyme (ACE), arginase, catalase, glutathione transferase (GST) and glutathione peroxidase (GSH-Px) activities, glutathione (GSH) and nitric oxide (NO) levels] associated with cognitive function in the brain of streptozotocin (STZ)-induced diabetic rats treated with acarbose (ACA). The rats were made diabetic by intraperitoneal administration of 0.1 M sodium-citrate buffer (pH 4.5) containing STZ [60 mg/kg b.w (BW)] and fed with diets containing 2 and 4% ML/MS. Acarbose (25 mg/kg BW) was administered by gavage daily for 14 days. The animals were distributed in eleven groups of eight animals as follows: control, STZ-induced, STZ?+?ACA, STZ?+?2% ML, STZ?+?ACA?+?2% ML, STZ?+?4% ML, STZ?+?ACA?+?4% ML, STZ?+?2% MS, STZ?+?ACA?+?2% MS, STZ?+?4% MS, STZ?+?ACA?+?4% MS. There were marked increase in AChE, BChE, arginase, ACE and concomitant decrease in catalase, GST, GSH-Px, activities and NO levels in STZ-diabetic group compared with the control. However, there was a decrease in AChE, BChE and ACE activities and concomitant increase in the antioxidant molecules in the groups fed with supplemented diets treated with/without ACA compared with the STZ-diabetic group. These findings suggest that ML/MS supplemented diet could prevent cognitive dysfunction-induced by chronic hyperglycemia.     

碧血胶囊治疗非酒精性脂肪性肝病的疗效观察

[目的]探讨中药复方碧血胶囊对非酒精性脂肪性肝病（NAFLD）的防治作用。[方法]取雄性SD大鼠70只,随机分为正常组、高脂饮食模型组、新伐他丁组、血脂康组及碧血胶囊低、中、高剂量组,每组10只。各治疗组给药30d后,行血脂、肝功能及肝组织病理学检测。[结果]碧血胶囊中、高剂量组明显降低NAFLD大鼠的丙氨酸氨基转移酶（ALT）、天冬氨酸转氨酶（AST）、胆汁酸（TBA）、总胆固醇（TC）水平,增加高密度脂蛋白胆固醇（HDL-C）水平,明显改善肝组织脂肪病变程度,与模型组比较差异有统计学意义（P〈0.05）。与阳性对照药新伐他丁、血脂康相比,差异无统计学意义（P〉0.05）。[结论]碧血胶囊能显著降低NAFLD的血脂水平,改善肝功能及肝组织脂肪病变,其疗效与新伐他丁相当。     

Nucleoside-nucleotide free diet protects rat colonic mucosa from damage induced by trinitrobenzene sulphonic acid.

BACKGROUND: Growing evidence suggests that intestinal recovery from injury induced by radiation, endotoxin, and protein deficiency is improved by the ingestion of nucleosides and nucleotides. AIM: This study examined the effect of dietary nucleosides and nucleotides supplementation on trinitrobenzene sulphonic acid induced colonic damage in experimental colitis. METHODS: Sprague-Dawley rats were randomised into two groups and fed nucleic acid free 20% casein diet (control) or this diet supplemented with 0.5% nucleoside-nucleotide mixture for four weeks. On the second week, colonic inflammation was induced in rats by intracolonic administration of 0.25 ml of 50% ethanol containing 25 mg of trinitrobenzene sulphonic acid. Additionally, other sets of rats were treated with 0.25 ml of 50% ethanol, 25 mg of trinitrobenzene sulphonic acid in 0.25 ml saline, or 0.25 ml of 0.9% saline. RESULTS: After two weeks, colon weight, macroscopic and microscopic damage scores, were significantly greater (p < 0.05) in the nucleoside-nucleotide supplemented group compared with the non-supplemented control groups. The same variables seen in the trinitrobenzene sulphonic acid-ethanol group fed nucleoside-nucleotide free diet were greater (p < 0.05) than in the rest of the groups fed nucleoside-nucleotide free diet and treated with ethanol, trinitrobenzene sulphonic acid in saline, or saline. Histologically, segmental ulceration and inflammation associated with significantly increased infiltration of polymorphonuclear leucocytes, macrophages, lymphocytes, fibroblasts were observed in the supplemented group compared with the controls. In the nucleoside-nucleotide supplemented group the epithelial damage, mucosal erosion, oedema, and coagulative necrosis of the muscularis propria was more extensive in comparison to the non-supplemented control groups. CONCLUSIONS: This study suggests that dietary nucleosides and nucleotides may aggravate colonic damage and inflammation in chemically induced experimental colitis in rats; and that nucleoside-nucleotide free diet combined with other pharmacological agents may offer a better response.