应用甲强龙与否治疗糖尿病合并突发性耳聋效果的临床观察

目的观察鼓室注射甲强龙与否治疗糖尿病合并突发性耳聋的效果。方法选取2012—2013年间收治的40例糖尿病合并突聋患者,将40例糖尿病合并突发性耳聋患者(46耳)随机分成具有可比性的对照组和治疗组各20例23耳,前者应用扩血管药和降糖药物治疗,后者加用鼓室注射甲强龙治疗,治疗结束后观察疗效。结果对照组治愈1耳,显效6耳,有效8耳,无效8耳,总有效率为65.22%;研究组治愈2耳,显效11耳,有效7耳,无效3耳,总有效率为86.96%,治疗组疗效优于对照组,差异有统计学意义(Zc=1.97,P0.05),但两组总有效率差异无统计学意义(χ2=2.99,P0.05)。结论鼓室注射甲强龙联合扩血管药和降糖药物是治疗糖尿病合并突聋的有效方法,值得临床推广应用。     

复方健耳剂对DBA/2J小鼠耳蜗组织超氧化物歧化酶1表达的影响

目的研究复方健耳剂对小鼠耳蜗组织超氧化物歧化酶(SOD)1表达的影响,探讨其预防老年性耳蜗感音神经性损害机制。方法选择断奶DBA/2J小鼠10只,随机分为对照组和中药组各5只,对照组小鼠为常规饲料与日常饮水喂养;中药组小鼠为常规饲料与中药溶液喂养;至4.3月龄时两组同时终止实验,取出耳蜗,利用Real Time PCR技术定量检测两组耳蜗组织SOD1的表达。结果中药组SOD1的表达比对照组高(P<0.05)。结论复方健耳剂通过对SOD1的表达影响可能是其有效对抗老年性耳蜗感音神经性损害的重要机制之一。     

钙蛋白酶和钙蛋白酶抑素在老年聋大鼠耳蜗中的表达

目的 确定钙蛋白酶在老年聋大鼠耳蜗中的表达和钙蛋白酶-钙蛋白酶抑素平衡变化与老年耳聋的相关性.方法 采用免疫组织化学染色确定钙蛋白酶在老年大鼠耳蜗中的表达水平和组织定位,采用即时PCR技术分析耳蜗提取物中钙蛋白酶和钙蛋白酶抑素 mRNA水平的变化.结果 钙蛋白酶主要分布在耳蜗组织的内外毛细胞、神经元细胞和血管纹.在青年组大鼠耳蜗组织中钙蛋白酶有低水平表达,在老年大鼠耳蜗中的表达明显高于青年组.不同程度耳聋的耳蜗毛细胞、神经元和血管纹的钙蛋白酶表达趋势相似.但钙蛋白酶在血管纹中表达低于神经元和毛细胞.在老年耳聋组,耳蜗提取物中的钙蛋白酶 mRNA水平比青年组增高5.7倍（P＜0.01）,而钙蛋白酶抑素的mRNA水平减低了3倍（P＜0.01）.结论钙蛋白酶-钙蛋白酶抑素系统平衡紊乱在老年耳蜗组织退化和听力障碍发生过程中有重要作用.     

复方健耳剂干预小鼠老年性耳蜗感音神经细胞凋亡径路

目的探讨中药复方健耳剂干预老年性耳蜗感音神经细胞凋亡作用可能径路。方法选择刚断奶C57BL/6J小鼠15只随机分为2月龄对照组、7月龄对照组、7月龄中药组各5只,其中2月龄对照组、7月龄对照组每日饮用自来水直到出生后2、7个月止,7月龄中药组每日饮用中药复方健耳剂直到出生后7个月止。各组期满立刻取出耳蜗,利用实时聚合酶链反应技术,检测耳蜗Fas配体(L)、细胞色素(cyt) C基因、含半胱氨酸的天冬氨酸蛋白水解酶(caspase)-3表达量。结果 7月龄对照组耳蜗cyt C、Fas L、caspase-3表达量均显著高于7月龄中药组和2月龄对照组(P<0. 05)。结论 C57BL/6J小鼠老年性耳蜗感音神经细胞凋亡可能均通过线粒体或细胞膜途径介导caspase引起程序性细胞死亡。该中药防治老年性聋关键作用机制之一可能与保护线粒体,防止cyt C外泄或稳定细胞膜,抑制Fas L,以阻止其触发caspase引起细胞程序性死亡径路有关。     

巴曲酶联合甲泼尼龙治疗突发性耳聋的临床效果观察

目的 观察巴曲酶联合甲泼尼龙治疗突发性耳聋的临床效果。方法 回顾性地分析2012年8月至2014年10月在解放军总医院海南分院耳鼻咽喉头颈外科就诊的110例（共118耳）突发性耳聋患者的资料，观察组57人（62耳）治疗方案中含巴曲酶、甲泼尼龙；对照组53人（56耳）治疗方案中不含巴曲酶、甲泼尼龙。根据纯音听阈图形将患者分为4组，中低频听力下降38耳、中高频听力下降51耳、平坦型12耳、全聋型17耳。结果 观察组经治疗后痊愈11耳（17.7%）、显效32耳（51.6%）、有效16耳（25.8%）、无效3耳（4.8%），总有效率95.16%；对照组治疗后痊愈6耳（10.7%）、显效21耳（37.5%）、有效20耳（35.7%）、无效9耳（16.1%），总有效率83.93%。两组比较差异具有统计学意义（P＜0.05）。中低频听力下降型耳聋预后最好、平坦型耳聋预后较好、中高频听力下降型耳聋预后较差、全聋型预后最差，两组有效率比较差异均具有统计学意义（P＜0.05）。结论 巴曲酶联合甲泼尼龙治疗突发性耳聋具有满意的临床效果，且安全可靠，值得临床推广，不同类型的突发性耳聋预后差别很大。     

长期维生素C治疗对大鼠听阈的影响

目的探讨长期使用氧自由基清除剂维生素C对大鼠老年性聋的影响。方法42只二级Wistar大鼠,随机分成2组:试验组饮用水中加入维生素C;对照组正常进食与饮水。检测2组大鼠内耳丙二醛含量、听性脑干诱发电位(ABR)客观反应阈、耳蜗内mtDNA4834bp缺失的变化。结果(1)大鼠11月龄时,对照组与实验组的ABR反应阈为(49.3±3.9)dBSPL与(49.7±4.4)dBSPL(P>0.05),耳蜗中丙二醛含量为(10.8±1.7)与(11.6±2.1)pmol/g,P<0.05;耳蜗内mtDNA4834bp缺失的发生率比较,差异无统计学意义(P>0.05);(2)大鼠24月龄时,对照组与实验组的ABR反应阈、耳蜗中丙二醛含量及耳蜗内mtDNA4834bp缺失的发生率比较,差异有统计学意义(P<0.01、P<0.01和P<0.05)。结论长期使用氧自由基清除剂维生素C可以减轻大鼠内耳膜脂质过氧化程度,降低大鼠耳蜗内mtDNA4834bp缺失的发生率,从而减轻其老年性聋的程度;氧自由基学说可能是老年性聋的发病机制。     

芪参降脂饮对高胆固醇血症大鼠主动脉ICAM-1表达量的影响

目的观察芪参降脂饮对高胆固醇血症大鼠主动脉ICAM-1的表达的影响.方法 24只SD大鼠随机分为3组:对照组8只,喂普通饲料;模型组8只,喂高脂饲料;中药组8只,喂高脂饲料,同时给予芪参降脂饮灌胃.6周后急性处死.取血测血脂;用免疫组织化学检测主动脉血管壁细胞间黏附分子-1(ICAM-1)蛋白表达水平.结果中药组大鼠血清胆固醇水平明显低于模型组(P<0.05),模型组大鼠主动脉血管壁ICAM-1蛋白表达量明显高于中药组(P<0.01).结论芪参降脂饮能够降低实验性高胆固醇血症大鼠血脂,抑制ICAM-1在主动脉血管壁的表达.     

花姜酮对燃煤型砷中毒大鼠肝组织Bax、Bcl-2蛋白表达及肝纤维化的影响

目的 探讨花姜酮对燃煤型砷中毒大鼠肝组织Bax、Bcl-2蛋白表达及肝纤维化的影响.方法 将18只健康清洁级断乳Wistar大鼠(体质量80～100 g)随机均分为三组,对照组大鼠喂标准饲料90 d后处死;造模治疗组大鼠喂含砷100 mg/kg的饲料,且由股静脉穿刺给予10 mg/kg花姜酮溶液,1次/周,持续90 d...     

特发性突聋糖皮质激素治疗的研究进展

糖皮质激素在世界范围内被用作特发性突聋的标准治疗。但由于全身性用药的不良反应，包括代谢并发症，如糖尿病、高血压、青光眼、胃肠道出血、骨质疏松或肱骨头缺血性坏死等，使得部分患者改为局部应用糖皮质激素。另外，局部应用糖皮质激素，亦可作为全身性应用糖皮质激素治疗特发性突聋无效患者的补救措施。局部应用糖皮质激素治疗特发性突聋的给药方法主要为耳后注射给药和鼓室内注射给药，前者倾向于低频或中频下降型耳聋患者，而后者倾向于高频下降型和全聋型患者，二者也可联合使用。在临床研究中，尽管耳后注射和鼓室内注射糖皮质激素对特发性突聋的治疗有一定疗效，但仍存在争议。二者相比，耳后注射应用方便，操作相对简单，且不良反应较少。     

胃痞颗粒治疗胃癌前病变的实验研究

[目的]观察胃痞颗粒对胃黏膜上皮异型增生大鼠胃黏膜上皮细胞凋亡及调控基因蛋白表达的影响。探讨胃痞颗粒治疗胃癌前病变的作用机制。[方法]采用N-甲基-N-硝基-N-亚硝基胍（MNNG）诱导造模。设空白组、模型组、胃痞颗粒Ⅰ组及Ⅱ组，进行常规病理检测、TUNEL细胞凋亡检测、Bcl-2、Fas、P53（突变型）蛋白表达检测。[结果]胃黏膜组织病理学变化，中、重度异型增生率胃痞颗粒Ⅰ、Ⅱ组与模型组相比明显降低（均P〈0．05）；P53（突变型）、Bcl-2基因蛋白表达，胃痞颗粒Ⅰ、Ⅱ组明显低于模型组（均P〈0．05）；Fas蛋白表达，胃痞颗粒Ⅰ、Ⅱ组均高于模型组，但前者差异无统计学意义（P〉0．05），后者差异有统计学意义（P〈0．05）。[结论]胃痞颗粒对大鼠实验性胃黏膜癌前病变有逆转治疗作用。     

Experiment to determine the effect of riboflavin deficiency at weaning on iron economy and heme synthesis

21-day-old female Norwegian Hooded rats were fed a riboflavin-deficient diet for 7 weeks. A control group consisted of individually weight-matched rats fed a complete diet. Reticulocytosis was induced by phlebotomy and heme synthesis measured in a reticulocyte-rich preparation in vitro. Concentrations of circulating iron and liver stores of ferritin iron and non-heme iron were measured. Riboflavin deficiency significantly impaired the process of accumulation and maintenance of hepatic iron stores but did not appear to influence the rate of heme synthesis in an in vitro system. A primary lesion in iron metabolism in young riboflavin-deficient rats may be at the level of iron absorption so that assimilated iron is diverted to the erythroid marrow at the expense of repleting iron stores.     

Mild zinc deficiency and dietary phytic acid accelerates the development of fulminant hepatitis in LEC rats

BACKGROUND AND AIM: Restriction of copper intake delays hepatic copper accumulation in Long-Evans Cinnamon (LEC) rats, which are animal models of Wilson's disease. Involvement of zinc is suggested to develop hepatitis in the disease; however, this has not been clarified. The aims of this study were to investigate the effects of mild zinc deficiency on the development of hepatitis and to determine the relationship between the absorption and hepatic levels of copper, zinc and iron. METHODS: Male LEC and F344 (wild type atp7b) rats were fed a low zinc, phytate-containing or control diet. The onset of hepatitis (Experiment 1), and absorptive rates of copper, zinc and iron and hepatitis indices in 4 weeks (Experiment 2) were observed. RESULTS: The onset of fulminant hepatitis in LEC rats was much earlier in the low zinc and phytate groups (mean 94.6 +/- 2.74 days and 82.8 +/- 3.56 days old, respectively) than in the control group (136 +/- 2.11 days old) with worse hepatitis indices. Hepatic copper levels were much higher in LEC rats than F344 rats, but were not largely different among the diet groups without prominent changes in copper absorption. Hepatic levels and intestinal absorption of zinc and iron were lower in the phytate group than in the control group. CONCLUSION: Mild zinc deficiencies caused by a low zinc or phytate-containing diet accelerate the onset of hepatitis in LEC rats without increasing copper absorption, and zinc and iron metabolism may be involved in the earlier onset of jaundice of LEC rats.     

Intervention effect of traditional Chinese medicine Yi Tang Kang on metabolic syndrome of spleen deficiency

Objective:To investigate effects of herbal compound Yi Tang Kang on the spleen deficiency metabolic syndrome.Methods:Forty male Wistar rats were randomly divided into two groups:the normal control group and the MS spleen deficiency syndrome group.The control group rats were fed with standard diet and water,while MS spleen deficiency syndrome group with high fat diet and low dose intraperitoneal injection of slreptozocin.which swam to the endurance limit.After 12 weeks,the MS spleen deficiency syndrome group was randomly divided into two groups,with 13 rats in each group.Flats in model group were fed with high fat diet and conlinuouly administered with daily saline,and rats in intervention group with high fat diet were trated with traditional Chinese medicines Yi Tang Kang by gavage,2 mL/200 g at the same lime every day.10 weeks later,the expression of serum proteomics was investigated through abdominal aortic puncture and separation of serum,using isotope labeling technique,high performance liquid chromatography and four bar-Orbitrap mass spectrometer.Results:After treatment with traditional Chinese medicine yitangkang,in the model group,important carboxylesterase and retinal guanylate cyclase 2 precursor were upregulated.As for intervention group,these indesxes were raised,but immunoglobulin IgG,carnitine acetyltransferase,tubulin beta-5,and Gan Lu sugar binding protein C were down-regulated.At the same time,some new biological active substances,such as protein tyrosine kinase,beta glucosidase were also found.Conclusions:Traditional Chinese medicines Yi Tang Kang could regulate glucose and lipid metabolism in rats with spleen deficiency syndrome.     

Polyunsaturated fatty acid deficiency reverses effects of alcohol on mitochondrial energy metabolism

BACKGROUND/AIMS: Polyunsaturated fatty acids (PUFA) deficiency is common in patients with alcoholic liver disease. The suitability of reversing such deficiency remains controversial. The aim was to investigate the role played by PUFA deficiency in the occurrence of alcohol-related mitochondrial dysfunction. METHODS: Wistar rats were fed either a control diet with or without alcohol (control and ethanol groups) or a PUFA deficient diet with or without alcohol (PUFA deficient and PUFA deficient+ethanol groups). After 6 weeks, liver mitochondria were isolated for energetic studies and fatty acid analysis. RESULTS: Mitochondria from ethanol fed rats showed a dramatic decrease in oxygen consumption rates and in cytochrome oxidase activity. PUFA deficiency showed an opposite picture. PUFA deficient+ethanol group roughly reach control values, regarding cytochrome oxidase activity and respiratory rates. The relationship between ATP synthesis and respiratory rate was shifted to the left in ethanol group and to the right in PUFA-deficient group. The plots of control and PUFA deficient+ethanol groups were overlapping. Phospholipid arachidonic over linoleic ratio closely correlated to cytochrome oxidase and oxygen uptake. CONCLUSIONS: PUFA deficiency reverses alcohol-related mitochondrial dysfunction via an increase in phospholipid arachidonic over linoleic ratio, which raises cytochrome oxidase activity. Such deficiency may be an adaptive mechanism.     

低硒大鼠microRNA表达谱的变化

目的 探讨低硒大鼠microRNA表达谱的变化。方法 将30只SD大鼠随机分为对照组、低硒组及补硒组,每组各10只,对照组喂养标准饲料,低硒组喂养低硒饲料,补硒组喂养低硒饲料14周后再给予亚硒酸钠补硒3周。各组喂养17周后,检测大鼠的血硒水平。提取各组大鼠心肌组织RNA进行microRNA基因芯片检测,寻找低硒大鼠与正常大鼠microRNA的表达差异。采用GO分析等生物学方法对差异性表达的microRNA基因进行深度的分析,并通过RT-qPCR进行验证。结果 成功构建了SD大鼠低硒模型（血硒含量0 .026 ng/L）,低硒组大鼠血硒水平与对照组相比明显降低(P<0.05),补硒后又明显增加（P<0.05）。通过microRNA基因芯片检测低硒组筛选出显著差异性表达基因共30个,上调基因中表达最显著的为:miR-374,miR-16,miR-199a-5p,miR-195和miR-30e*,下调基因中表达最显著的为:miR-3571,miR-675和miR-450a*。 其中miR-374表达量最高,与低硒密切相关。结论 低硒大鼠中miR-374,miR-16,miR-199a-5p,miR-195,miR-30e*,miR-3571,miR-675,miR-450a*表达显著异常,其中miR-374与低硒关系最为密切。为MicroRNA在克山病的诊断及治疗方面研究提供实验依据。     

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.     

饮食调整治疗大鼠非酒精性脂肪性肝炎

目的:观察单纯饮食改变治疗大鼠非酒精性脂肪性肝炎(NASH)的作用。方法:30只SD大鼠随机分为3组(每组n=10):正常组喂普通饲料;模型组喂高脂饲料;饮食治疗组在高脂饮食12周后恢复正常饲料喂养。16周后处死动物。结果:正常饮食能显著降低造模大鼠的体重、肝指数、转氨酶,还能改善肝脏脂肪变性和炎症坏死的程度。结论:单纯恢复正常饮食即可治疗大鼠NASH。     

The Effects of Iron Deficiency, Protein Deficiency and Worm Infestation upon Disaccharidase Activity in the Rat

The effect of iron deficiency anaemia, protein deficiency and worm infestation upon intestinal disaccharidase activity in the rat was assessed following the observation that these factors may have contributed to the premature onset of lactase deficiency in man. Adaptation of intestinal lactase occurred between eight and ten weeks of age in young rats fed a 10% lactose diet. Iron deficiency anaemia depressed jejunal and ileal lactase activity. Sucrase and maltase activities were not significantly affected by iron deficiency. Adaptation of intestinal lactase was prevented by both protein deficiency and combined iron/protein deficiency. Sucrase activity was not significantly depressed by either of these and in many instances activity was higher than the control group. Similar changes were noted with maltase. Worm infestation with Nippostrongylus brasi-liensis consistently depressed jejunal lactase and maltase activities, but had little effect on sucrase activity. It was concluded that intestinal lactase in particular was depressed by a number of environmental factors and adaptation of lactase thereby prevented.     

Effects of Alcohol, Carbon Tetrachloride, and Choline Deficiency on Iron Metabolism in the Rat

The effects of alcohol on hepatic iron uptake and intestinal iron transport were studied in rats fed a nutritionally replete liquid diet containing varying quantities of ethanol. Results were compared with those from animals exposed to carbon tetrachloride (CCI₄) to produce hepatocellular necrosis or a choline-deficient diet to produce steatosis and cirrhosis. A high ethanol intake for 4 or 10 weeks produced hepatic steatosis. CCU produced hepatocellular necrosis. Choline deficiency was associated with steatosis ± cirrhosis. Intestinal iron transport was unaffected by ethanol, CCU, or choline deficiency. Hepatic iron uptake was significantly depressed in rats consuming 11.7 g/kg/day ethanol (p < 0.01) for 4 weeks. Choline-deficient animals studied at 14 weeks also had significantly decreased hepatic iron uptake (p < 0.01); results were similar in the cirrhotic and noncirrhotic animals. Conversely, CCI₄ exposure produced a significant 5-fold increase in hepatic iron uptake (p < 0.001). Results suggest that ethanol consumption, fatty liver, and cirrhosis are not responsible for any increase in iron absorption or of hepatic iron uptake in the rat model. Acute hepatocellular injury is followed by increased hepatic iron uptake.     

Overproduction of insulin in the chromium-deficient rat.

The hypothesis that the insulin secretory hyperresponsiveness observed in rats with diet-induced insulin resistance may be a basic characteristic of dietary chromium (Cr) deficiency was evaluated. Two groups of weanling rats were fed ad libitum a purified diet containing 64% sucrose, 20% casein, 5% corn oil, and the recommended levels of vitamins and minerals without added Cr. Cr-deficient (-Cr) rats were provided with distilled drinking water only, while Cr-supplemented (+Cr) rats received water containing 5 ppm Cr as CrCl3. A third group of rats fed a commercial chow diet served as sucrose controls. Effects of Cr deficiency were assessed by comparing fasting levels of glucose, insulin, and plasma lipids in blood samples collected biweekly from the -Cr and +Cr groups over a 3-month period. Both groups of rats fed the low-Cr sucrose diet developed a transient hyperinsulinemia and hyperlipidemia relative to the chow-fed control rats. There were significant effects of Cr supplementation on plasma triglycerides during the initial 2 weeks of dietary adaptation. Effects of the low-Cr diet were evaluated after the 12-week period by comparing the insulin response area and glucose clearance during a 40-minute intravenous glucose tolerance test (IVGTT). The rates of glucose clearance (KG) in -Cr and +Cr rats were similar (4.2 +/- 1.0 and 4.3 +/- 0.8%/min, respectively) and were comparable to the K(G) in chow-fed rats (4.6 +/- 0.8). In contrast, insulin secretory responses in -Cr rats were exaggerated (area, 14,083 +/- 3,399 microU/mL x min), being twofold greater (P < .05) relative to the +Cr group (6,183 +/- 864). The insulin secretory response area in chow-fed rats (7,081 +/- 408 microU/mL x min) was similar to the value in the +Cr group. These observations provide support for the hypothesis that Cr deficiency can lead to elevated insulin secretory responses to glucose.