Therapeutic effect of DA-9601 on chronic reflux gastritis induced by sodium taurocholate in rats

AIM: To investigate the therapeutic effects of DA-9601 on sodium taurocholate (TCA)-induced chronic reflux gastritis in SD rats.METHODS: In this study, we have investigated the therapeutic effects of DA-9601 on chronic erosive and atrophic gastritis induced by 6 mo of TCA administration (5 mmol/L in drinking water) in SD rats. RESULTS: Four weeks of DA-9601 administration (0.065%, 0.216% in rat chow), following the withdrawal of TCA treatment, resulted in a significant decrease in total length of erosions in rats in a dose-dependent manner. Furthermore, the indicators of atrophic gastritis, such as reduced mucosal thickness and reduction in the number of parietal cells, were improved by the administration of DA-9601 in a dose-related manner. DA-9601 also attenuated inflammatory cell infiltration and the proliferation of collagenous fiber in the gastric mucosa. The improvement in the reduction of the gastric mucus was observed in the rats receiving a high dose of DA-9601 (0.216%). The therapeutic effect of DA-9601 on experimental chronic erosive gastritis was superior to that of rebamipide (1.08% in rat chow). Biochemical analyses showed increased mucosal prostaglandin E2 and reduced glutathione levels by DA-9601 treatment. CONCLUSION: We suggest that DA-9601 is apromising agent for the treatment of chronic erosive and atrophic gastritis with an etiological factor of bile reflux. Increasedmucosal prostaglandin E2 and reduced glutathione by DA-9601 treatment may be therapeutic mechanisms for chronic erosive and atrophic gastritis.

Pioglitazone attenuates the severity of sodium taurocholate-induced severe acute pancreatitis

AIM: To determine the effect of pioglitazone, a specific peroxisome proliferator-activated receptor-γ (PPARγ) ligand, on development of severe acute pancreatitis (SAP) and expression of nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas. METHODS: Male Sprague-Dawley (SD) rats (160-200 g) were randomly allocated into three groups (n = 18 in each group): severe acute pancreatitis group, pioglitazone group, sham group. SAP was induced by retrograde infusion of 1 mL/kg body weight 5% sodium taurocholate (STC) into the biliopancreatic duct of male SD rats. Pioglitazone was injected intraperitoneally two hours piror to STC infusion. Blood and ascites were obtained for detecting amylase and ascitic capacity. Pancreatic wet/dry weight ratio, expression of NF-κB and ICAM-1 in pancreatic tissues were detected by immunohistochemical staining. Pancreatic tissue samples were stained with hematoxylin and eosin (HE) for routine optic microscopy. RESULTS: Sham group displayed normal pancreatic structure. SAP group showed diffuse hemorrhage, necrosis and severe edema in focal areas of pancreas. There was obvious adipo-saponification in abdominal cavity. Characteristics such as pancreatic hemorrhage, necrosis, severe edema and adipo-saponification were found in pioglitazone group, but the levels of those injuries were lower in pioglitazone group than those in SAP group. The wet/dry pancreatic weight ratio, ascetic capacity, serum and ascitic activities of anylasein the SAP group were significantly higher than those in the sham group and pioglitazone group respectively (6969.50 ± 1368.99 vs 2104.67 ± 377.16, 3.99 ± 1.22 vs 2.48 ± 0.74, P < 0.01 or P < 0.05). According to Kusske criteria, the pancreatic histologic score showed that interstitial edema, inflammatory infiltration, parenchyma necrosis and parenchyma hommorrhage in SAP group significantly differed from those in the sham group and pioglitazone group (7.17 ± 1.83 vs 0.50 ± 0.55, 7.67 ± 0.82 vs 6.83 ± 0.75, P < 0.01, P < 0.05. The expression of NF-κB and ICAM-1 in sham group was lower than that in SAP group and pioglitazone group (0.50 ± 0.55 vs 33 ± 1.21, P < 0.01). There was a significant difference in the expression of NF-κB and ICAM-1 between SAP group and pioglitazone group (7.50 ± 1.05 vs 11.33 ± 1.75, 0.80 ± 0.53 vs 1.36 ± 0.54, P < 0.01 or P < 0.05) at 12 h after the induction of pancreatitis. CONCLUSION: Pioglitazone attenuates the severity of SAP. The beneficial effect of pioglitazone is multifactorial due to its anti-inflammatory activities, most likely through the inhibition of ICAM-1 expression and NF-κB activation. Specific ligands of PPARγ may represent the novel and effective means of clinical therapy for SAP.

De novo mutation loci and clinical analysis in a child with sodium taurocholate cotransport polypeptide deficiency: A case report

BACKGROUND Sodium taurocholate cotransport polypeptide(NTCP)deficiency disease is a genetic metabolic disorder due to mutations in the SLC10A1 gene and impaired bile acid salt uptake by the basolateral membrane transport protein NTCP in hepatocytes.A variety of clinical manifestations and genetic mutation loci have been reported for this disease.However,specific therapeutic measures are lacking,and the long-term effects are unknown.CASE SUMMARY An infant with elevated bile acids and behavioral neurodevelopmental delay failed to respond to bile acid-lowering therapy.Genetic testing for metabolic liver disease revealed that the child had NTCP deficiency due to the SLC10A1 mutation:c.422dupA(p.Y141X),which is a novel mutation site.The current followup revealed a gradual decrease in bile acid levels after 1 year of age,but the child still had behavioral neurodevelopmental delays.CONCLUSION The clinical manifestations,genetic characteristics,treatment and long-term prognosis due to NTCP deficiency remain poorly defined and need to be further confirmed by more studies and reports.

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 proliferative environment for the germs.

Pancreatic blood perfusion in sodium taurocholate－induced pancreatitis in rats

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三种急性胰腺炎大鼠模型的制备及特点比较

背景:建立稳定可靠的急性胰腺炎动物模型对于了解其发病机制、病理生理学特点及临床用药具有重大意义。国内外研究表明,雨蛙素、L-精氨酸、牛磺胆酸钠均能诱导急性胰腺炎,但是其病理生理学特点、模型特点变化规律尚不明确。目的:采用雨蛙素、L-精氨酸、牛磺胆酸钠制备大鼠急性胰腺炎模型,观察不同时段模型特点变化规律。方法:96只健康雄性SD大鼠随机分为正常组、雨蛙素组、L-精氨组、牛磺胆酸组,每组24只,每组内分为12,24,48 h 3个亚组,每个亚组8只。正常组不做处理,其余3组制备急性胰腺炎模型:雨蛙素组采用雨蛙素6次腹腔注射,间隔1 h;L-精氨酸组采用L-精氨酸2次腹腔注射,间隔1 h;牛磺胆酸钠采用胆胰管逆行注射牛磺胆酸钠诱导急性胰腺炎模型。考察各组大鼠存活率、胰腺大体形态、胰腺脏器指数、淀粉酶、脂肪酶、谷丙转氨酶、谷草转氨酶、尿素氮、肌酐水平,苏木精-伊红染色观察胰腺组织病理特征并进行胰腺损伤评分,评估大鼠不同时段模型特点变化规律。结果与结论:(1)雨蛙素组大鼠总存活率100%,L-精氨酸组为88%,牛磺胆酸钠组为96%;(2)各组模型大鼠胰腺脏器指数均有所升高;雨蛙素组大体观察可见胰腺水肿、分叶模糊、疏松;L-精氨酸组胰腺腺体增大增厚并伴有点片状出血;牛磺胆酸钠胰腺组织出现不同程度充血水肿伴散在点片状出血坏死;(3)各组模型组大鼠血清谷丙转氨酶、谷草转氨酶、尿素氮、肌酐水平与淀粉酶、脂肪酶水平变化一致,雨蛙素组可能在12 h达到峰值(P <0.05),随后呈下降趋势;L-精氨酸24 h达到最高峰(P <0.05),48 h明显下降;牛磺胆酸钠组血清淀粉酶、脂肪酶在12 h维持在较高水平并且有缓慢下降的趋势(P <0.05);(4)与正常组相比,光镜下观察雨蛙素组胰腺腺泡轻度水肿,小叶间隙增宽,炎性细胞较多;L-精氨酸组小叶间隙增宽,大量炎性细胞浸润,片状坏死点;牛磺胆酸钠组胰腺水肿明显,结构紊乱,出现大量坏死灶及炎性细胞浸润;(5)与正常组相比,3种模型诱导急性胰腺炎胰腺病理评分在各个时间点差异均有显著性意义(P <0.05),且同组随着时间的推移病理评分增加,说明胰腺组织损害逐渐加重;同一时间不同模型组相比,病理评分存在差异,且以牛磺胆酸钠组病理评分最高,L-精氨酸组次之,雨蛙素组最低;(6)结果提示,在相同时间点分析3种模型,病情最重的是牛磺胆酸钠组,以胰腺的出血坏死为主要特征;其次是L-精氨酸组,以坏死为主要特征,病情最轻为雨蛙素组,以水肿为主要特征;雨蛙素和L-精氨酸组血清生化指标在48 h有所好转,提示这两种模型可能有自愈倾向属于自限性病程;牛磺胆酸钠组血清生化指标在12 h后缓慢下降,因此认为在48 h后或者更长时间内牛磺胆酸钠组胰腺的损伤可能不会有所缓解。

不同厂家八宝惊风散中人工牛黄胆汁酸类活性成分的含量测定及差异分析

目的建立同时测定八宝惊风散中人工牛黄有效成分(胆酸、猪去氧胆酸和牛磺胆酸钠)含量的方法,比较不同厂家样品中3个成分的含量差异。方法采用超高效液相串联质谱法测定3个厂家9批八宝惊风散中胆酸、猪去氧胆酸和牛磺胆酸钠的含量,色谱柱为Phenomenex Luna®C18,流动相为乙腈-水(梯度洗脱),流速为0.5 mL/min,柱温为40℃,进样量为2μL。质谱采用负离子单四极杆模式,胆酸、猪去氧胆酸和牛磺胆酸钠的m/z分别为407.2、392.2、514.2。以3个成分的含量为指标,对9批样品进行聚类分析和主成分分析。结果胆酸、猪去氧胆酸和牛磺胆酸钠的线性范围分别为5.48~548.40、5.38~538.40、4.74~474.05 ng/mL(r≥0.9993);精密度、重复性、稳定性(24 h)的RSD均不高于3.7%(n=6),平均回收率分别为103.3%、103.3%、101.6%,RSD分别为3.3%、3.4%、4.2%(n=6)。9批样品中胆酸、猪去氧胆酸、牛磺胆酸钠的含量分别为0.702~1.711、0.599~2.049、0.664~1.752 mg/g。A厂家样品中3个成分的平均含量较高,批间差异最小;C厂家样品中3个成分的平均含量最低,批间差异较大。聚类分析基本可以区分不同厂家的样品;以主成分综合得分为指标进行聚类分析,结果与含量聚类分析结果基本一致。结论成功建立了同时测定八宝惊风散中人工牛黄3个胆汁酸类有效成分含量的方法。各厂家样品中3个成分的含量存在较大差异。

水飞蓟宾对利福平和异烟肼致肝损伤中胆汁酸转运体Ntcp与Bsep的影响

目的 初步探讨水飞蓟宾能否通过激动Nrf2/ARE信号通路,激活下游胆汁酸相关的转运体牛磺胆酸钠转运蛋白(Ntcp)及胆盐输出泵(Bsep)Bsep的表达,从而改善异烟肼/利福平(INH/RFP)INH/RFP引起的肝损伤。方法:选用SPF级ICR小鼠随机分成5组:对照组(CON组),模型组(IR组),水飞蓟宾干预组(SY50组,SY100组,SY200组),除对照组外,干预组及IR组根据体质量给予75 mg/kgINH+150 mg/kgRFP,对照组给予空白溶剂,干预组分别同时给予水飞蓟宾低剂量50 mg/kg(IR+SY50),中剂量100 mg/kg(IR+SY100)以及高剂量200 mg/kg(IR+SY200),连续灌胃给药14 d。第15天给予异氟烷吸入麻醉后摘眼球取血,离心后用于生化指标测定,取脏组织于10%福尔马林固定用于病理切片、HE染色;4%多聚甲醛固定用于目标蛋白免疫组化测定;Western blot测定目标蛋白Ntcp、Bsep及核Nrf2的表达。结果 与CON组相比,IR组均能够引起生化指标ALT、AST、TBil、DBil、ALP、TBA的显著变化,与IR组相比,低剂量的水飞蓟宾干预组ALT、Tbil、TBA降低明显,中剂量的水飞蓟宾能显著降低ALT、AST、Tbil、TBA,高剂量的水飞蓟宾能显著降低除ALP以外的所有指标,差异有统计学意义(P<0.05)。IR组Ntcp,Bsep蛋白表达均下调,而水飞蓟宾能显著上调这些蛋白的表达,IR组下调Nrf2核蛋白的表达,与水飞蓟宾合用后,Nrf2核蛋白的表达显著上调。结论 水飞蓟宾可能通过激活Nrf2入核,调控下游胆汁酸转运体Ntcp、Bsep的表达,治疗INH/RFP引起的肝损伤。

钠离子牛磺胆酸共转运多肽缺陷病及其对母胎影响的研究进展

钠离子牛磺胆酸共转运多肽(sodium-taurocholate cotransporting polypeptide,NTCP)缺陷病是一种溶质载体家族10成员1(solute carrier family 10 member 1,SLC10A1)双等位基因突变引起的胆汁酸代谢障碍性疾病,分布具有区域和种族差异,其中SLC10A1 c.800C>T(p.Ser267Phe)是我国的高频突变。NTCP缺陷病患儿主要表现为病理性黄疸,少部分有生长、运动和神经系统发育迟缓的表现,成年患者临床症状和体征不明显,生化检查提示血清总胆汁酸水平升高、部分伴有转氨酶和25-羟维生素D3水平降低。NTCP缺陷病性高胆汁酸血症需与乙型肝炎病毒感染、丁型肝炎病毒感染、自身免疫性肝炎及妊娠期肝内胆汁淤积症等鉴别,妊娠合并NTCP缺陷病性高胆汁酸血症对母胎的影响迄今少有相关报道。综述NTCP缺陷病的分子遗传机制、临床表现、实验室检查、诊断、治疗及其对母胎的影响,为该病患者的明确诊断和正确干预提供依据。

人工蛇胆的主要成份对动物心脏及血压的影响

目的 :探讨人工蛇胆及其主要成份———牛磺胆酸钠 (TCANa)对动物心脏及血压的影响。方法 :分别用人工蛇胆、TCANa 2 5mg·kg 1iv ,观察其对大鼠正常血压及由麻黄碱所致的大鼠高血压的影响 ;以 10 %人工蛇胆 ,TCANa溶液 15ml灌注于离体蛙心 ,观察离体蛙心的收缩幅度和频率 ;以人工蛇胆、TCANa 2 5mg·kg 1iv,观察其对家兔心电图的影响。结果 :人工蛇胆、TCANa均能显著地降低大鼠的血压及由麻黄碱引起的高血压 ;使离体蛙心的收缩幅度及频率逐渐降低 ,二者无显著性差异 ;二者对家兔心电图无明显影响。结论

水溶性壳聚糖降血脂作用的化学机理(Ⅰ)──水溶性壳聚糖及其衍生物对胆酸盐的结合能力研究

通过壳聚糖氧化裂解 ,制备了分子量为 80 0 0的水溶性壳聚糖 ,并通过烷基化反应合成了二乙氨乙基壳聚糖、二甲氨基 ( 1 -甲基 )乙基壳聚糖及二乙基甲基铵乙基壳聚糖 .在体外测定了水溶性壳聚糖及其衍生物对胆酸盐 (牛磺胆酸钠和甘氨胆酸钠 )的结合能力及其影响因素 .结果表明 ,水溶性壳聚糖结合胆酸盐的能力主要取决于其阳离子化程度 .修饰后的壳聚糖结合胆酸盐的能力增强 ,说明引入更多的胺基或铵基有利于对胆酸盐的结合 .

三种不同造模方法建立大鼠急性胰腺炎模型的对比

目的采用雨蛙肽、L-精氨酸、牛磺胆酸钠作为诱导剂建立大鼠急性胰腺炎(AP)动物模型,通过大鼠病理评分、血清生化及炎症细胞因子指标检测,找出一种操作简单、重复性好的大鼠AP造模方法。方法采用不用造模方法处理后的大鼠在不同时间点采集血液及胰腺标本。检测指标有淀粉酶(AMY)、谷丙转氨酶(ALT)、尿素氮(BUN)、肌酐(Cr)、Ca^(2+)、超氧化物歧化酶(SOD)、白介素(IL)-6、IL-10、肿瘤坏死因子(TNF)-α及胰腺组织病理评分。结果雨蛙肽组大鼠血清检查结果及胰腺病理均符合轻型AP改变,L-精氨酸及牛磺胆酸钠组血清检查结果及胰腺病理均符合重症AP改变。结论三种方法均可成模,大鼠AP模型病情最重的是牛磺胆酸钠诱导组,其次为L-精氨酸诱导组,病情最轻为雨蛙肽诱导组。

肠壁穿刺逆行胰胆管注射牛黄胆酸钠重症急性胰腺炎造模

目的建立一种操作简单、病变典型且稳定性好的大鼠重症急性胰腺炎(SAP)模型。方法46只健康雄性SD大鼠分为SAP组和对照组,SAP组经肠壁穿刺逆行胰胆管注射5%牛黄胆酸钠,对照组同法注射等量0.9%生理盐水。两组大鼠分别于注射后3、6、12 h检测血清淀粉酶水平、胰腺组织的湿/干质量比率及病理组织学评分,观察24 h生存指数。结果SAP组各时间段血清淀粉酶和胰腺病理组织学评分均显著高于对照组,胰腺组织湿/干质量比率在注射后6、12 h显著高于对照组;其造模后24 h的总死亡率为70%(7/10)。结论经肠壁穿刺逆行胰胆管注射牛黄胆酸钠成功诱发大鼠SAP,其模型操作简单、可重复性好。

黑鱼鱼胆抗炎活性成分研究

目的研究黑鱼鱼胆的抗炎成分活性。方法采用萃取、硅胶柱层析等方法进行分离纯化,然后通过氢谱、碳谱对分离出的单体进行结构鉴定,利用小鼠脾淋巴细胞增殖实验和脂多糖(lipopolysaccharide,LPS)诱导小鼠巨噬细胞RAW264.7释放一氧化氮(nitrogen monoxide,NO)实验评价黑鱼鱼胆抗炎活性成分。结果利用活性追踪的方法分离得到化合物牛黄胆酸钠(C1)和化合物牛黄鹅去氧胆酸钠(C2),且两个化合物对刀豆蛋白A(Concanavalin A,Con A)诱导小鼠脾淋巴细胞增殖实验的细胞相对活力分别为65.9%±11.7%、60.5%±9.4%,与模型组相比差异均具有极显著性(P<0.01);对LPS诱导小鼠巨噬细胞RAW264.7释放NO的量分别为(16.4±1.9)、(15.5±1.7)μmol·L^(-1),与模型组相比差异均具有极显著性(P<0.01)。结论黑鱼鱼胆中牛黄胆酸钠和牛黄鹅去氧胆酸钠具有一定的抗炎活性且对正常脾淋巴细胞和巨噬细胞无毒性作用。

牛磺胆酸钠致急性胰腺炎时大鼠胰腺微血流的变化

作者观察了４２只大鼠用不同浓度牛磺胆酸钠诱导的急性出血坏死性胰腺炎时平均动脉压、胰腺微区血流量、血清淀粉酶和脂肪酶及胰腺病理形态的变化。发现在大鼠胰腺炎早期，平均动脉压尚无明显改变时，胰腺微区血流量降低：且随着诱导剂浓度的增加，血清淀份酶和脂肪酶进一步升高，胰腺病理损害加重，胰腺微血流进一步恶化。表明胰腺炎早期即可出现明显的胰腺微血流障碍；胰腺微血流障碍的程度与胰腺炎时释放入血的胰酶及胰腺炎的严重程度一致。

大鼠重症急性胰腺炎模型制备方法的建立与探讨

目的建立一种操作简单,诱导成功率高且病变典型的重症急性胰腺炎(SAP)大鼠模型。方法 36只健康雄性SD大鼠随机分为模型组(n=18)和对照组(n=18)。模型组用微量输液泵经胰胆管逆行注入3.5%牛磺胆酸钠诱导SAP大鼠模型;对照组仅翻动胰腺和十二指肠。观察两组大鼠术后3h、6h、12h腹水及血清淀粉酶、脂肪酶的变化,观察胰腺组织大体形态以及病理改变,并进行评分。结果模型组胰腺组织结构破坏明显,其大体及病理评分均显著高于对照组(P<0.01),腹水量、血清淀粉酶、脂肪酶也均较对照组显著增加(P<0.01)。结论逆行胰胆管注射牛磺胆酸钠能成功诱导大鼠SAP,具有创伤小、操作简便、可重复性好及诱导成功率高的特点,是一种较为理想的SAP动物模型制备方法 。

胆酸盐在酸性介质中自聚集作用的共振瑞利散射光谱及其分析应用研究

研究了牛磺胆酸钠、甘牛胆酸钠、胆酸钠和脱氧胆酸钠等四种胆酸盐在酸性介质中的聚集作用对共振瑞利散射光谱的影响及其分析应用.结果表明:在一定浓度的HCl,H2SO4或HNO3溶液中,四种胆酸盐均能自聚集形成粒径增大的聚集体.该聚集体能导致溶液RRS显著增强,并产生了新的RRS光谱.不同胆酸盐在同种介质中的反应产物具有相似的光谱特征,最大RRS波长分别位于349(HNO3介质),359(H2SO4介质)和369nm(HCl介质).在一定范围内,胆酸盐的浓度与散射强度(ΔIRRS)成正比.对于不同的体系其检出限在12.0～21.8ng/mL之间.方法灵敏度高,选择性较好,而且十分简便快速.可用于市售蛇胆川贝液和血清样品中胆酸盐的测定.

逆行胰胆管注射牛磺胆酸钠诱导重症急性胰腺炎模型多器官损害观察

探索逆行胰胆管注射牛磺胆酸钠诱导大鼠重症急性胰腺炎(Severe acute pancreatitis,SAP)模型及胰腺外多器官损害情况。采用12周龄SD大鼠35只,随机分为对照组和模型组,各3组。模型组逆行胰胆管注射牛磺胆酸钠诱导大鼠重症急性胰腺炎模型,对照组仅开腹后拨动十二指肠降部。观察造模后6 h、12 h胰腺和腺外器官病理和血清学指标、腹水及48 h内生存率。结果:SAP模型大鼠48 h内90%死亡,胰腺进行性水肿、坏死,大量腹水渗出,心、肺、肝、肾均有不同程度受损。SD大鼠逆行胰胆管注射牛磺胆酸钠诱导的动物模型,是研究重症急性胰腺炎胰腺坏死、水肿和多器官进损害的良好模型。

乳杆菌耐胆汁、降解结合胆盐和同化胆固醇能力的研究

对8株植物乳杆菌的胆汁耐受力、降解结合胆盐能力以及同化胆固醇能力进行了研究。不同的菌株在添加了牛胆汁的MRS中生长速度具有明显差异,同化胆固醇能力也明显不同,而降解结合胆盐的能力没有明显区别。分析发现,菌株的胆汁耐受力和降解结合胆盐能力,胆汁耐受力和同化胆固醇能力,以及降解结合胆盐能力和同化胆固醇能力之间都没有明显的相关性。

不同程度急性胰腺炎大鼠早期TNF、LPS及酶学的变化

采用胰管内逆行注入不同浓度牛磺胆酸钠造成程度不同的大鼠急性胰腺炎（ＡＰ）的模型，观察不同程度ＡＰ大鼠早期肿瘤坏死因子（ＴＮＦ）、内毒素（ＬＰＳ）及酶学的改变，结果表明轻、重胰腺炎（ＡＥＰ、ＡＮＰ）组ＬＰＳ水平造模后２４小时后明显升高，升高的程度以重型组最剧。轻、重胰腺炎组血中ＴＮＦ水平造模术后均急剧升高，两组相比有显著性变化。各组血中淀粉酶的水平术后１２小时达到高峰。说明在ＡＰ的早期，胰酶的活化，细胞因子的诱生参与机体超强的炎症反应过程，是造成ＡＰ早期病理损害的主要原因。而来自肠源性细菌的严重感染和内毒素血症导致了后期病理生理的恶性循环，形成急性胰腺炎病损变化的第二个“高峰”。