血清总胆汁酸测定及相关生化指标在肝脏疾病变化分析

目的　用血清胆汁酸及相关指标评价不同肝病特异性 ,敏感性及临床意义。方法　使用酶终点法及速率法测定肝脏疾病患者血清总胆汁酸及相关生化指标AST、ALT、AKP、γ -GT ,并对各种肝病TBA及相关生化指标进行比较分析。结果　餐前胆汁酸在慢性肝炎、肝硬化、肝癌灵敏度高达 78.4% ,98.0 % ,82 .7% ,其升高幅度依次为急性肝炎 >肝癌 >肝硬化 >胆汁淤积性肝病 >慢性肝炎 >脂肪肝。胆汁酸、γ -GT持续升高 ,ALT/AST长期倒置 ,与肝病的慢性化有关。结论　胆汁酸及相关指标测定可以客观地对各种肝病作较全面的分析     

Effect of DW2282 on the induction of methemoglobinemia, hypoglycemia or WBC count and hematological changes

DW2282,(S)-(+)-4-phenyl-1-[1-(4-aminobenzoyl)-indoline-5-sulfonyl] -4,5-dihydro-2-imidazolone hydrochloride, is a new anticancer agent which is thought to exhibit a characteristic mechanism of action in the inhibition of tumor growth. In this study, we estimated the toxicities of DW2282 in mice. When mice were orally dosed for five consecutive days at the dosages of 50, 100 and 150 mg/kg, DW2282 did not induce methemoglobinemia and hypoglycemia at any of these doses. However, increased ALT and AST values were observed in the 150 mg/kg dosing group, and white blood cells (WBC) were significantly decreased at all doses. However, the changes in WBC count, ALT and AST immediately reversed after the cessation of drug administration. In addition, we found that DW2282 did not cause an increase in hemolysis in human blood. Taken together, these data suggested that DW2282 may have a relatively low level of toxicity, and that there may be a quick recovery from any toxicity it does produce.     

吗啡依赖大鼠血清尿酸及ALT、AST的检测分析

目的：检测吗啡依赖大鼠血清肝功能生化指标及核苷酸代谢参数的变化.方法：Wistar大鼠35只,随机分成5组,每组7只.第1组为对照组,给予0.9%氯化钠注射液；第2组给予盐酸吗啡20～95 mg&;#8226;kg 1&;#8226;d 1,分2次,ip,共7 d；第3组在给予盐酸吗啡的同时,给予嘌呤碱基混悬液100 mg&;#8226;kg 1&;#8226;d 1,ig,第8天给予盐酸纳洛酮4 mg&;#8226;kg 1,ip,观察戒断体征；第4组用嘌呤核苷混悬液替代嘌呤碱基混悬液,其余同第3组；第5组给予盐酸吗啡和盐酸纳洛酮,用量和用法同第3组.采用Beckman丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)及尿酸检测试剂盒测定相应指标.结果：发现了吗啡依赖大鼠血清尿酸水平升高,ALT及 AST酶活性升高.结论：吗啡可引起组织细胞嘌呤核苷酸分解代谢增强,引起肝脏功能的损伤.     

益肾活血胶囊抗病毒性心肌炎的实验研究

目的　探讨益肾活血胶囊对病毒性心肌炎的治疗作用。方法　选用BALB/C小鼠 6 0只,随机分为正常对照组、模型组、益肾活血胶囊组、阳性药物组,每组分别给药后,测定LDH和AST含量,并进行组织病理学检测,各区测定值采用t检验进行组间比较。结果　益肾活血组小鼠LDH、AST水平较模型组明显降低,(p <0 0 0 1);组织病理学检测发现,心脏组织病理改变程度较模型组明显减轻。结论　益肾活血胶囊对于病毒性心肌炎模型小鼠有一定的治疗作用。     

2.5Gy中子辐射对小鼠心肌细胞损伤的实验研究

〔目的〕利用 2 .5Gy 90 %的中子射线照射BALB/C小鼠 ,研究小鼠血清中反映心肌细胞损伤程度的天门冬氨酸氨基转移酶 (AST)、乳酸脱氢酶 (LDH)和肌酸激酶 (CK)、丙氨酸氨基转移酶 (ALT)活力的变化情况 ,以确定 2 .5Gy中子辐射对小鼠心肌细胞损伤的情况。〔方法〕采用二级BALB/C雄性小鼠作为实验动物 ,共计 78只。实验期间在军事医学科学院实验动物中心统一饲养。将上述小鼠分为 2组 ,包括 1个对照组和 1个实验组。采用北京清华大学的中子源分别对各动物组进行 90 %中子照射 ,照射剂量为 2 .5Gy(66只 ) ,对照组 12只。分别在照射动物之后的 6h、12h、1d、3d、5d、7d、10d、14d、2 1d、2 8d和 41d采取静脉血 ,进行AST、LDH、CK和ALT的活性测定。采用MicrocalOrigin软件包进行数理统计分析。〔结果〕2 .5Gy中子照射 5d后血清AST、LDH、CK和ALT活力均有明显升高 ,直到于照射后 2 1d～ 2 8d后仍然未恢复至正常状态 ,均显著高于正常对照组 (P <0 .0 5 )。〔结论〕2 .5Gy中子辐射可以引起心肌细胞损伤 ,进而引起血清AST、LDH、CK和ALT活力不同程度的升高。     

茵陈五苓散对大鼠酒精性肝损伤防治作用的研究

目的观察茵陈五苓散对大鼠酒精性肝损伤血清ALT、AST和病理组织学的影响，为临床酒精性肝损伤的防治提供实验依据。方法采用白酒灌胃造模，50只Wistar大鼠随机分成正常组、模型组、预防1组、预防2组、治疗组，分别于实验第5周、第9周末尾静脉取血，分离血清，测定ALT、AST。并于第9周取血后肝脏取材，常规HE染色，光镜观察。结果模型组血清ALT、AST明显升高，预防1、2组、治疗组血清ALT、AST均低于模型组，差异具有显著性（均P〈0．01）。模型组成功建立酒精性肝损伤病理学模型，预防组、治疗组病理学改变较模型组显著减轻。结论茵陈五苓散能有效地预防和治疗大鼠酒精性肝损伤。     

A Ca2+ chelator ameliorates chromium (VI)-induced hepatocyte L-02 injury via down-regulation of voltage-Dependent anion channel 1 (VDAC1) expression

Hexavalent chromium could result in cell malfunctions. Intracellular Ca²⁺ ([Ca²⁺]_i) content and VDAC1 expression are both important features related to cell survial. This study aimed to explore the mechanism of cell injury induced by Cr(VI) and tentatively offer clues to repairing this cell damage using [Ca²⁺]_i and VDAC1. L-02 hepatocytes were treated with Cr(VI)/BAPTA, and the levels of [Ca²⁺]_i and cell injury associated with Cr(VI) were determined in addition to the effect of BAPTA. The expression of VDAC1 in Cr(VI)-induced cells was evaluated. The results showed a dose-dependent elevation of the level of VDAC1 and the mRNA level of the VDAC1 biogenesis-related gene Sam50. BAPTA could ameliorate less severe damage induced by 4 μM Cr(VI) via reducing VDAC1 and Sam50. Additionally, cell injury caused by less than 4 μM Cr(VI) could be ameliorated by VDAC1 knockdown. Taken together, the findings of this study suggest that inhibition of intracellular Ca^2± overload could protect cells from damage and that VDAC1 plays a considerable role in Cr(VI)-induced liver injury.