ERK信号蛋白在吗啡预处理减轻大鼠全心缺血/再灌注损伤中的作用

目的探讨细胞外信号调节激酶(extracellular signaling-regulated kinase,ERK)在吗啡预处理减轻大鼠全心缺血/再灌注损伤中的作用。方法健康成年♂SD大鼠,采用随机数字表法分为6组(n=10):对照组(control,CON)、缺血/再灌注组(ischemia/reperfusion,I/R)、缺血预处理组(ischemia preconditioning,IPC)、吗啡1μmol·L^-1预处理组(morphine preconditioning,MPC)、MPC+ERK抑制剂PD98059组(MPD)、ERK抑制剂PD98059对照组(PD)。利用Langendorff灌流系统对各组大鼠离体心脏在进行相应处理后,化学比色法检测基线、再灌注5、10 min时冠脉流出液乳酸脱氢酶(lactate dehydrogenase,LDH)活性;同时利用充水球囊置入左心室持续监测左心室发展压(left ventricular developed pressure,LVDP)。2,3,5-氯化三苯基四氮唑(triphenyltetrazolium chloride,TTC)染色测量梗死区(infarct size,IS)、缺血危险区(area at risk,AAR)体积及IS/AAR比值;Western blot检测心肌组织ERK磷酸化水平。结果与I/R组比较,MPC组IS和IS/AAR减小,再灌注5、10 min时LDH活性降低,再灌注结束时LVDP升高,心肌组织磷酸化ERK(p-ERK)相对表达量增加;ERK抑制剂PD98059阻断MPC的保护作用,增加心肌梗死面积,升高再灌注5、10 min时LDH活性,降低再灌注末LVDP,此外,PD98059抑制MPC诱导的ERK磷酸化。结论吗啡预处理可能通过诱导ERK磷酸化水平升高而减轻大鼠全心缺血/再灌注损伤。     

TFPI对大鼠DIC状态的检测

目的:本研究应用大鼠内毒素血症模型,通过监测大鼠动脉血血小板数(PLT)、纤维蛋白原(FIB)、凝血酶原时间(PT)、部分凝血活酶时间(APTT)及组织因子途径抑制物(TFPI),探讨其在诊断中的意义,为DIC的发现提供新的实验室证据,以期实行早期治疗,降低死亡率.方法:雌雄各半Wistar大鼠16只,随机分为两组:正常对照组(N,n=8),DIC组(P,n=8),P组首次注射内毒素(1 mg/kg),P组24 h后再次注射内毒素(1 mg/kg),经动脉采血;所采血样分别用双抗体夹心ELISA法测定TFPI,全自动血常规分析仪测定PLT,全自动血凝分析仪测定FIB、PT及APTT.结果:与N组相比,P组PLT、FIB减少,PT、APTT延长,TFPI含量增加,P＜0.05.结论:大鼠血浆TFPI出现降低(DIC状态),其数值始终高于正常状态,ELISA法测定的TFPI灵敏准确,提示TFPI对DIC有诊断价值.     

叶黄素对阿霉素所致大鼠心、肾损伤的保护作用

目的 探讨叶黄素对阿霉素所致大鼠心、肾毒性的保护作用及其机制.方法 采用单次腹腔注射阿霉素(10mg/kg)造成大鼠实验性心、肾病模型,研究注射阿霉素前、后叶黄素灌胃对大鼠血液生化学指标、组织生化指标及病理组织学的影响.结果 心、肾病模型组大鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、血尿素氮(BUN)、肌酐(Cr)含量均明显高于对照组,心、肾组织匀浆中丙二醛(MDA)含量显著增加,而谷胱甘肽过氧化物酶(GSH-Px)及超氧化物歧化酶(SOD)活性显著下降.叶黄素(20mg·kg-1·d-1)可降低心、肾损伤大鼠血清AST、ALT、LDH、CK、BUN及Cr水平,改善阿霉素损伤大鼠心、肾病理组织学变化,并降低心、肾组织匀浆MDA水平,提高组织GSH-Px及SOD活性.结论 叶黄素通过抗氧化作用对大鼠阿霉素心、肾损伤产生保护和治疗作用.     

PD98059对HL60细胞Ras-MEK1/2-ERK1/2信号转导影响的研究

目的探讨MEK1抑制剂PD98059对HL60细胞Ras-MEK1/2-ERK1/2信号转导以及细胞增殖的影响。方法四唑盐比色试验(MTT)法检测PD98059对HL60细胞增殖的抑制作用,流式细胞术观察PD98059对HL60细胞凋亡和G0/G1期阻滞的影响,半定量反转录-聚合酶链反应(RT-PCR)测定PD98059对HL60细胞ERK2、p27、Skp2基因表达的影响,免疫组织化学SP法检测ERK2、p27、Skp2蛋白表达的改变情况。结果 PD98059能够抑制HL60细胞的生长,该抑制作用具有浓度及时间依赖性(P<0.05)。PD98059能够促进HL60细胞凋亡,该作用具有浓度及时间依赖性(P<0.05);PD98059作用HL60细胞48h,随着浓度的增加G0/G1期阻滞增强(P<0.05)。PD98059可使HL60细胞ERK2、Skp2的mRNA及蛋白表达量减少,p27的mR-NA及蛋白表达量增加(P<0.05)。结论 PD98059能够抑制HL60细胞的生长,诱导细胞发生G0/G1期阻滞,促进其凋亡,这可能是通过PD98059阻断Ras-MEK1/2-ERK1/2信号转导,影响了ERK2、Skp2、p27等的表达而实现的。     

MAPK通路在瑞芬太尼预处理减轻心衰大鼠离体心脏缺血/再灌注损伤中的作用

目的探讨MAPK信号通路在瑞芬太尼预处理减轻心力衰竭大鼠离体心脏缺血/再灌注损伤中的作用。方法成年♂SD大鼠,尾静脉注射阿霉素,制备慢性心力衰竭模型,通过随机数字表将54只模型大鼠分为9组(n=6):假手术组(sham)、缺血/再灌注组(IR)、瑞芬太尼预处理组(RPC)、ERK抑制剂PD98059+RPC组(RPD)、p38抑制剂SB203580+RPC组(RSB)、JNK抑制剂SP600125+RPC组(RSP)以及抑制剂对照组(PD、SB和SP)。化学比色法检测再灌注5min和10 min时冠脉流出液中乳酸脱氢酶(LDH)的活性,再灌注末行TTC染色并计算心肌梗死面积,通过Power Lab系统记录血流动力学。结果与IR组相比,RPC可以明显降低梗死面积与缺血危险区的比值(IS/AAR),同时,也可以降低再灌注5 min及10 min LDH活性;而JNK抑制剂SP600125几乎完全取消RPC的保护作用,明显增加IS/AAR,并升高再灌注5 min LDH活性;ERK抑制剂PD98059也可部分阻断RPC的保护作用;而p38抑制剂SB203580对RPC的保护作用则无明显影响。血流动力学结果显示,与IR相比,RPC及加入MAPK抑制剂后对离体心脏缺血/再灌注损伤后心功能影响差异无统计学意义。结论 JNK和ERK信号通路可能在瑞芬太尼预处理减轻心力衰竭大鼠离体心脏缺血/再灌注损伤中发挥重要作用。     

二烯丙基二硫对D-氨基半乳糖/脂多糖所致小鼠急性肝损伤的保护作用

目的研究二烯丙基二硫(diallyl disulfide, DADS)对D-氨基半乳糖/脂多糖(D-galactosamine/lipopolysaccharide, D-gal/LPS)诱导的小鼠急性肝损伤是否有保护作用。方法 SPF级雄性ICR小鼠72只,随机分为6组:对照组,DADS对照组,D-gal/LPS模型组和DADS低、中、高剂量干预组(DADS+D-gal/LPS),每组12只。DADS对照组、DADS低、中、高剂量干预组小鼠分别灌胃给予不同剂量的DADS(80、20、40和80 mg/kg·bw),给予DADS 1 h后,DADS干预组和D-gal/LPS模型组小鼠腹腔注射D-gal(500 mg/kg·bw)/LPS(10μg/kg·bw),8 h后称量小鼠体重,取血并分离血清,检测血清丙氨酸转氨酶(alanine aminotransferase, ALT)、天冬氨酸转氨酶(aspartate aminotransferase, AST)、乳酸脱氢酶(lactate dehydrogenase, LDH)活力和总胆红素(total bilirubin, TBil)的水平;取出肝脏,称重并计算肝脏系数;将肝左叶制作石蜡切片,通过苏木素-伊红(HE)染色对肝进行组织病理学检查。结果与对照组相比,DADS对照组无明显异常,各组小鼠的肝脏系数差异无统计学意义;D-gal/LPS模型组小鼠的存活率为92%,血清ALT、AST、Tbil和LDH水平明显升高(P0.05), HE染色显示肝小叶出现大面积的出血性坏死,同时可见嗜酸性小体,表明肝细胞发生凋亡。与D-gal/LPS模型组相比,20、40和80 mg/kg·bw的DADS干预组小鼠存活率均为100%;ALT、AST活力和Tbil含量均明显降低(P0.05),其中给予80 mg/kg·bw的DADS干预后ALT、AST、Tbil和LDH分别降低了88.5%、84.2%、35.3%和77.2%;HE染色示肝脏出血性坏死区域明显减少,仅20 mg/kg·bw的DADS干预组有局部肝细胞坏死灶,40和80 mg/kg·bw的DADS干预组已无明显肝细胞坏死。结论 DADS对D-gal/LPS诱导的急性肝损伤有明显的保护作用。     

α-硫辛酸通过激活ERK信号通路促进神经突触生长

目的探讨α-硫辛酸(LA)促进神经突触生长的可能机制。方法将体外培养的小鼠神经母细胞瘤N2a细胞分为对照组(A组)、细胞外信号调节蛋白激酶(ERK)抑制剂PD98059 40μM组(B组)、LA 500μM组(C组)和PD98059 40μM+LA 500μM组(D组)。用光学显微镜观察细胞突触生长情况,Western blot法检测ERK表达水平。结果与A组相比,C组突触生长、ERK激活水平增加(P<0.01);而D组能明显抑制C组上述观察指标的增加过程(P<0.01)。结论 LA对神经细胞突触生长的促进作用可能是通过激活ERK依赖性信号通路来实现的。     

亚慢性染毒纳米碳酸钙大鼠组织病理学研究

目的通过观察亚慢性染毒纳米碳酸钙大鼠器官组织病理学变化,初步探讨纳米碳酸钙的毒性和可能靶器官。方法选取健康SD大鼠100只,随机分为对照组、微米碳酸钙组(200 mg/kg)、纳米碳酸钙组(12.5、50和200 mg/kg)。滴鼻染毒,每周5次,连续12周。染毒结束24 h后处死大鼠,腹主动脉采血,全自动生化分析仪检测天冬氨酸转氨酶(AST)及丙氨酸转氨酶(ALT)活性和肌酐(Cr)、尿素氮(BUN)含量,取大鼠心、肝、脾、肺、肾、脑海马组织进行病理观察。结果对照组大鼠各器官均未见异常。微米碳酸钙组大鼠肺泡壁充血水肿,炎性细胞侵润。纳米碳酸钙组大鼠肺泡壁充血水肿,炎性细胞浸润,局部肺不张,部分小血管出现玻璃样变;支气管黏膜萎缩、剥脱,大量炎性细胞浸润。高剂量纳米碳酸钙组大鼠肾小球肿胀,肝细胞脂肪样变。纳米碳酸钙各组大鼠血清ALT活性和BUN含量显著高于对照组(P0.05),高剂量组大鼠血清BUN含量显著高于微米碳酸钙组(P0.05)。结论亚慢性染毒纳米碳酸钙可导致大鼠肺、肝、肾组织病理学损伤。     

番茄红素对大鼠肝脏缺血再灌注损伤的保护作用

目的研究番茄红素(lycopene,LP)对大鼠肝脏缺血再灌注损伤的保护作用。方法将80只SPF级雄性SD大鼠随机分为5组:假手术组、肝脏缺血再灌注模型对照组、番茄红素(5、10和20 mg/kg)治疗组,每组16只;术后番茄红素各治疗组连续4周灌胃给予相应剂量番茄红素治疗,假手术组和肝缺血再灌注模型组分别灌胃给予等体积的生理盐水,每天1次。检测各组大鼠血清中转氨酶(ALT和AST)、碱性磷酸酶(ALP)活性,丙二醛(MDA)含量以及总抗氧化能力(T-AOC)水平;检测肝脏组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性;通过苏木精-尹红(HE)染色观察各组肝脏组织病理学改变。结果与假手术组相比,肝脏缺血再灌注模型对照组大鼠血清中ALT、AST、ALP活性和MDA含量均显著升高(P<0.01),T-AOC水平显著降低(P<0.01);肝脏组织中SOD、GSH-Px、CAT活性均显著降低(P<0.01),且肝脏组织出现明显的病理学改变。与肝脏缺血再灌注模型对照组相比,番茄红素(5、10和20 mg/kg)治疗组大鼠血清中ALT、AST活性和MDA含量均显著降低(P<0.05,P<0.01);番茄红素(10和20 mg/kg)治疗组大鼠血清中ALP活性均显著降低,且T-AOC水平显著升高(P<0.05,P<0.01),肝脏组织中SOD和CAT活性显著升高(P<0.05,P<0.01);番茄红素(20 mg/kg)治疗组大鼠肝脏组织中GSH-Px活性显著升高(P<0.01);番茄红素各治疗组肝组织病理性改变出现不同程度的改善。结论番茄红素对大鼠肝脏缺血再灌注损伤具有保护作用,该作用可能与番茄红素能够有效改善抗氧化酶系统活性,减轻自由基损伤,改善肝功能有关。     

ERK抑制剂对心肺复苏后大鼠心肌缺血再灌注损伤和能量代谢的作用研究

目的 探讨 ERK抑制剂 PD98059对于心脏骤停/心肺复苏（CA/CPR）后大鼠心肌能量代谢和心肌缺血再灌 注损伤的作用。方法 36只大鼠按随机数字表法分为假手术（Sham）组（n=6）、模型（CA）组（n=15）和 PD98059（PD） 组（n=15）。Sham组只单纯行手术操作;CA组和 PD组经食道交流电刺激诱导心室颤动（VF）建立大鼠 CA/CPR模型, 恢复自主循环（ROSC）后,PD组立即静脉注射 PD98059（0.3 mg/kg）,CA组立即静脉注射等量生理盐水。观察复苏后 24 h存活情况,采集血清检测心肌肌钙蛋白 I,同时取心肌组织进行 HE染色、ATP含量测定,并采用蛋白免疫印迹法 检测磷酸化 ERK（p-ERK）的表达水平。结果 复苏后 24 h,各组存活情况为 Sham组 6只、CA组 6只、PD组 13只。与 Sham组比较,CA和 PD组血清心肌肌钙蛋白 I水平升高;PD组血清心肌肌钙蛋白 I水平较 CA组下降（P＜0.05）。PD 组 ATP含量较 CA组明显升高（P＜0.05）,心肌病理损伤程度也较 CA组明显减轻。与 Sham组比较,CA和 PD组大鼠 心肌组织 p-ERK的表达水平升高;PD组 p-ERK表达水平较 CA组下降（P＜0.05）。结论 ERK抑制剂 PD98059治疗 能够改善心肺复苏后心肌能量代谢障碍,减轻心肌缺血再灌注损伤。     

Subacute toxicity of uranyl acetate in Swiss-Albino mice

Subacute effects of uranyl acetate were investigated in laboratory mice (Mus musculus, Swiss-Albino). Uranyl acetate was administrated to mice during a period of 5 days with dietary consumption ad libitum. Effects of uranyl acetate on food and water consumption, body weight changes; plasma urea nitrogen (BUN), creatinine concentrations and activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were assayed by time-course experiment. Glutathione S-transferase (GST) and catalase (CAT) activities were also determined in liver tissues on day 5. Distribution of radioactivity in liver, kidney and brain was detected by scintillation spectrometry. The results indicated that uranyl acetate was accumulated in examined tissues, with highest accumulation being in brain. Some of the biochemical biomarkers (BUN, creatinine, ALP) were significantly increased (P<0.05) in the exposure group compared to control animals. Also, BUN and/or creatinine levels and/or ALT and AST activities significantly increased (P<0.01 or P<0.05) with UA exposure on day 3 and/or day 5 compared with results of day 1.     

Comparative evaluation of the protective effect of selenium and garlic against liver and kidney damage induced by mercury chloride in the rats

The present study was designed to compare the protective effect of selenium and garlic against liver and kidney damage induced by (ip) injection of 0.5 mg/kg mercury chloride (HgCl(2)) in rats. Thirty-six Sprague-Dawley rats were used in the present experiment and divided into six groups: one group was orally given (1 ml) saline and served as a control group; two groups of rats were given either selenium (0.1 mg/kg) or garlic (63 mg/kg) alone, once daily an oral dose for 30 successive days; other two groups of rats were given either selenium or garlic alone, once daily a dose for 15 successive days prior to HgCl(2) injection and on the next 15 successive days simultaneously with HgCl(2) injection; and the last group of rats was injected ip with HgCl(2) for 15 days and at the end of the experiment (which lasted 30 days), blood samples for the biochemical analysis were obtained from all rats after being lightly anesthetized with ether, and specimens of kidney and liver were removed and prepared for histochemical study. Computer image analysis was applied to liver and kidney tissues to evaluate the DNA density and DNA ploidy pattern in different groups. The results revealed that the rats injected with HgCl(2) showed a significant increase in levels of blood urea nitrogen (BUN), serum creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST) by 29.3%, 62.5%, 29.46% and 30.61%, respectively, while alkaline phosphatase (ALP) showed a significant decrease by 22.6% as compared with saline control group. Rats that were given selenium in combination with the HgCl(2) injection showed a significant decrease in BUN, Serum creatinine, ALT and AST levels, while ALP was significantly increased as compared with HgCl(2) group. Also rats that were given garlic in combination with HgCl(2) injection showed a significant decrease in BUN, Serum creatinine, ALT and AST levels, although serum ALP level showed an increase as compared to HgCl(2) group. Rats that had been orally administered selenium or garlic alone did not show any significant changes in the serum level of BUN, Serum creatinine, ALT and AST but there was a significant decrease in ALP level as compared with saline control group. The cytometric results revealed that injection of HgCl(2) induced an increase in the DNA density in kidney tissues with an increase in aneuploid cells and decrease in diploid cells. However, DNA density decreased in liver tissues with mild decrease in diploid cells and little percentage of aneuploid cells. We can conclude that oral administration of either selenium or garlic produces a significant protection against liver and kidney damage induced by the HgCl(2) injection, but garlic appears to be more protective.     

左布比卡因硬膜外麻醉对腹部手术病人心肌酶的影响

目的:观察局部麻醉药(局麻药)左布比卡 因硬膜外麻醉对手术病人心肌酶谱的影响,并与布 比卡因作对比,评估其临床应用的安全性。方法:择 期行胆囊切除手术的病人60例,均行硬膜外麻醉, 随机双盲分成2组,左布比卡因组30例、布比卡因 组30例,2组分别用0.56%左布比卡因,或用0.56 %布比卡因,总量均为13mL;注射局麻药前及术后 24h取静脉血测定肝、肾功能及心肌酶谱。结果:2 组术后ALT,AST,BUN,Cr,LDH,α 羟丁酸脱氢酶 (BDH),肌酸激酶(CK)均有增高;与术前比较有显 著差异(P<0.05或P<0.01),组间比较除CK, BDH外均无显著差异(P>0.05),左布比卡因组和布比卡因组CK的增加值分别为(440±s120)U·L-1和(530±135)U·L-1,2组比较差异有非常显著意义(P<0.01)。2组麻醉疗效比较,差异无显著意义。结论:左布比卡因和布比卡因行硬膜外麻醉效果均较好,但以心肌酶的部分指标作比较左布比卡因更安全。     

参芎葡萄糖注射液联合前列腺素E_1脂微球载体制剂治疗CRF失代偿期患者的临床观察

目的:观察参芎葡萄糖注射液联合前列腺素E1脂微球载体制剂治疗慢性肾功能衰竭(CRF)失代偿期患者的疗效及安全性。方法:将我院148例CRF失代偿期患者随机分成2组:对照组70例,给予低盐低脂优质蛋白饮食,口服复方α-酮酸片,配合降压、降糖、控制感染等对症治疗;治疗组78例,在对照组治疗基础上应用参芎葡萄糖注射液联合前列腺素E1脂微球载体制剂。观察治疗前后尿素氮(BUN)、肌酐(Scr)、24h尿蛋白、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)及纤维蛋白原(FIB)等指标。结果:与治疗前比较,2组BUN、Scr、24h尿蛋白显著下降(P<0.05或P<0.01),且治疗组与对照组比较,下降更为显著(P<0.05);治疗组治疗后PT、APTT均延长,FIB有所下降(P<0.05或P<0.01)。2组均未见严重不良反应发生。结论:参芎葡萄糖注射液联合前列腺素E1脂微球载体制剂能够明显改善CRF失代偿期患者的肾功能,延缓其病情进展。     

妊娠期高血压疾病患者肝肾功能监测的临床意义

目的探讨妊娠期高血压疾病(HDCP)患者肝肾功能指标监测的临床意义。方法分析109例HDCP患者(包括妊娠高血压组、轻度子痫前期组和重度子痫前期组)和66例健康妊娠组的初诊建卡时及孕末期血清尿素氮(BUN)、肌酐(Cr)、尿酸(UA)、谷丙转氨酶(ALT)和谷草转氨酶(AST)等指标,了解其变化情况及与HDCP的关联性。结果各组间孕末期UA值均显著高于初诊建卡时。与健康妊娠组相比,重度子痫前期组孕末期UA值和Cr值改变显著(P<0.01)。各组间孕末期BUN、ALT和AST指标变化也无显著差异(P>0.05)。结论在HDCP孕妇的肝肾功能各项指标中,血清UA对于预测HDCP的发展意义最显著。     

药物依赖者肝、心、肾功能损伤的报告

本文报告100例海洛因及盐酸二氢埃托啡成瘾者肝、心、肾功能的损伤情况。抽取空腹晨血,分别测定谷丙转氨酶(GPT)、谷草转氨酶(GOT)、乳酸脱氢酶(LDH)、硷性磷酸酶(ALP)、γ-谷氨酰转肽酶(γ-GT),β_2-微球蛋白(β_2-MG),尿素氮(BUN),肌酐(Cr)。结果与对照组相应的数据比较,除BUN外,均有非常显著性差异。表明滥用者的肝、心、肾均受到不同程度的损伤。同时用海洛因和盐酸二氢埃托啡两种药患者的损伤程度要重于单用海洛因者。结果还表明,盐酸二氢埃托啡不但严重损伤脏器,而且完全能致身体依赖性。     

实验性兔羊水栓塞血浆凝血指标的含量变化

目的　观察兔羊水栓塞 ( AFE)后血浆凝血指标的动态变化。方法　采用怀孕家兔制作羊水栓塞动物模型 ,将不同性质的自身羊水注入兔血循环 ,分别在羊水注入前、注入后 5、45 m in从兔心脏取血 ,用血凝仪检测血浆中各项凝血指标包括纤维蛋白原定量 ( FIB)、血浆凝血酶原时间 ( PT)、凝血酶凝固时间 ( TT)、活化部分凝血活酶时间 ( APTT)的动态变化。结果　注入羊水后 PT、TT、APTT时间显著延长 ( P<0 .0 1) ,FIB则显著降低 ( P<0 .0 1) ,而对照组无显著变化 ( P>0 .0 5 )。结论　凝血指标的动态变化表明羊水栓塞早期有发生弥漫性血管内凝血 ( DIC)的趋势 ,胎盘提取液中的某些成分可能加重了 DIC的严重程度     

Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats.

Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl(2); Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl(2) induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects.     

妊娠期糖尿病患者血脂游离脂肪酸与新生儿动脉血气血乳酸心肌酶的变化研究

目的 探讨妊娠期糖尿病患者血脂、游离脂肪酸(FFA)水平与新生儿动脉血气、血乳酸(LAC)、心肌酶水平的变化.方法 选取2019年7月至2020年7月在西安高新区医院定期体检与分娩且确诊的妊娠期糖尿病患者102例作为研究组,选取同期在本院进行定期体检的健康孕妇102名作为对照组,回顾性分析2组人群的资料.对2组人群的血...     

溶血标本对标本中生化指标准确性的影响分析

目的 讨论标本溶血对生化检验结果产生的影响.方法 120例进行身体检查的健康体检者,均抽取空腹静脉血4 ml,并将静脉血标本分为2份,每份2 ml,选取其中120份标本作为常规组,另120份标本作为溶血组.常规组进行常规的生化检验,溶血组诱导溶血之后进行生化检验.比较两组天门冬氨酸氨基转移酶(AST)、谷丙转氨酶(AL...