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甲醛熏蒸软木塞对胶囊制剂崩解时限的影响

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松花粉对甘油诱导大鼠急性肾衰竭的保护作用

目的：研究松花粉对甘油诱发大鼠急性肾衰竭（acute renal failure,ARF）的保护作用及机制。方法：采用双侧后肢注射50%甘油溶液（10 mL·kg-1）诱发大鼠成急性肾衰竭模型,检测大鼠血清肌酐（Scr）、血清尿素氮（BUN）的含量,肾组织中超氧化物歧化酶（SOD）的活性,谷胱甘肽（GSH）、丙二醛（MDA）的含量,同时测定肾组织中一氧化氮（NO）的含量和诱导型一氧化氮合酶（iNOS）的活性;HE染色观察肾病理组织形态学变化。结果：与空白组大鼠相比,模型组大鼠血清Scr和BUN的含量明显上升,肾组织中SOD的活性和GSH的含量显著降低,MDA的含量显著升高;组织病理检查发现,模型组大鼠肾小管损伤明显,肾皮质细胞部分脱落,肾小球肿胀,间质炎性侵润明显。给予松花粉治疗后,可显著降低ARF大鼠血清Scr和BUN,升高肾组织中SOD的活性、GSH的含量,降低MDA的含量,同时发现,松花粉可明显降低肾组织中NO的含量和iNOS的活性,并显著降低肾组织损伤。结论：松花粉对甘油致大鼠ARF具有治疗作用,其作用机制可能与抑制iNOS的活性,降低体内NO过多产生,降低NO相关的脂质过氧化过程有关。     

卡托普利对甘油诱导的急性肾衰的保护作用及其机制探讨

目的研究卡托普利对甘油诱导的横纹肌溶解性急性肾衰的保护作用及其机制。方法用50%（v/v）的甘油按8mL.kg^-1后肢肌内注射建立急性肾衰的动物模型。所有大鼠单笼饲养,药物处理组每日分别以卡托普利和依那普利灌胃共7d,第7d损伤组和药物处理组禁水24h后注射甘油,注射甘油后饮水不限,24h后处死动物。通过检测血浆晚期氧化蛋白产物（AOPP）水平、肾组织形态学变化、超氧化物歧化酶（SOD）、血管紧张素转换酶（ACE）和谷胱甘肽过氧化物酶（GSH-Px）活性等查明AOPP是否与急性肾衰有关,并阐明卡托普利对其的保护作用及其机制。结果给大鼠后肢肌内注射50%（v/v）的甘油能诱导横纹肌溶解性急性肾衰,降低SOD、GSH-Px的活性和NO浓度,升高血尿素氮（BUN）、肌酐（Cr）浓度、AOPP和脂质过氧化产物（MDA）水平。卡托普利（30mg·kg^-1）能减轻肾损害和改善肾功能,逆转SOD、GSH-Px的活性、NO和AOPP水平的改变,而依那普利（30mg·kg^-1）和低剂量的卡托普利（10mg·kg^-1）保护作用不明显。结论卡托普利（30mg·kg^-1）对横纹肌溶解所致急性肾衰具有明显的保护作用,该作用可能与其抗氧化作用有关,而且可能是巯基依赖性的。     

Protective role of caffeic acid phenethyl ester (cape) on gentamicin-induced acute renal toxicity in rats

The toxicity of gentamicin (GEN) in the kidney seems to relate to the generation of reactive oxygen species (ROS). Caffeic acid phenethyl ester (CAPE) has been demonstrated to have antioxidant, free radical scavenger and anti-inflammatory effects. It has been proposed that antioxidant maintain the concentration of reduced glutathione (GSH) may restore the cellular defense mechanisms and block lipid peroxidation thus protect against the toxicity of wide variety of nephrotoxic chemicals. We investigated the effects of CAPE on GEN-induced changes in renal malondialdehyde (MDA), a lipid peroxidation product, nitric oxide (NO) generation, superoxide dismutase (SOD), catalase (CAT) activities, GSH content, blood urea nitrogen (BUN) and serum creatinine (Cr) levels. Morphological changes in the kidney were also examined. A total of 32 rats were equally divided into four groups which were: (1) control, (2) injected with intraperitoneally (i.p.) GEN, (3) injected with i.p. GEN+CAPE and (4) injected with i.p. CAPE. GEN administration to control rats increased renal MDA and NO generation but decreased SOD and CAT activities, and GSH content. CAPE administration with GEN injections caused significantly decreased MDA, NO generation and increased SOD, CAT activities and GSH content when compared with GEN alone. Serum level of BUN and Cr significantly increased as a result of nephrotoxicity. CAPE also, significantly decreased serum BUN and Cr levels. Morphological changes in the kidney due to GEN, including tubular necrosis, were evaluated qualitatively. In addition, CAPE reduced the degree of kidney tissue damage induced by GEN. Both biochemical findings and histopathological evidence showed that administration of CAPE reduced the GEN-induced kidney damage. Our results indicated that CAPE acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level. Thus, CAPE could be effectively combined with GEN treatment.     

大黄和泽泻提取物对二甘醇致小鼠肾脏损伤的保护作用研究

目的:研究大黄和泽泻提取物对二甘醇(DEG)致小鼠肾脏损伤的保护作用及其机制。方法:采用ig给予DEG方法建立小鼠肾脏损伤模型,ig给予大黄和泽泻提取物后测定血清中肌酐(Cr)和尿素氮(BUN)浓度,测定超氧化物歧化酶(SOD)和谷胱甘肽过氧化酶(GSH-PX)活性及丙二醛(MDA)含量变化。结果:小鼠ig给予DEG后有明显中毒表现,肾脏体质量比增加,血清中Cr和BUN水平升高,肾组织SOD和GSH-PX活性降低、MDA含量增加;给予大黄和泽泻提取物后小鼠中毒表现明显减轻,肾脏体质量比减少,血清中Cr和BUN水平明显降低,肾组织SOD和GSH-PX活性升高、MDA含量降低。结论:大黄和泽泻提取物对DEG所致小鼠肾脏损伤具有明显的保护作用,该作用与其改善肾脏抗氧化酶活性及抑制脂质过氧化反应有关。     

益气补肾方药对顺铂致大鼠肾脏氧化损伤的保护作用

目的:探讨不同剂量中药对顺铂(DDP)所致大鼠肾脏氧化损伤的保护作用。方法:实验大鼠分为正常对照组、DDP模型组、低剂量中药组(10.8 g·kg^-1)、中剂量中药组(21.6 g·kg^-1)和高剂量中药组(32.4 g·kg^-1)。DDP模型组和3个中药组一次性尾静脉注射DDP (8 mg·kg^-1),正常对照组注射等量生理盐水。注射DDP当天起,3个中药组每日灌服相应剂量的中药煎剂。检测血清尿素氮(BUN)、肌酐(Cr)、肾皮质丙二醛(MDA)、一氧化氮(NO)含量和超氧化物歧化酶(SOD)、诱导型一氧化氮合酶(iNOS)的活性。结果:灌服中剂量中药组的大鼠与DDP模型组相比肾脏系数、BUN、Cr含量显著降低,肾皮质SOD活性显著升高,MDA、NO含量以及iNOS活性显著降低。结论:适当剂量的益气补肾方药可有效拮抗DDP所致的肾毒性,抑制DDP诱导的肾脏氧化损伤。     

抗癌药顺铂对小鼠的耳、肾和肝毒性及其机制的研究

目的　以小鼠为实验对象建立抗癌药顺铂毒性研究的实验动物模型 ,并探讨其毒性作用产生的可能机制 ,为进一步对顺铂毒性作用的防治研究提供科学参考资料。方法　选择♂昆明种小鼠 ,经腹腔连续注射顺铂 5d ,观察不同剂量顺铂对小鼠的听力、肾脏和肝脏的毒性作用及肝和肾组织抗氧化系统各指标的变化。结果　顺铂可引起小鼠体重明显下降、全频率的听力阈值升高 ,肝和肾的脏器系数、血清尿素氮 (BUN)含量和丙氨酸氨基转换酶 (ALT)活性等指标的异常 ,并呈剂量依赖关系。此外 ,顺铂还可引起肝和肾抗氧化及氧化损伤指标的异常。结论　 3 0～ 4 0mg·kg-1b w的顺铂可引起小鼠出现明显的听力、肾和肝组织的损伤。氧化损伤是抗癌药顺铂产生其毒性作用的可能机制之一 ,但对于不同的脏器和在不同的给药时期 ,其发挥的作用不同     

Ameliorative effects of gallic acid on gentamicin-induced nephrotoxicity in rats

Abstract

The major side effect of gentamicin (GEN) is nephrotoxicity which in turn restricts the clinical use of this drug. In this study, the effect of gallic acid (GA) on gentamicin-induced nephrotoxicity was studied. A total number of 28 male Wistar rats were randomly divided into four experimental groups: control, GEN (100 mg/kg/day), GEN + GA (30 mg/kg/day), GA (30 mg/kg/day). All drug administrations were done intraperitoneally (i.p) for eight consecutive days. Twenty-four hours after the last administration, blood samples were collected to determine serum creatinine (Cr), blood urea nitrogen (BUN). The right kidney was used for histological examination. Malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activity were assayed in left renal tissue. Results showed a significant increase in the levels of MDA, NO, Cr, and BUN and decrease of GSH, CAT, GPx, and SOD by GEN administration. Co-administration with GA showed reduction in the levels of MDA, NO, Cr, and BUN and increase in GSH, CAT, GPx, and SOD. Also, the nephroprotective effect of GA was confirmed by the histological examination of the kidneys. The results of our study showed that GA exerts a significant nephroprotective effect against GEN-induced nephrotoxicity.     

Oral erdosteine administration attenuates cisplatin-induced renal tubular damage in rats.

The effect of oral erdosteine on tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities are investigated in the cisplatin model of acute renal failure in rats. A single dose of cisplatin caused kidney damage manifested by kidney histology as well as increases in plasma creatinine and blood urea nitrogen (BUN) levels. Treatment with free radical scavenger erdosteine attenuated increases in plasma creatinine and BUN, and tissue MDA and NO levels, and provided a histologically-proven protection against cisplatin-induced acute renal failure. Erdosteine also reduced depletion in the tissue CAT, GSH-Px, and SOD activities. These results show that erdosteine may be a promising drug for protection against cisplatin-induced nephrotoxicity. However, further studies with different doses of erdosteine are warranted for clarifying the issue.     

小儿碳酸氢盐透析液的制备及临床应用

目的：探讨适用于小儿急性肾功能衰竭(ARF)的血液透析液的制备。方法：制备无糖碳酸氢盐透析液．用于我院小儿急性肾功能衰竭患者。结果：ARF患者透析后血BUN、Cr显著下降,同时酸中毒和电解质紊乱纠正或改善。结论：无糖碳酸氢盐透析液用于ARF患儿疗效确切。值得临床推广使用。     

重症急性胰腺炎引起肾损伤及川芎嗪干预研究

目的：探讨重症急性胰腺炎引起肾损伤时血栓素（TXA2）、前列环素（PGI2）、内毒素（ET）及肾脏氧自由基（OFR）的变化。方法：144只SD大鼠随机分为空白对照组、胰腺炎组（SAP组）、实验组川芎嗪（治疗组）,每组48只。对照组开腹后仅翻动十二指肠;SAP组经胆胰管逆行注射3.5%牛磺胆酸钠0.1ml/100g建立大鼠SAP模型。分别于造模后3、6、12h抽血测定TXA2、PGI2、ET、尿素氮（BUN）、肌酐（Cr）浓度和肾组织OFR的含量,观察胰腺及肾脏病理改变。结果：SAP组造模后各时点Cr、BUN、TXA2、ET及肾脏丙二醛（MDA）含量比对照组升高明显,胰腺及肾脏病理改变严重;实验组各时点的以上各物质含量均明显减低,6、12h肾脏损害轻微。结论：川芎嗪通过改善微循环,减少ET入血,清除OFR等,改善SAP引起的肾损伤。