AUTHENTICATIONOFTHECHINESEDRUG“KUDIDAN”（HERBAELEPHANTOPI）ANDITSSUBSTITUTESUSINGRANDOMPRIMEDPOLYMERASECHAINREACTION（PCR）

ＡＵＴＨＥＮＴＩＣＡＴＩＯＮＯＦＴＨＥＣＨＩＮＥＳＥＤＲＵＧ“ＫＵＤＩＤＡＮ”（ＨＥＲＢＡＥＬＥＰＨＡＮＴＯＰＩ）ＡＮＤＩＴＳＳＵＢＳＴＩＴＵＴＥＳＵＳＩＮＧＲＡＮＤＯＭＰＲＩＭＥＤＰＯＬＹＭＥＲＡＳＥＣＨＡＩＮＲＥＡＣＴＩＯＮ（ＰＣＲ）ＨＣａ...     

阿尼西坦及其胶囊的HPLC测定

阿尼西坦及其胶囊的ＨＰＬＣ测定邵东（上海复旦大学化学系，上海２００４３３）ＤＥＴＥＲＭＩＮＡＴＩＯＮＯＦＡＮＩＲＡＣＥＴＡＭＵＭＡＮＤＩＴＳＣＡＰＳＵＬＥＳＢＹＨＰＬＣ￥ＳＨＡＯＤｏｎｇ（ＤｅｐａｒｔｍｅｎｔｏｆＣｈｅｍｉｓｔｒｙ，ＦｕｄａｎＵｎｉｖ...     

西咪替丁及其制剂的双点电位测定法

西咪替丁及其制剂的双点电位测定法杜志茂（宝鸡市药品检验所陕西７２１００１）ＤＯＵＢＬＥ－ＰＯＩＮＴＰＯＴＥＮＴＩＯＭＥＴＲＩＣＡＳＳＡＹＯＦＣＩＭＥＴＩＤＩＮＥＡＮＤＩＴＳＰＲＥＰＡＲＡＴＩＯＮＳ￥ＤＵＺｈｉ－Ｍａｏ（ＢａｏｊｉＩｎｓｔｉｔｕｔｅｆｏ...     

人参皂甙对顺铂所致大鼠肾损害的保护作用

通过药物与肾皮质薄片直接孵育法和注射给药法观察了人参皂甙（Ｇｉｎ）对顺铂（ＣＰ）所致大鼠肾损害的作用。结果表明：ＣＰ１．０ｍｍｏｌ·Ｌ￣（－１）在含有对氨基马尿酸（ＰＡＨ）的生理盐水溶液中与肾薄片孵育１２０ｍｉｎ，导致薄片中ＰＡＨ的蓄积明显减少，Ｇｉｎ８０ｍｇ·Ｌ￣（－１）增加ＰＡＨ的蓄积并抑制ＣＰ引起的ＰＡＨ蓄积减少。ＣＰ７．５ｍｇ·ｋｇ￣（－１）ｉｐ导致时间依赖性的血浆尿素氮（ＢＵＮ）升高，肾皮质组织中超氧化物歧化酶（ＳＯＤ）活性降低和脂质过氧化代谢产物丙二醛（ＭＤＡ）升高Ｇｉｎ５０ｍｇ·ｋｇ￣（－１）每日２次ｉｐ抑制ＣＰ所致的ＢＵＮ和ＭＤＡ升高及ＳＯＤ活性降低，推测Ｇｉｎ对ＣＰ所致大鼠肾损害的保护作用可能与其增强肾小管细胞的内在反应性和抗脂质过氧化作用有关。     

羧甲基纤维素钠胶浆制备方法的比较

羧甲基纤维素钠胶浆制备方法的比较印嘉骏（江苏武进中医院，江苏２１３１６１）ＣＯＭＰＡＲＩＳＯＮＯＦＰＲＥＰＡＲＡＴＩＯＮＯＦＣＡＲＢＯＸＹＭＥＴＨＹＬＣＥＬＬＵＬＯＳＥＳＯＤＩＵＭＭＵＣＩＬＡＧＥ￥ＹＩＮＪｉａ－Ｊｕｎ（ＷｕｊｉｎＨｏｓｐｉｔａｌｏｆ...     

红景天中糖组份的分析

红景天中糖组份的分析ＣＯＭＰＯＳＩＴＩＯＮＡＮＡＬＹＳＩＳＯＦＰＯＬＹＳＡＣＣＨＡＲＩＤＥＩＮＲＨＯＤＩＯＬＡ骆传环舒融（北京放射医学研究所，北京１００８５０）ＬＵＯＣｈｕａｎ－Ｈｕａｎ，ＳＨＵＲｏｎｇ（ＢｅｉｊｉｎｇＩｎｓｔｉｔｕｔｅｏｆＲａｄｉａ...     

从甘草酸粗品制取甘草酸单钾盐

从甘草酸粗品制取甘草酸单钾盐邓国斌（兰州二七六五化工厂，甘肃７３００２０）ＰＲＥＰＡＲＡＴＩＯＮＯＦＭＯＮＯＰＯＴＡＳＳＩＵＭＧＬＹＣＹＲＲＨＩＺＩＮＡＴＥＦＲＯＭＣＲＵＤＥＧＬＹＣＹＲＲＨＩＺＩＣＡＣＩＤ￥ＤｅｎｇＧｕｏ－Ｂｉｎ（ＴｈｅＣｈｅｍｉｃ...     

复方利血平薄膜包衣片研究

复方利血平薄膜包衣片研究朱忠，黄国顺，李晓华（广州华乐制药厂，广东５１０５１０）ＳＴＵＤＩＥＳＯＮＣＯＭＰＯＵＮＤＲＥＳＥＲＰＩＮＥＴＡＢＬＥＴＳ￥ＺＨＵｚｈｏｎｇ；ＨＵＡＮＧＧｕｏ－Ｓｈｕｎ；ＬＩＸｉａｏ－Ｈｕａ（ＧｕａｎｇｚｈｏｕＨｕａｌｅＰｈａ...     

银杏苦内酯对急性胰腺炎大鼠的治疗作用及机制

观察血小板活化因子受体特异性拮抗刘银杏苦内酯（ＢＮ５２０２１）对牛磺胆酸钠诱导的急性胰腺炎（ＡＰ）大鼠的治疗作用及其对胰腺组织丙二醛（ＭＤＡ）．ＳＯＤ和Ｃａ２＋的影响。结果表明：ＢＮ５２０２１显著降低ＡＰ大鼠死亡率，延长平均存活时间、降低血清淀粉酶活性、减轻胰组织病理损伤；显著降低胰组织Ｃａ２＋含量和ＭＤＡ含量、提高ＳＯＤ活性。提示ＢＮ５２０２１对ＡＰ大鼠有一定治疗作用，此与其抑制钙超载、清除自由基有关。     

一种含硫、非β－内酰胺结构的β－内酰胺酶抑制剂6001

一种含硫、非β－内酰胺结构的β－内酰胺酶抑制剂６００１β－ＬＡＣＴＡＭＡＳＥＩＮＨＩＢＩＴＯＲ６００１，ＡＮＯＶＥＬＮＯＮ－β－ＬＡＣＴＡＭＳＵＬＦＵＲＣＯＮＴＡＩＮＩＮＧＣＯＭＰＯＵＮＤＰＲＯＤＵＣＥＤＢＹＳＴＲＥＰＴＯＭＹＣＥＳ刘，林文良，潘雅辉...     

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.     

二氢吡啶类钙拮抗剂对多柔比星肾毒性的影响

目的观察二氢吡啶类钙拮抗剂对多柔比星(Dox)肾毒性的影响。方法Dox单次6.5 m.gkg-1尾静脉注射诱导大鼠肾损伤,造模后次日大鼠分别ig硝苯地平15 m.gkg-1.d-1,尼群地平10 m.gkg-1.d-1,氨氯地平5 m.gkg-1.d-1,连续30 d,于给药后d 10,20和30收集各组大鼠24 h尿液测尿蛋白含量,于末次给药4 h后处死大鼠,测血清尿素氮和肌酐含量,测肾皮质还原型谷胱甘肽(GSH),丙二醛(MDA),一氧化氮(NO)含量及谷胱甘肽-S-转移酶(GST),过氧化物歧化酶(SOD),一氧化氮合酶(NOS)活性。结果硝苯地平组大鼠于给药d 10和d 20对Dox肾毒性的尿蛋白有增加作用,给药d 30时,对尿蛋白,血清尿素氮和肌酐均无明显影响,对肾组织GSH,MDA,NO含量及GST,SOD,NOS活性也无明显改变;尼群地平组大鼠于给药d 10,20和30时,对Dox肾毒性的尿蛋白及血清尿素氮和肌酐含量均有升高作用,并明显增加肾组织MDA,NO含量及NOS活性,显著降低GSH含量及GST,SOD活性;氨氯地平对Dox所致的尿蛋白,血清尿素氮和肌酐含量的升高具有降低作用,并明显降低肾组织MDA,NO含量及NOS活性,显著增加GSH含量及GST,SOD活性。结论硝苯地平对Dox肾毒性无明显影响,尼群地平则有加重作用,氨氯地平对Dox肾毒性具有保护作用。     

Differential effects of dihydropyridine calcium antagonists on doxorubicin-induced nephrotoxicity in rats

The aim of this study was to compare the roles of dihydropyridine calcium antagonists nifedipine, nitrendipine, amlodipine on doxorubicin (DXR)-induced nephrotoxicity in rats using biochemical, histopathological and immunohistochemical approaches. Male Sprague-Dawley rats were randomly divided into five experimental groups: control; DXR; DXR+nifedipine (15 mg/kg); DXR+nitrendipine (10 mg/kg); DXR+amlodipine (5 mg/kg). Results showed that treatment with DXR alone caused significant changes in the levels of urinary protein, serum creatinine (SCr), and blood urea nitrogen (BUN). Co-administration with amlodipine effectively reversed the effect of DXR on these parameters. In contrast, nifedipine and nitrendipine either had no effect or worsened DXR induced changes in the levels of urinary protein, SCr and BUN. Furthermore, DXR treatment caused significant increases in the levels of malondialdehyde (MDA), nitric oxide (NO), nitric oxide synthase (NOS) and significant decreases in the levels of reduced glutathione (GSH), glutathione-S-transferase (GST), and superoxide dismutase (SOD). These effects were significantly reduced by co-administration with amlodipine but not affected by nifedipine and worsened by nitrendipine. In addition to the biochemical changes, histopathological studies showed that DXR caused significant structural damages in the kidneys. Glomerular cell apoptosis, a decrease in Bcl-2 expression and an increase in Bax expression were observed in all rats treated with DXR. Co-administration with amlodipine effectively reversed the effect of DXR while nifedipine and nitrendipine had no effect. In conclusion, this study clearly indicated that amlodipine protected against DXR-induced nephrotoxicity while nifedipine and nitrendipine had no effect.     

葡甲胺对顺铂所致大鼠肾毒性的预防作用

目的　研究葡甲胺 (N MG)对顺铂 (CDDP)所致大鼠肾毒性的预防作用及其可能机制。方法　大鼠1次腹腔注射 5mg/kgCDDP动物模型 ,于CDDP处理前 1h经口给予N MG预处理。检测指标包括血尿素氮BUN、尿蛋白、尿铂 (Pt) ,肾组织匀浆中NOS、NO、MDA、SOD及肾组织Pt含量 ,同时观察抗肿瘤活性。结果　给药后第 3、5天N MG预处理组可明显预防CDDP所致大鼠肾功能损害 ,降低肾组织中NOS、NO、及MDA含量 ,增加SOD活性 (P <0 0 5或P <0 0 1)。另外 ,给药后第 3天尿Pt(0 .42 5 μg/mgCr)排泄量非常显著地高于CDDP组(0 2 45 μg/mgCr,P <0 0 1) ,肾组织Pt含量于给药后第 3、5天显著低于CDDP组 (P <0 0 5 )。N MG预处理对荷瘤小鼠的肿瘤抑制率与CDDP组无显著性差异。结论　N MG预处理能明显预防CDDP所致大鼠的肾损害 ,其预防作用机制可能是N MG促进Pt经尿排出 ,并减少了肾组织Pt蓄积 ,从而CDDP产生的自由基减少 ,脂质过氧化程度减轻。N MG对CDDP抗肿瘤活性无明显影响。     

Effect of recombinant human basic fibroblast growth factor on acute inflammation in mice and rats.

AIM: To investigate the anti-inflammatory effects of recombinant human basic fibroblast growth factor (rh-bFGF). METHODS: Several inflammation models such as croton oil-induced ear swelling, carrageenan-induced hind paw edema, and acute peritonitis in rats or mice were prepared. Superoxide dismutase (SOD) activity was measured by hydroxyamine method, nitric oxide (NO) concentration by Griess reaction assay, nitric oxide synthase (NOS) activity by NADPH-diaphoras stain assay, N-acetyl-beta- D-glucosaminidase (NAG) activity by colorimetry, prostaglandin E2 (PGE2) production by radioimmunoassay (RIA), malondialdehyde (MDA) content by thiobarbituric acid (TBA) fluorescence technique, and protein content by Coomassie brilliant blue method in peritoneal exudate in rats. RESULTS: Recombinant human bFGF 2, 4 kU/kg im inhibited croton oil-induced ear swelling and carrageenan-induced paw edema in mice. In addition, rh-bFGF 2, 4 kU/kg im reduced neutrophil counts in the rat peritoneal exudate, and lessened protein content in peritoneal exudate in rats and mice. In the rat peritonitis induced by carrageenan, rh-bFGF 4 kU/kg decreased the MDA and NO levels, inhibited the NOS activity, augmented the SOD activity, and lowered the production of PGE(2) in exudate. However, rh-bFGF had no effect on NAG content. CONCLUSION: Recombinant human bFGF has an anti-inflammatory effect and its mechanisms are related to the inhibition of NOS activity, reduction of NO, MDA, and PGE(2) content, and increase of SOD activity.     

The protective effect of captopril on nicotine-induced endothelial dysfunction in rat

This study was designed to examine the in vivo and in vitro effects of captopril, an angiotensin-converting enzyme inhibitor, on nicotine-induced endothelial dysfunction in rats. Endothelial dysfunction was induced by exposing isolated rat mesenteric arteries to nicotine (0.01, 0.1, or 1 mM) for 24 hr using an organ culture system, or by treating rats with nicotine (2 mg/kg/day, intraperitoneally) for 4 weeks. The protective effects of captopril were tested by exposing isolated mesenteric arteries to captopril (0.01, 0.03, or 0.1 mM) + nicotine (0.1 mM) for 24 hr, or by treating rats with captopril (3 mg/kg/day, intravenously) + nicotine (2 mg/kg/day, intraperitoneally) for 4 weeks. Exposure of the isolated mesenteric arteries to nicotine induced a significant concentration -dependent inhibition of endothelium-dependent relaxation. Co-culture of segments of mesenteric artery with captopril (0.03 or 0.1 mM) attenuated the nicotine-induced impairment of vasorelaxation in a dose-dependent manner. Administration of nicotine to rats for 4 weeks significantly impaired endothelium-dependent relaxation compared with control rats. This impairment was accompanied by a reduction in nitrite/nitrate, nitric oxide (NO) synthase (NOS), and superoxide dismutase (SOD) activities in the serum and aorta. Chronic captopril treatment not only improved the impairment of endothelium-dependent relaxation, but also prevented the reduction of nitrite/nitrate contents and of NOS and SOD activities in the serum and aorta. However, there were no significant differences in serum angiotensin-converting enzyme activity among the three groups. These results indicate that captopril can be used to attenuate nicotine-induced endothelial dysfunction, an effect that may be related not only to antioxidation, but also to enhancing NO production by preventing the decrease in NOS.     

川芎嗪对顺铂所致大鼠肾氧化损伤的保护作用

目的探讨川芎嗪（TMP）对顺铂（DDP）所致大鼠肾氧化损伤影响。方法将32只SD大鼠随机分成4组各8只：DDP+TMP 50 mg&#8226;kg－1&#8226;d－1组和DDP+TMP 100 mg&#8226;kg－1&#8226;d－1组分别腹腔注射TMP 50和100 mg&#8226;kg－1&#8226;d－1,连续5 d;对照组和DDP组给予0.9%氯化钠溶液,均5 mL&#8226;kg－1。给药第3天,除对照组外,其他3组腹腔注射DDP,8 mg&#8226;kg－1。实验第5天收集代谢笼中大鼠24 h尿,测尿蛋白含量;处死大鼠后测血清尿素氮（BUN）、肌酐（SCr）、24 h尿蛋白、肾皮质丙二醛（MDA）、还原型谷胱甘肽（GSH）、过氧化物歧化酶（SOD）、谷胱甘肽 S 转移酶（GST）活性及肾皮质一氧化氮（NO）含量、一氧化氮合酶（NOS）活性。结果与DDP组比较,DDP+TMP50 mg&#8226;kg－1&#8226;d－1组和DDP+TMP100 mg&#8226;kg－1&#8226;d－1组大鼠24 h尿蛋白分别下降41.45%和65.33%;BUN分别下降18.12%和57.51%;SCr分别下降14.39%和48.89%（P＜0.05或P＜0.01）;与DDP组比较,DDP+TMP 100 mg&#8226;kg－1&#8226;d－1组大鼠肾皮质MDA、NO含量及NOS活力分别降低36.73%,45.39%,22.86%（P＜0.05）,GSH含量和SOD、GST活性分别为DDP组的1.33,1.66,1.57倍（P＜0.05）。结论TMP对DDP所致大鼠肾氧化性损伤具有保护作用。     

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。     

黄芪注射液抗大鼠全脑缺血再灌注损伤机制

目的探讨黄芪注射液抗大鼠全脑缺血再灌注损伤机制。方法采用改良的Pulsinelli四血管法,复制大鼠全脑缺血15 min再灌注7 d损伤模型,应用生化法检测海马组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、一氧化氮合酶（NOS）的活性和丙二醛（MDA）、一氧化氮（NO）的含量,并观察黄芪注射液对上述指标的影响。结果与假手术组比较,模型组海马组织SOD、GSH-Px活力下降,NOS活力明显升高;MDA、NO含量升高（P〈0.05）。与模型组比较,黄芪注射液治疗组SOD、GSH-Px活力升高,NOS活力明显下降;MDA、NO含量下降（P〈0.05）。结论黄芪注射液对大鼠全脑缺血再灌注损伤有保护作用,机制与提高机体抗氧化能力,抑制脂质过氧化反应,减少自由基损伤有关。     

贝那普利和维生素E对糖尿病肾病大鼠氧化应激的影响

目的:观察贝那普利及维生素E对糖尿病肾病(DN)大鼠肾脏一氧化氮合成酶(NOS)活性、一氧化氮(NO),超氧化物歧化酶(SOD)、丙二醛(MDA)含量及血清总抗氧化能力的影响,探讨两者在DN中的可能作用机制。方法:注射链佐脲菌素制作DN模型,分为4组,A组:正常对照组;B组:糖尿病肾痛模型组;C组:贝那普利治疗组;D组:贝那普利 维生素E治疗组。于第12周检测24h尿蛋白定量(TP)、血清胱蛋白酶抑制剂C(Cys C)、糖化血红蛋白(HbAlc),血清总抗氧化能力,肾组织NOS、NO、SOD、MDA含量。结果:与A组相比,B组TP、CysC、HbAlc、肾组织血糖、MDA明显升高(P<0.01),而血清总抗氧化能力,肾组织NO、NOS、SOD明显降低(P<0.01)。与B组相比,C组TP、CysC、HbAlc、肾组织血糖显著降低(P<0.01),MDA亦下降(P<0.05),而总抗氧化能力增强(P<0.05),SOD升高(P<0.01)。与C组相比,D组TP、肾组织血糖下降更加显著(P<0.01),MDA下降(P<0.05),而NO、NOS、SOD明显升高(P<0.05或P<0.01),总抗氧化能力增强(P<0.05)。结论:贝那普利能降低TP、HbAlc、肾组织血糖、MDA,增加NO、NOS、SOD,维生素E可增加血清总抗氧化能力,清除自由基而有肾保护作用。两者对治疗DN氧化应激有协同作用。