应《网络安全法》要求，自2017年10月1日起，未进行实名认证将不得使用互联网跟帖服务。为保障您的帐号能够正常使用，请尽快对帐号进行手机号验证，感谢您的理解与支持！

24小时热门版块排行榜    

小木虫论坛-学术科研互动平台 » 生物医药区 » 新药研发 » 快捷药讯 » 【求助】氧化型谷胱甘肽二钠注射液的原研商信息或其他文献均可
31/1返回列表
查看: 1085  |  回复: 2
只看楼主 @他人 存档 新回复提醒 (忽略) 收藏    在APP中查看

hypharm

铜虫 (初入文坛)

[交流] 【求助】氧化型谷胱甘肽二钠注射液的原研商信息或其他文献均可

求助：氧化型谷胱甘肽二钠注射液由俄罗斯 Pharma BAM公司生产。
英文名称：Glutatione oxidized disodium salt
的相关文献及资料。万分感谢各位。
回复此楼

» 猜你喜欢

» 抢金币啦！回帖就可以得到:

查看全部散金贴
1楼 2010-12-15 20:12:05
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

ronalbeck

银虫 (正式写手)
★
koria0727(金币+1):多谢参与。 2010-12-17 09:18:13
hypharm(金币+5): 2010-12-19 14:48:19
1题目Role of oxidative stress and intracellular glutathione in the sensitivity to apoptosis induced by proteasome inhibitor in thyroid cancer cells.
Authors:du ZX; Zhang HY; Meng X; Guan Y; Wang HQ
Abstract:
BACKGROUND: The proteasome inhibitor bortezomib has shown impressive clinical activity alone and in combination with conventional and other novel agents for the treatment of multiple myeloma (MM) and some solid cancers. Although bortezomib is known to be a selective proteasome inhibitor, the downstream mechanisms of cytotoxicity and drug resistance are poorly understood. METHODS: Proteasome activity, intracellular glutathione (GSH) and ROS levels, as well as activities of GSH synthesis enzymes were measured using spectrophotometric methods. Cell death was analyzed using flow cytometry and caspase activity assay. The expression level of GSH synthesis enzymes were measured using real-time RT-PCR. RESULTS: At concentrations that effectively inhibited proteasome activity, bortezomib induced apoptosis in FRO cells, but not in ARO cells. Bortezomib elevated the amount of glutathione (GSH) and the treatment with bortezomib increased the level of mRNA for GCL, a rate-limiting enzyme in glutathione synthesis. Furthermore, depletion of GSH increases apoptosis induced by bortezomib, in contrast, repletion of GSH decreases bortezomib-mediated cell death. CONCLUSION: GSH protects cells from proteasome inhibition-induced oxidative stress and glutathione-dependent redox system might play an important role in the sensitivity to proteasome inhibition-induced apoptosis.
Source:BMC Cancer [BMC Cancer] 2009; Vol. 9, pp. 56. Date of Electronic Publication: 2009 Feb 16
2Impairment of endothelial function induced by glyc-oxidized lipoprotein a [Lp(a)].
Authors:Galle J; Winner B; Conzelmann E; Wanner C
Source:Cellular And Molecular Biology (Noisy-Le-Grand, France) [Cell Mol Biol (Noisy-le-grand)] 1998 Nov; Vol. 44 (7), pp. 1035-45.
Abstract:diabetic patients develop endothelial dysfunction early in the course of the disease. Atherogenic lipoproteins such as LDL and Lp(a) are important risk factors for endothelial dysfunction and undergo nonenzymatic glycation in hyperglycaemia. Here we assessed whether glycation of Lp(a) potentiates its damaging influence on endothelial function. Human Lp(a) was glycated by dialyzation for 7 days against buffer containing 200 mmol/l glucose, or sham-treated without glucose and oxidized by incubation with Cu++. The degree of glycation accounted to 32 +/- 4%, and glycation rendered Lp(a) more susceptible to oxidative modification when exposed to Cu++. Isolated rings of rabbit aorta were superfused with physiological salt solution, and isometric tension was recorded. Incubation of the aortic rings with sham-treated or with 30 microg/ml glycated Lp(a), not oxidized, had no influence on acetylcholine-induced, endothelium-dependent relaxation. Exposure of the aortic rings to 30 microg/ml oxidized non-glycated (ox) Lp(a) caused a significant inhibition (19% at 1 microM acetylcholine) of the endothelium-dependent relaxation. Incubation of aortic rings with 30 microg/ml oxidized glycated (glyc-ox) Lp(a) attenuated endothelium-dependent relaxation more potently than oxLp(a) (by 34% at 1 microM acetylcholine). The presence of diethyl-dithio-carbamate (DDC), an inhibitor of the endogenous superoxide dismutase (SOD), potentiated the inhibition of relaxation induced by oxLp(a) and by glyc-oxLp(a) [38% inhibition at 1 microM acetylcholine for oxLp(a), and 49% inhibition at 1 microM acetylcholine for glyc-oxLp(a)]. Co-incubation with the O2- scavenger 4,5-dihydroxy-1,3-benzene disulfonic acid disodium salt (TIRON) prevented the inhibition of relaxation by the oxidized lipoproteins, suggesting that enhanced NO-inactivation by O2- could be the underlying mechanism for the impairment of endothelium-dependent dilations by ox- and glyc-oxLp(a). The concentration of lysophosphatidycholine, a lipoprotein oxidation product and stimulus for O2- formation, was significantly enhanced in oxLp(a) and in glyc-oxLp(a) compared to native lipoproteins. Conclusion: Glycation enhances the endothelium-damaging influence of oxLp(a), presumably by enhancing oxidative stress. The likely mechanism for attenuation of endothelium-dependent dilations is increased formation of O2-, resulting in inactivation of nitric oxide. This mechanism may play an important role in diabetic patients and may contribute to disturbed organ perfusion.

[ Last edited by ronalbeck on 2010-12-16 at 14:45 ]
赞一下(1人) 回复此楼
2楼2010-12-16 14:43:58
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖

hypharm

铜虫 (初入文坛)
引用回帖:
Originally posted by hypharm at 2010-12-15 20:12:05:
求助：氧化型谷胱甘肽二钠注射液由俄罗斯 Pharma BAM公司生产。
英文名称：Glutatione oxidized disodium salt
的相关文献及资料。万分感谢各位。

《需要质量标准、处方工艺、原料物理化学性质类的文献》
赞一下 回复此楼
3楼2010-12-19 14:47:59
已阅   回复此楼   关注TA 给TA发消息 送TA红花 TA的回帖
相关版块跳转 我要订阅楼主 hypharm 的主题更新
31/1返回列表
普通表情 龙 兔 虎 猫 高级回复 (可上传附件)
信息提示
关闭
请填处理意见
关闭