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α-硫辛酸通过抑制体内氧化应激降低2型糖尿病患者尿足细胞标记蛋白的排泄。

The alpha-lipoic acid decreases urinary podocalyxin excretion in type 2 diabetics by inhibiting oxidative stress in vivo.

作者信息

Lin Haiyan, Ye Shandong, Xu Jiang, Wang Wei

机构信息

Department of Endocrinology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui, China; Department of Internal Medicine, Maanshan Maternal and Child Health Care Center, Maanshan, Anhui, China.

Department of Endocrinology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui, China.

出版信息

J Diabetes Complications. 2015 Jan-Feb;29(1):64-7. doi: 10.1016/j.jdiacomp.2014.09.011. Epub 2014 Sep 30.

Abstract

OBJECTIVE

To observe the effects of Alpha-lipoic acid (ALA) on oxidative stress (OS) in vivo and urinary podocalyxin (PCX, the glomerular podocyte marker protein) excretion in type 2 diabetics and explore its possible protective mechanisms on glomerular podocytes.

METHODS

Thirty-six type 2 diabetics were recruited as observation group and treated with ALA on the basis of initial therapy for six months, and 30 healthy subjects were selected as control group. FBG, HbA1c, serum glutathione peroxidase (SGSH-Px), superoxide dismutase (SSOD) activity, urinary malondialdehyde (UMDA), 8-hydroxy-deoxyguanosine (U8-OHdG), albumin (UALB), creatinine (UCr) and urinary PCX (UPCX) were determined at baseline and after six months' observation.

RESULTS

Compared with the control group, the ratios of UMDA/UCr (UMCR), U8-OHdG/UCr (U8CR), UALB/UCr (UACR) and UPCX/UCr (UPCR) increased markedly, SGSH-Px and SSOD decreased significantly in the diabetics (P<0.01); after sixth month treatment, the levels of UMCR, U8CR, UACR and UPCR reduced and SGSH-Px and SSOD increased markedly in the observation group (P<0.05) with no significant changes in FBG and HbA1c. UPCR had positive correlation with UACR, UMCR and U8CR (r=0.720, r=0.661, r=0.698, P<0.01), and negative correlation with SGSH-Px and SSOD in the diabetics (r=-0.608, r=-0.559, P<0.01).

CONCLUSION

ALA can provide some protection against glomerular podocyte injury in type 2 diabetics, which may be related partly to its effects in alleviating enhanced OS and strengthening antioxidant ability in vivo.

摘要

目的

观察α-硫辛酸(ALA)对2型糖尿病患者体内氧化应激(OS)及尿足突细胞标记蛋白(PCX)排泄的影响,并探讨其对肾小球足细胞可能的保护机制。

方法

选取36例2型糖尿病患者作为观察组,在初始治疗基础上加用ALA治疗6个月,选取30例健康受试者作为对照组。于基线期及观察6个月后测定空腹血糖(FBG)、糖化血红蛋白(HbA1c)、血清谷胱甘肽过氧化物酶(SGSH-Px)、超氧化物歧化酶(SSOD)活性、尿丙二醛(UMDA)、8-羟基脱氧鸟苷(U8-OHdG)、白蛋白(UALB)、肌酐(UCr)及尿PCX(UPCX)。

结果

与对照组相比,糖尿病患者UMDA/UCr(UMCR)、U8-OHdG/UCr(U8CR)、UALB/UCr(UACR)及UPCX/UCr(UPCR)比值明显升高,SGSH-Px及SSOD明显降低(P<0.01);观察组治疗66个月后,UMCR、U8CR、UACR及UPCR水平降低,SGSH-Px及SSOD明显升高(P<0.05),FBG及HbA1c无明显变化。糖尿病患者UPCR与UACR、UMCR及U8CR呈正相关(r=0.720,r=0.661,r=0.698,P<0.01),与SGSH-Px及SSOD呈负相关(r=-0.608,r=-0.559,P<0.01)。

结论

ALA对2型糖尿病患者肾小球足细胞损伤具有一定保护作用,可能与其减轻体内增强的氧化应激及增强抗氧化能力有关。

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