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6-姜酚,生姜的一种生物活性化合物,通过调节氧化应激和炎症减轻链脲佐菌素诱导的糖尿病大鼠的肾损伤。

6-Gingerol, a Bioactive Compound of Ginger Attenuates Renal Damage in Streptozotocin-Induced Diabetic Rats by Regulating the Oxidative Stress and Inflammation.

作者信息

Almatroodi Saleh A, Alnuqaydan Abdullah M, Babiker Ali Yousif, Almogbel Mashael Abdullah, Khan Amjad Ali, Husain Rahmani Arshad

机构信息

Department of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.

Department of Medical Biotechnology, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.

出版信息

Pharmaceutics. 2021 Feb 28;13(3):317. doi: 10.3390/pharmaceutics13030317.

DOI:10.3390/pharmaceutics13030317
PMID:33670981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7997342/
Abstract

The aim of present study is to investigate the role of 6-gingerol in ameliorating the renal injury in streptozotocin (STZ)-induced diabetic rats. The diabetes was induced by using a single dose of freshly prepared STZ (55 mg/kg body weight) intraperitoneally which causes the degeneration of pancreatic Langerhans islet β-cells. The diabetic rats were treated with oral gavage of 6-gingerol (10 mg/kg b.w.). The treatment plan was continued for 8 weeks successively and the body weight and fasting blood glucose levels were weekly checked. The biochemical parameters like lipid profile, kidney profile, antioxidant enzyme levels, lipid peroxidation and anti-inflammatory marker levels were investigated after the treatment plant. The pathological condition of kidneys was examined by haematoxylin-eosin (H&E) staining besides this analysis of NF-B protein expression by immuno-histochemistry was performed. Some of the major parameters in diabetes control vs. normal control were reported as fasting blood glucose (234 ± 10 vs. 102 ± 8 mg/dL), serum creatinine (109.7 ± 7.2 vs. 78.9 ± 4.5 μmol/L) and urea (39.9 ± 1.8 vs. 18.6 mg/dL), lipid profile levels were significantly enhanced in diabetic rats. Moreover, diabetic rats were marked with decreased antioxidant enzyme levels and increased inflammatory markers. Treatment with 6-gingerol significantly restored the fasting blood glucose level, hyperlipidaemia, () and inflammatory marker levels, NF-B protein expression and augmented the antioxidant enzyme levels in the kidneys of diabetic rats. The kidney damage was significantly normalized by the treatment of 6-gingerol and it provides an evidence that this novel compound plays a significant role in the protection of kidney damage. These findings demonstrate that 6-gingerol reduces lipid parameters, inflammation and oxidative stress in diabetic rats, thereby inhibiting the renal damage. Our results demonstrate that use of 6-gingerol could be a novel therapeutic approach to prevent the kidney damage associated with the diabetes mellitus.

摘要

本研究的目的是探讨6-姜酚在改善链脲佐菌素(STZ)诱导的糖尿病大鼠肾损伤中的作用。通过腹腔注射单剂量新鲜配制的STZ(55mg/kg体重)诱导糖尿病,这会导致胰腺朗格汉斯胰岛β细胞变性。给糖尿病大鼠口服灌胃6-姜酚(10mg/kg体重)。连续8周持续该治疗方案,并每周检查体重和空腹血糖水平。治疗方案结束后,研究脂质谱、肾脏指标、抗氧化酶水平、脂质过氧化和抗炎标志物水平等生化参数。除了通过免疫组织化学分析NF-κB蛋白表达外,还用苏木精-伊红(H&E)染色检查肾脏的病理状况。与正常对照组相比,糖尿病对照组的一些主要参数如下:空腹血糖(234±10 vs. 102±8mg/dL)、血清肌酐(109.7±7.2 vs. 78.9±4.5μmol/L)和尿素(39.9±1.8 vs. 18.6mg/dL),糖尿病大鼠的脂质谱水平显著升高。此外,糖尿病大鼠的抗氧化酶水平降低,炎症标志物增加。用6-姜酚治疗可显著恢复糖尿病大鼠肾脏的空腹血糖水平、高脂血症、(此处原文缺失内容)和炎症标志物水平、NF-κB蛋白表达,并提高抗氧化酶水平。6-姜酚治疗可使肾脏损伤明显恢复正常,这证明这种新型化合物在保护肾脏损伤中起重要作用。这些发现表明,6-姜酚可降低糖尿病大鼠的脂质参数、炎症和氧化应激,从而抑制肾脏损伤。我们的结果表明,使用6-姜酚可能是预防糖尿病相关肾脏损伤的一种新型治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/2f8bc30d24b2/pharmaceutics-13-00317-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/17508b7f49e5/pharmaceutics-13-00317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/b4f82b862188/pharmaceutics-13-00317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/26d80f3a458b/pharmaceutics-13-00317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/0c544602362d/pharmaceutics-13-00317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/5a8d098ace7a/pharmaceutics-13-00317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/21023452de7c/pharmaceutics-13-00317-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/b31763aabf1c/pharmaceutics-13-00317-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/2f8bc30d24b2/pharmaceutics-13-00317-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/17508b7f49e5/pharmaceutics-13-00317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/b4f82b862188/pharmaceutics-13-00317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/26d80f3a458b/pharmaceutics-13-00317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/0c544602362d/pharmaceutics-13-00317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/5a8d098ace7a/pharmaceutics-13-00317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/21023452de7c/pharmaceutics-13-00317-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/b31763aabf1c/pharmaceutics-13-00317-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6178/7997342/2f8bc30d24b2/pharmaceutics-13-00317-g008.jpg

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