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糖尿病大鼠辅助干预和抗逆转录病毒治疗后的肾脏组织病理学和生化变化。

Renal histopathological and biochemical changes following adjuvant intervention of and antiretroviral therapy in diabetic rats.

作者信息

Offor Ugochukwu, Edwin Coleridge Stephen Naidu, Ogedengbe Oluwatosin Olalekan, Jegede Ayoola Isaac, Peter Aniekan Imo, Onyemaechi Okpara Azu

机构信息

Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa.

Department of Preclinical Sciences, School of Health Care Sciences, Faculty of Health Sciences, University of Limpopo, South Africa.

出版信息

Iran J Basic Med Sci. 2019 Nov;22(11):1359-1367. doi: 10.22038/ijbms.2019.31848.7663.

DOI:10.22038/ijbms.2019.31848.7663
PMID:32128103
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7038428/
Abstract

OBJECTIVES

Diabetic nephropathy (DN) is an important primary cause of end-stage kidney disease. This study explores the mechanisms of the reno-protective effects of () in diabetic rats following treatment with highly active antiretroviral therapy (HAART) regimen triplavar.

MATERIALS AND METHODS

Adult male Sprague-Dawley rats (n=48) were divided into 7 groups (A-G).Treatment groups (B-G) had 7 animals per group and control group (Group A) had 6 animals per group. Diabetes was induced with streptozotocin (STZ) by intraperitoneal injection (STZ 45 mg/kg body weight). The animals were euthanized on the tenth week with kidneys removed for examination and blood obtained via cardiac puncture.

RESULTS

Key renal parameters showed no albuminuria, normal blood urea nitrogen (BUN), serum creatinine and electrolytes in all groups treated with Untreated diabetic (Group B) and HAART treated diabetic (Group C) showed severe albuminuria, a significantly raised BUN and serum creatinine (<0.05) and gross electrolyte disturbances. Blood glucose levels were consistently and significantly raised in all groups not receiving the adjuvant (<0.05). Levels of oxidative stress enzymes Superoxide dismutase (SOD), Catalase and activities of Reduced Gluthaione (GSH) and Malondiadehyde (MDA) were significantly lower in all groups not receiving . Histopathology in untreated diabetic and HAART treated animals showed severe degenerative changes in the glomeruli and inflammatory cellular infiltration while treated animals showed an essentially normal glomerular appearance with capillary loops and normal cytoarchitecture.

CONCLUSION

extract administration improved blood glucose levels, reinstates renal function, reduces body weight loss and restores hyperglycemia.

摘要

目的

糖尿病肾病(DN)是终末期肾病的一个重要主要病因。本研究探讨高效抗逆转录病毒治疗(HAART)方案三联药物治疗后()对糖尿病大鼠肾脏保护作用的机制。

材料与方法

成年雄性Sprague-Dawley大鼠(n = 48)分为7组(A - G)。治疗组(B - G)每组7只动物,对照组(A组)每组6只动物。通过腹腔注射链脲佐菌素(STZ,45 mg/kg体重)诱导糖尿病。在第十周对动物实施安乐死,取出肾脏进行检查,并通过心脏穿刺采集血液。

结果

所有接受(此处原文缺失药物名称)治疗组关键肾脏参数显示无蛋白尿、血尿素氮(BUN)、血清肌酐和电解质正常。未治疗的糖尿病组(B组)和接受HAART治疗的糖尿病组(C组)显示出严重蛋白尿、BUN和血清肌酐显著升高(<0.05)以及明显的电解质紊乱。所有未接受辅助(此处原文缺失药物名称)组血糖水平持续且显著升高(<0.05)。所有未接受(此处原文缺失药物名称)组氧化应激酶超氧化物歧化酶(SOD)、过氧化氢酶水平以及还原型谷胱甘肽(GSH)和丙二醛(MDA)活性显著降低。未治疗的糖尿病动物和接受HAART治疗动物的组织病理学显示肾小球有严重退行性改变和炎性细胞浸润,而接受(此处原文缺失药物名称)治疗动物的肾小球外观基本正常,有毛细血管袢且细胞结构正常。

结论

提取物给药改善了血糖水平,恢复了肾功能,减少了体重减轻并纠正了高血糖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/c064497b312a/IJBMS-22-1359-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/e032176323fe/IJBMS-22-1359-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/980dc347b58e/IJBMS-22-1359-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/4219c3e28cff/IJBMS-22-1359-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/526d02f9a899/IJBMS-22-1359-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/c064497b312a/IJBMS-22-1359-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/e032176323fe/IJBMS-22-1359-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/980dc347b58e/IJBMS-22-1359-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/4219c3e28cff/IJBMS-22-1359-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/526d02f9a899/IJBMS-22-1359-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ef/7038428/c064497b312a/IJBMS-22-1359-g005.jpg

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