Akomolafe Seun F, Olasehinde Tosin A, Adewale Omowumi O, Ajayi Olubunmi B
Department of Biochemistry, Faculty of Science, Ekiti State University, Ado Ekiti, Nigeria.
Department of Biochemistry, University of Fort Hare Alice, Eastern Cape, 5700, South Africa.
Biol Trace Elem Res. 2021 Jan;199(1):197-204. doi: 10.1007/s12011-020-02113-y.
The protective effect of curcumin on potassium bromate (KBrO)-induced renal damage was investigated in vivo. Treatment with KBrO (20 mg/kg bw) caused a significant increase in arginase and adenosine deaminase (ADA) activities in rats' kidney. However, oral administration of curcumin (20 mg/kg bw) caused a significant reduction in ADA and arginase activities in KBrO + CUR group. Furthermore, nitric oxide level was significantly low in KBrO group compared with the control. After treatment with curcumin in KBrO + CUR group, nitric oxide levels increased significantly (P < 0.05). Determination of some kidney biomarkers revealed elevated levels of creatinine, serum urea, and electrolytes (Na and Cl) in KBrO-treated rats. Curcumin effectively reduced the levels of these renal function parameters in KBrO + CUR groups and were not significantly different from the control. Antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities as well as glutathione (GSH) levels were significantly low with concomitant higher levels of malondialdehyde (MDA) after treatment with KBrO. Curcumin caused a significant increase in SOD, CAT, and GPX activities including GSH levels with lower production of MDA in kidney homogenates of rats in KBrO + CUR. Curcumin ameliorated corpuscular degeneration in the kidney tissue and exhibited protection against tubular necrosis. These results revealed the protective effect of curcumin against KBrO-induced renal toxicity by preventing degradation of ADA and arginine, improving antioxidant status and histopathological changes in rats' kidney.
在体内研究了姜黄素对溴酸钾(KBrO)诱导的肾损伤的保护作用。用KBrO(20毫克/千克体重)处理导致大鼠肾脏中精氨酸酶和腺苷脱氨酶(ADA)活性显著增加。然而,口服姜黄素(20毫克/千克体重)使KBrO+CUR组的ADA和精氨酸酶活性显著降低。此外,与对照组相比,KBrO组的一氧化氮水平显著降低。在KBrO+CUR组用姜黄素处理后,一氧化氮水平显著升高(P<0.05)。一些肾脏生物标志物的测定显示,KBrO处理的大鼠中肌酐、血清尿素和电解质(钠和氯)水平升高。姜黄素有效降低了KBrO+CUR组中这些肾功能参数的水平,且与对照组无显著差异。用KBrO处理后,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPX)等抗氧化酶活性以及谷胱甘肽(GSH)水平显著降低,同时丙二醛(MDA)水平升高。姜黄素使KBrO+CUR组大鼠肾脏匀浆中的SOD、CAT和GPX活性以及GSH水平显著升高,MDA产生减少。姜黄素改善了肾组织中的细胞变性,并表现出对肾小管坏死的保护作用。这些结果揭示了姜黄素通过防止ADA和精氨酸降解、改善抗氧化状态以及大鼠肾脏的组织病理学变化,对KBrO诱导的肾毒性具有保护作用。