Role of Some Natural Antioxidants in the Modulation of Some Proteins Expressions against Sodium Fluoride-Induced Renal Injury.

Role of Some Natural Antioxidants in the Modulation of Some Proteins Expressions against Sodium Fluoride-Induced Renal Injury.
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DOI:
10.1155/2018/5614803
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发表时间:
2018
影响因子:
--
通讯作者:
Hasan IH
Hasan IH
中科院分区:
生物学3区
文献类型:
--
作者:
Alhusaini AM;Faddah LM;El Orabi NF;Hasan IH

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本工作的目的是寻找 N-乙酰半胱氨酸 (NAC) 和/或百里醌 (THQ) 在预防氟化钠 (NaF) 引起的急性肾损伤中的作用。 将大鼠分为五组:G1为正常组(对照),G2为腹腔注射10mg/kg NaF中毒,G3为10mg THQ/kg,G4为20mg NAC/kg,G5为THQ和NAC联合治疗。之前的治疗每天与 NaF 一起口服,持续四个星期。 NaF中毒的大鼠血清尿素、肌酐、尿酸、肾脂质过氧化、一氧化氮和TNF-α水平显着升高,而超氧化物歧化酶(SOD)和谷胱甘肽(GSH)水平降低。 Toll样受体4(TLR4)、脂质运载蛋白、血管粘附分子1(VCAM-1)和BAX蛋白表达上调,而Bcl-2和NF-E2相关因子2(Nrf2)蛋白表达下调。 DNA片段也被放大。组织学分析显示,NaF 导致肾皮质破坏,包括肾小球、近端和远端曲管消失、肾小管细胞空泡化、局灶性坏死和细胞浸润。 THQ 和 NAC 补充剂抵消了 NaF 诱导的肾毒性,肾 GSH 和 SOD 的增加反映了这一点。 THQ 和 NAC 改善了所有改变的蛋白质表达,改善了肾脏结构,并减少了 DNA 碎片。 氧化应激在增强 NaF 毒性中的作用表明 NAC 和 THQ 通过多种机制对氟化物毒性具有肾脏保护作用。
The aim of the present work is to find the effects of N-acetylcysteine (NAC) and/or thymoquinone (THQ) in the protection against acute renal injury induced by sodium fluoride (NaF). Rats were distributed into five groups: G1 was normal (control), G2 was intoxicated with 10mg/kg NaF i.p., G3 was treated with 10mg THQ /kg, G4 was treated with 20mg NAC /kg, and G5 was treated with a combination of THQ and NAC. The previous treatments were given daily along with NaF for four weeks orally. Rats intoxicated with NaF showed a significant increase in serum urea, creatinine, uric acid, renal lipid peroxidation, nitric oxide, and TNF-α levels, whereas the activity of superoxide dismutase (SOD) and glutathione (GSH) level was reduced. The expressions of Toll-like receptor-4 (TLR4), Lipocalin, vascular adhesion molecule-1(VCAM-1), and BAX proteins were upregulated, whereas Bcl-2 and NF-E2-related factor 2 (Nrf2) proteins expressions were downregulated. DNA fragmentation was also amplified. Histological analysis revealed that NaF caused a destructive renal cortex in the form of the glomerular corpuscle, the obliterated proximal and distal convoluted tubules, vacuolization in tubular cells focal necrosis, and cell infiltration. THQ and NAC supplementation counteracted NaF-induced nephrotoxicity as reflected by the increase in renal GSH and SOD. THQ and NAC ameliorated all the altered proteins expressions, improved renal architecture, and declined DNA fragmentation. The role of oxidative stress in the enhancement of NaF toxicity suggested the renoprotective effects of NAC and THQ against the toxicity of fluoride via multiple mechanisms.
百里醌在癌症中的分子和治疗潜力的综述。
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