首页> 外文期刊>Tissue and Cell >Bradykinin potentiating factor isolated from Buthus occitanus venom has a protective effect against cadmium-induced rat liver and kidney damage.
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Bradykinin potentiating factor isolated from Buthus occitanus venom has a protective effect against cadmium-induced rat liver and kidney damage.

机译:从<鱼中提取的缓激肽增强因子对镉诱导的大鼠肝肾损害具有保护作用。

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摘要

Bradykinin and its related peptides are widely distributed in venomous animals, including scorpion. A peptide fraction isolated from the venom of the Egyptian scorpion Buthus occitanus was proved to have a bradykinin-potentiating activity. The aim of the present study was conducted to investigate whether the treatment with bradykinin potentiating factor (BPF) offers more beneficial effects in reversing cadmium-induced oxidative stress in rat liver and kidney. Adult male rats, equally divided into control and two treated groups, 10 animals in each group. group (I) was orally given (1 ml) saline and served as a control group; group (II) of rats was given cadmium chloride (4 mg/kg) alone, once daily an oral dose for 7 successive days; group (III) of rats was given ip injection (1 ml) BPF, once daily a dose for 7 successive days prior to CdCl2 treatment and on the next 7 successive days with the same dose of cadmium as group II. Both organs were subjected to histopathological analysis with the light microscope. The activities of alanine aminotransferase (ALT), asparate aminotransferase (AST) and alkaline phosphatase (ALP) in serum were measured as indicators of the liver function. As parameters of the kidney function, creatinine, uric acid and urea concentrations in serum were determined. Also, malondialdehyde (MDA), reduced glutathione (GSH), super oxide dismutase (SOD) and catalase (CAT) were determined in both tissues. Cd exposure caused a significant decrease or inhibition in the activities of GSH, SOD, and CAT, with significant increase in the level of MDA, in versus to control groups in both liver and kidney. Also, when Cd was treated in co-administration with BPF induced increase or stimulation in the activity of GSH, SOD, and CAT, with significant decrease in the level of MDA when compared to Cd group in both organs. Histopathological changes of liver and kidney were also in accordance with the biochemical findings. Our data showed that Cd treatment induced histopathological alteration in the liver, severe hydropic degeneration in centrolobular zones. Inflammatory cells infiltration around the congested central vein and an obvious injury in some renal tubules. Bradykinin potentiating factor (BPF) administration prevented the histopathological alterations which observed in Cd-groups and both liver and kidney had essentially normal appearance in histopathological examination. In conclusion, BPF markedly ameliorated cadmium-induced liver and kidney tissue damage as evidenced by histological and biochemical examinations and acts as a potent scavenger of free radicals to protect the liver and kidney against the deleterious effect of acute cadmium intoxication.
机译:缓激肽及其相关肽广泛分布在包括蝎子在内的有毒动物中。事实证明,从埃及蝎子“ Buthus occitanus”的毒液中分离出的肽片段具有缓激肽激活作用。进行本研究的目的是研究缓激肽增强因子(BPF)的治疗是否在逆转镉诱导的大鼠肝脏和肾脏的氧化应激中提供更有益的作用。成年雄性大鼠平均分为对照组和两个治疗组,每组10只动物。 (I)组口服生理盐水(1ml)作为对照组。 (II)组的大鼠单独给予氯化镉(4 mg / kg),每天一次口服,连续7天; (III)组的大鼠接受 ip 注射(1 ml)BPF,每天一次,在CdCl 2 处理之前连续7天服用,然后在接下来的7天连续服用与第二组的镉剂量相同。用光学显微镜对两个器官进行组织病理学分析。测定血清中丙氨酸氨基转移酶(ALT),天冬氨酸氨基转移酶(AST)和碱性磷酸酶(ALP)的活性,作为肝功能的指标。测定血清中的肌酐,尿酸和尿素浓度作为肾脏功能的参数。此外,在两个组织中都测定了丙二醛(MDA),还原型谷胱甘肽(GSH),超氧化物歧化酶(SOD)和过氧化氢酶(CAT)。与肝脏和肾脏的对照组相比,镉暴露导致GSH,SOD和CAT活性显着降低或抑制,MDA水平显着升高。同样,当镉与BPF并用时,会引起GSH,SOD和CAT活性的增加或刺激,与两个器官中的Cd组相比,MDA的水平均显着下降。肝脏和肾脏的组织病理学变化也与生化结果一致。我们的数据表明,镉治疗可引起肝脏组织病理学改变,在小叶中心区发生严重的水样变性。炎性细胞浸润在充血的中心静脉周围,并且在一些肾小管中明显受损。缓激肽增强因子(BPF)的使用可以防止组织病理学改变,这种改变在Cd组中观察到,并且肝脏和肾脏在组织病理学检查中的外观都基本正常。总之,组织学和生化检查证明,BPF明显减轻了镉诱导的肝和肾组织损伤,并作为有效的自由基清除剂,保护肝脏和肾脏免受急性镉中毒的有害影响。

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