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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Protective effects of kolaviron and gallic acid against cobalt-chloride-induced cardiorenal dysfunction via suppression of oxidative stress and activation of the ERK signaling pathway
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Protective effects of kolaviron and gallic acid against cobalt-chloride-induced cardiorenal dysfunction via suppression of oxidative stress and activation of the ERK signaling pathway

机译：甲钴铁和没食子酸通过抑制氧化应激和激活ERK信号通路对氯化钴诱导的心肾功能不全的保护作用

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摘要

Cobalt (Co) toxicity is a potential public health problem due to recent renewed use of Co in orthopedic implants, dietary supplements, and blood doping in athletes and horses. We investigated the protective roles of kolaviron (KV), a bi-flavonoid of Garcinia kola, and gallic acid (GA) on cobalt chloride (CoCl2)-induced cardiorenal damage in rats. CoCl2 caused significant increases (p < 0.05) in serum creatine kinase-myocardial band (CK-MB), lactate dehydrogenase (LDH), aspartate transaminase (AST), xanthine oxidase (XO), urea, creatinine, malondialdehyde, H2O2, nitric oxide, as well as C-reactive protein expression, along with significant (p < 0.05) reduction in cardiac and renal expression of extracellular signal regulated kinase (ERK) and the activities of superoxide dismutase, catalase, and glutathione S-transferase. KV and GA prevented the toxic effects of CoCl2 by stimulating ERK expression and reversing Co-induced biochemical changes. Administration of CoCl2 alone did not significantly alter ECG patterns in the rats, although co-treatment with KV (200 mg/kg) produced QT-segment prolongation and also appeared to potentiate Co hypotension. Histopathology of the heart and kidneys of rats treated with KV and GA confirmed the biochemical data. KV and GA thus protected against cardiac and renal damage in Co intoxication via antioxidant and (or) cell survival mechanisms, possibly involving ERK activation.
机译：钴（Co）毒性是潜在的公共卫生问题，这是由于最近在整形外科植入物，膳食补充剂和运动员和马匹中的血液掺杂中重新使用了Co。我们调查了藤黄可乐的一种双黄酮，克拉维铁（KV）和没食子酸（GA）对氯化钴（CoCl2）诱导的大鼠心脏肾损伤的保护作用。 CoCl2导致血清肌酸激酶-心肌带（CK-MB），乳酸脱氢酶（LDH），天冬氨酸转氨酶（AST），黄嘌呤氧化酶（XO），尿素，肌酐，丙二醛，H2O2，一氧化氮显着增加（p <0.05）以及C反应蛋白的表达，以及心脏和肾脏中细胞外信号调节激酶（ERK）的表达以及超氧化物歧化酶，过氧化氢酶和谷胱甘肽S-转移酶的活性显着（p <0.05）降低。 KV和GA可通过刺激ERK表达并逆转Co诱导的生化变化来防止CoCl2的毒性作用。单独给予CoCl2并没有显着改变大鼠的ECG模式，尽管与KV（200 mg / kg）共同治疗会导致QT段延长，并且也似乎增强了Co低血压。用KV和GA治疗的大鼠心脏和肾脏的组织病理学证实了其生化数据。因此，KV和GA可通过抗氧化剂和（或）细胞存活机制（可能涉及ERK激活）在Co中毒时保护其免受心脏和肾脏损害。

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