Abstract：
BACKGROUND: Hexavalent chromium (CrVI) is known to be a potentially hepatotoxic and nephrotoxic contaminant in humans and other animals, whose toxicity is associated with oxidative stress and inflammation. The aim of this study was to evaluate the potential protective effect of chlorogenic acid (CGA), which has known anti-inflammatory and antioxidant effects, on potassium dichromate (PDC)-induced acute hepatotoxicity and nephrotoxicity in rats.
RESULTS: Thirty-six Wistar albino rats were treated with CGA (10, 20, or 40 mg/kg, intraperitoneally) and/or PDC (15 mg/kg/day, intraperitoneally) as a single dose. Serum, liver, and kidney tissues were examined biochemically, histopathologically, and immunohistochemically. Compared to the control group, a significant increase in interleukin-6 (IL-6) levels and a significant decrease in serum and renal reduced glutathione (GSH) levels, liver catalase (CAT), tumour necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) levels were observed in the PDC group. The administration of PDC led to histopathological and immunohistochemical changes in rat liver and kidney tissues. With the administration of CGA, especially at the 10 mg/kg dosage, the above-mentioned parameters approached normal levels.
CONCLUSIONS: CGA had antioxidant and anti-inflammatory effects that alleviated PDC-induced acute hepato- and nephrotoxicity.
RESULTS: Thirty-six Wistar albino rats were treated with CGA (10, 20, or 40 mg/kg, intraperitoneally) and/or PDC (15 mg/kg/day, intraperitoneally) as a single dose. Serum, liver, and kidney tissues were examined biochemically, histopathologically, and immunohistochemically. Compared to the control group, a significant increase in interleukin-6 (IL-6) levels and a significant decrease in serum and renal reduced glutathione (GSH) levels, liver catalase (CAT), tumour necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) levels were observed in the PDC group. The administration of PDC led to histopathological and immunohistochemical changes in rat liver and kidney tissues. With the administration of CGA, especially at the 10 mg/kg dosage, the above-mentioned parameters approached normal levels.
CONCLUSIONS: CGA had antioxidant and anti-inflammatory effects that alleviated PDC-induced acute hepato- and nephrotoxicity.
摘要：
背景：已知六价铬（CrVI）是人类和其他动物的潜在肝毒性和肾毒性污染物，其毒性与氧化应激和炎症有关。本研究的目的是评估绿原酸（CGA）的潜在保护作用，具有已知的抗炎和抗氧化作用，重铬酸钾（PDC）诱导的大鼠急性肝毒性和肾毒性。
结果：36只Wistar白化病大鼠接受CGA（10、20或40mg/kg，腹膜内）和/或PDC（15mg/kg/天，腹膜内）作为单剂量。血清,肝脏,肾脏组织进行了生化检查，组织病理学,和免疫组织化学。与对照组相比,白细胞介素-6（IL-6）水平显着增加，血清和肾脏还原型谷胱甘肽（GSH）水平显着降低，肝脏过氧化氢酶（CAT），肿瘤坏死因子-α（TNF-α），在PDC组中观察到白细胞介素1β（IL-1β）水平。PDC的给药导致大鼠肝脏和肾脏组织的组织病理学和免疫组织化学改变。随着CGA的管理，特别是在10毫克/千克的剂量，上述参数接近正常水平。
结论：CGA具有抗氧化和抗炎作用，可减轻PDC诱导的急性肝和肾毒性。
结果：36只Wistar白化病大鼠接受CGA（10、20或40mg/kg，腹膜内）和/或PDC（15mg/kg/天，腹膜内）作为单剂量。血清,肝脏,肾脏组织进行了生化检查，组织病理学,和免疫组织化学。与对照组相比,白细胞介素-6（IL-6）水平显着增加，血清和肾脏还原型谷胱甘肽（GSH）水平显着降低，肝脏过氧化氢酶（CAT），肿瘤坏死因子-α（TNF-α），在PDC组中观察到白细胞介素1β（IL-1β）水平。PDC的给药导致大鼠肝脏和肾脏组织的组织病理学和免疫组织化学改变。随着CGA的管理，特别是在10毫克/千克的剂量，上述参数接近正常水平。
结论：CGA具有抗氧化和抗炎作用，可减轻PDC诱导的急性肝和肾毒性。
