Applied Nutrition Division, Defence Food Research Laboratory, DRDO, Siddhartha Nagar, Mysore, 570011, India.
Biol Trace Elem Res. 2018 Jul;184(1):154-164. doi: 10.1007/s12011-017-1172-2. Epub 2017 Oct 9.
The aim of the study was to assess the protective effect of Picrorhiza kurroa hydroalcoholic extract (PCK), a glycoside-rich extract, against potassium dichromate (PDC)-induced liver oxidative stress in Wistar albino rats. Thirty-six male Wistar rats were divided into six groups: the control group (which received distilled water), the SIL group (which received 60 mg/kg silymarin), the PDC group (which received 30 mg/kg KCrO), and the treatment groups (which received 25, 50, 100 mg/kg PCK). Administration of PDC resulted in increased levels of liver enzymes such as alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP); up-regulated peroxidation biomarkers, i.e., thiobarbutric acid-reactive species (TBARS) and protein carbonyls in serum; and decreased activities of antioxidant enzymes like superoxide dismutase (SOD) and catalase (CAT) significantly in the liver tissue. Gene expression studies of tumor necrosis factor (TNF), mitogen-activated protein kinase (MAPK), growth arrest, and DNA damage-inducible protein (GADD45) revealed that there was a liver damage at the molecular level, and histopathological studies further confirmed the morphological changes by PDC administration. However, PCKs at 50 and 100 mg/kg promoted significant restoration of liver enzyme levels and the activities of antioxidant enzymes were kept close to the values of the control and SIL groups. Our current study confirms that the active compounds present in the PCK might have conferred a strong protection against potassium dichromate-induced oxidative stress.
本研究旨在评估佩枯果水醇提取物(PCK)——一种富含糖苷的提取物——对 Wistar 白化大鼠重铬酸钾(PDC)诱导的肝氧化应激的保护作用。36 只雄性 Wistar 大鼠被分为六组:对照组(给予蒸馏水)、SIL 组(给予 60mg/kg 水飞蓟素)、PDC 组(给予 30mg/kg KCrO)和治疗组(给予 25、50、100mg/kg PCK)。PDC 的给药导致血清中转氨酶如丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和碱性磷酸酶(ALP)水平升高;过氧化生物标志物如硫代巴比妥酸反应性物质(TBARS)和蛋白羰基水平上调;肝组织中超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等抗氧化酶的活性显著降低。肿瘤坏死因子(TNF)、丝裂原活化蛋白激酶(MAPK)、生长停滞和 DNA 损伤诱导蛋白(GADD45)的基因表达研究表明,在分子水平上存在肝损伤,组织病理学研究进一步证实了 PDC 给药引起的形态变化。然而,50 和 100mg/kg 的 PCK 显著促进了肝酶水平的恢复,并且抗氧化酶的活性接近对照组和 SIL 组的水平。我们目前的研究证实,PCK 中存在的活性化合物可能对重铬酸钾诱导的氧化应激具有很强的保护作用。