Cadmium (Cd) is a hazardous heavy metal that adversely affects the vital body organs particularly liver. Eriocitrin (ERCN) is a plant-based flavonoid that is well-known for its wide range of pharmacological potential. This research trial was aimed to determine the ameliorative potential of ERCN against Cd provoked hepatotoxicity in rats. Twenty-four rats () were apportioned into control, Cd treated (5 mg/kg), Cd (5 mg/kg) + ERCN (25 mg/kg) and only ERCN (25 mg/kg) administrated group. Expressions of Nrf2/Keap1 pathway and apoptotic markers were assessed through qRT-PCR. The levels of inflammatory and liver function markers were evaluated by using standard ELISA kits. Cd exposure reduced the expression of Nrf2 and anti-oxidant genes as well as the activity of catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione (GSH) contents while escalating the expression of Keap1. Furthermore, Cd intoxication augmented malondialdehyde (MDA) and reactive oxygen species (ROS) levels in hepatic tissues. Exposure to Cd resulted in a notable elevation in the levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Cd administration upregulated nuclear factor-kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels as well as cyclooxygenase-2 (COX-2) activity. Furthermore, Cd administration upsurged Bax and Caspase-3 expression while reducing the expression of Bcl-2. Moreover, Cd intoxication disrupted the normal architecture of hepatic tissues. However, supplementation of ERCN significantly (p < 0.05) ameliorated the aforementioned disruptions induced by Cd intoxication. ERCN treatment remarkably ameliorated the hepatic tissues owing to its antioxidant, anti-inflammatory, and anti-apoptotic potentials. These findings underscore the therapeutic potential of ERCN to counteract the adverse effects of environmental pollutants on hepatic tissues.

中文翻译：

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圣草次苷通过调节 Nrf2/keap1 通路改善镉引起的大鼠肝毒性

镉 (Cd) 是一种有害的重金属，会对重要的身体器官特别是肝脏产生不利影响。圣草次苷 (ERCN) 是一种植物黄酮类化合物，以其广泛的药理潜力而闻名。这项研究试验的目的是确定 ERCN 对镉引起的大鼠肝毒性的改善潜力。将24只大鼠分为对照组、Cd处理组（5mg/kg）、Cd（5mg/kg）+ERCN（25mg/kg）组和仅给予ERCN（25mg/kg）组。通过 qRT-PCR 评估 Nrf2/Keap1 通路和凋亡标记物的表达。使用标准 ELISA 试剂盒评估炎症和肝功能标志物的水平。镉暴露降低了 Nrf2 和抗氧化基因的表达以及过氧化氢酶 (CAT)、谷胱甘肽还原酶 (GSR)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GPx)、谷胱甘肽 S-转移酶 (GST) 和谷胱甘肽的活性(GSH) 内容，同时升级 Keap1 的表达。此外，镉中毒会增加肝组织中的丙二醛（MDA）和活性氧（ROS）水平。暴露于镉会导致丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）和天冬氨酸转氨酶（AST）水平显着升高。镉给药上调核因子-κ B (NF-κB)、白介素-1 β (IL-1β)、肿瘤坏死因子-α (TNF-α) 和白细胞介素-6 (IL-6) 水平以及环氧合酶 - 2 (COX-2) 活性。此外，Cd 施用增加了 Bax 和 Caspase-3 的表达，同时降低了 Bcl-2 的表达。此外，镉中毒破坏了肝组织的正常结构。然而，补充 ERCN 显着（p < 0.05）改善了上述由镉中毒引起的干扰。 ERCN 治疗因其抗氧化、抗炎和抗凋亡潜力而显着改善了肝组织。这些发现强调了 ERCN 对抗环境污染物对肝组织不利影响的治疗潜力。