Omidifar Navid, Nili-Ahmadabadi Amir, Gholami Ahmad, Dastan Dara, Ahmadimoghaddam Davoud, Nili-Ahmadabadi Hossein
Biotechnology Research Center, Department of Pathology, School of Medicine, and Clinical Education Research Center, Zeinabieh Hospital, Shiraz University of Medical Sciences, Shiraz, Iran.
Medicinal Plants and Natural Products Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Evid Based Complement Alternat Med. 2020 Jun 17;2020:7457504. doi: 10.1155/2020/7457504. eCollection 2020.
Thirty-six male Wistar rats were divided into six groups: groups 1, 2, and 3 received vehicle, Cd (100 mg/L/day by drinking water), and extract (200 mg/kg/day; orally), respectively. Groups 4, 5, and 6 were Cd groups which were treated with extract (50, 100, and 200 mg/kg/day, respectively). After 2 weeks, liver enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) and also oxidative stress biomarkers including lipid peroxidation (LPO), total antioxidant capacity (TAC), total thiol molecule (TTM), and the histopathological changes were determined using standard procedure.
The findings showed that Cd caused a remarkable rise in levels of serum hepatic enzymes such as ALT ( < 0.001), AST ( < 0.01) and ALP ( < 0.001) compared with the control group. In addition, Cd led to the decreasing of the levels of TTM ( < 0.001) and TAC ( < 0.001) and increasing of LPO ( < 0.001) in liver tissue in comparison with the control group. In this regard, remarkable vascular congestion, hepatocellular degeneration, and vacuolization were observed in hepatic tissue of Cd-treated rats. Following the administration of extract, a significant improvement was observed in the functional and oxidative stress indices of hepatic tissue alongside histopathologic changes.
The current study indicated that the extract might prevent hepatic oxidative injury by improving oxidant/antioxidant balance in rats exposed to Cd.
36只雄性Wistar大鼠被分为六组：第1、2和3组分别接受赋形剂、镉（通过饮水，100毫克/升/天）和提取物（200毫克/千克/天；口服）。第4、5和6组是镉处理组，分别用提取物（50、100和200毫克/千克/天）进行处理。2周后，使用标准程序测定肝酶如丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）和碱性磷酸酶（ALP），以及氧化应激生物标志物，包括脂质过氧化（LPO）、总抗氧化能力（TAC）、总硫醇分子（TTM），并观察组织病理学变化。
研究结果表明，与对照组相比，镉导致血清肝酶如ALT（P<0.001）、AST（P<0.01）和ALP（P<0.001）水平显著升高。此外，与对照组相比，镉导致肝组织中TTM水平降低（P<0.001）和TAC水平降低（P<0.001），以及LPO升高（P<0.001）。在这方面，在镉处理大鼠的肝组织中观察到明显的血管充血、肝细胞变性和空泡化。给予提取物后，肝组织的功能和氧化应激指标以及组织病理学变化均有显著改善。
当前研究表明，提取物可能通过改善镉暴露大鼠的氧化/抗氧化平衡来预防肝脏氧化损伤。
