Hormone Evaluation Department, National Organization for Drug Control and Research, Giza 12611, Egypt.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, Minia 61519, Egypt.
Biomed Pharmacother. 2021 Feb;134:111102. doi: 10.1016/j.biopha.2020.111102. Epub 2020 Dec 15.
Ginger has been proposed as quite a promising candidate for cancer prevention. The purpose of this study was to assess the chemo-preventive effects of ginger. Furthermore, this study investigated the possible mechanisms of a standardized extract drawn from the rhizomes of ginger against diethylnitrosamine (DEN)-induced liver cancer in Wistar rats. The chemo-preventive effects of ginger at doses of 75 mg/kg, 150 mg/kg and 300 mg/kg per day were determined using a liver cancer model which was induced by DEN (Ali et al., 2008) and 2-acetylaminofluorene (2-AAF) in rats. Ginger attenuated carcinogenic changes after 22 weeks of cancer induction by decreasing the quantity and occurrences of hepatic dyschromatic nodules and positive focal areas as well as decreasing the amount of placental glutathione S-transferase (GST) in the livers of DEN/2-AAF-treated rats. Moreover, in rats, ginger counteracts DEN-influenced oxidative stress and decreases myeloperoxidase, malondialdehyde and protein carbonyl concentrations in the liver. This was determined by observing the restoration of superoxide dismutase, catalase, GST and glutathione. Immunohistochemical bleaching in rat livers showed that ginger prevented the increase in cell-positive numbers for Ki-67, cyclooxygenase-2 and nuclear factor kappa B p65. Ginger also inhibited the number of positive cells in DEN/2-AAF-treated rats for TUNEL, M30 and caspase-3 liver tissues. This research shows that ginger has an important chemo-preventative impact on liver cancer by inhibiting the growth of cells and inducing apoptosis. By reducing oxidative and inflammatory damage, ginger protects rat liver against cancer.
生姜被认为是预防癌症的有前途的候选物。本研究旨在评估生姜的化学预防作用。此外,本研究还研究了从生姜根茎中提取的标准化提取物对 Wistar 大鼠二乙基亚硝胺(DEN)诱导肝癌的可能机制。使用 DEN(Ali 等人,2008 年)和 2-乙酰氨基芴(2-AAF)诱导的肝癌模型确定了生姜在 75mg/kg、150mg/kg 和 300mg/kg/天剂量下的化学预防作用。生姜通过减少肝色素性结节和阳性灶的数量和发生以及降低 DEN/2-AAF 处理大鼠肝脏中的胎盘谷胱甘肽 S-转移酶(GST)的量来减轻癌症诱导后 22 周的致癌变化。此外,生姜在大鼠中对抗 DEN 诱导的氧化应激并降低肝中的髓过氧化物酶、丙二醛和蛋白质羰基浓度。通过观察超氧化物歧化酶、过氧化氢酶、GST 和谷胱甘肽的恢复来确定这一点。大鼠肝脏中的免疫组化褪色表明,生姜可防止 Ki-67、环氧化酶-2 和核因子 kappa B p65 阳性细胞数量增加。生姜还抑制了 DEN/2-AAF 处理大鼠中 TUNEL、M30 和 caspase-3 肝组织中阳性细胞的数量。这项研究表明,生姜通过抑制细胞生长和诱导细胞凋亡对肝癌具有重要的化学预防作用。通过减少氧化和炎症损伤,生姜保护大鼠肝脏免受癌症侵害。