Department of Food Science and Nutrition, Pusan National University, Busan 609-735, Republic of Korea.
Department of Pharmacy, Northern Jiangsu People's Hospital Affiliated to Yangzhou University (Clinical Medical College of Yangzhou University), Yangzhou, Jiangsu 225001, P.R. China.
Mol Med Rep. 2014 Mar;9(3):1061-7. doi: 10.3892/mmr.2014.1884. Epub 2014 Jan 7.
The present study investigated the protective effect of methanolic extract from Fuzhuan brick‑tea (FME) on hydrogen peroxide (H2O2)‑induced oxidative stress in the human intestinal epithelial adenocarcinoma cell line Caco‑2. Caco‑2 cells were pretreated with different concentrations (50, 100 and 200 µg/ml) of FME for 2 h and then exposed to H2O2 (1 mM) for 6 h. FME did not exhibit a significant cytotoxic effect and increased the cell viability following H2O2 treatment by decreasing lipid peroxidation in Caco‑2 cells. To investigate the protective effect of FME on H2O2‑induced oxidative stress in Caco‑2 cells, the levels of intracellular glutathione (GSH) and the activity of the endogenous antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH‑px) and glutathione S‑transferase (GST), were determined. FME significantly increased the level of GSH and the activity of antioxidant enzymes. The results from the present study demonstrated that FME has a protective effect on H2O2‑induced oxidative damage in Caco‑2 cells through the inhibition of lipid peroxidation and the increase in the activity of antioxidant enzymes. In addition, FME reduced the H2O2‑induced expression of interleukin‑8 at both the mRNA and protein levels in Caco‑2 cells.
本研究探讨了茯砖茶甲醇提取物(FME)对人肠上皮腺癌细胞系 Caco-2 中过氧化氢(H2O2)诱导的氧化应激的保护作用。Caco-2 细胞用不同浓度(50、100 和 200 µg/ml)的 FME 预处理 2 h,然后用 H2O2(1 mM)处理 6 h。FME 没有表现出明显的细胞毒性作用,并且通过降低 Caco-2 细胞中的脂质过氧化作用,增加了 H2O2 处理后的细胞活力。为了研究 FME 对 Caco-2 细胞中 H2O2 诱导的氧化应激的保护作用,测定了细胞内谷胱甘肽(GSH)的水平和内源性抗氧化酶过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-px)和谷胱甘肽 S-转移酶(GST)的活性。FME 显著增加了 GSH 的水平和抗氧化酶的活性。本研究的结果表明,FME 通过抑制脂质过氧化作用和增加抗氧化酶的活性,对 H2O2 诱导的 Caco-2 细胞氧化损伤具有保护作用。此外,FME 降低了 H2O2 诱导的 Caco-2 细胞中白细胞介素-8 的表达,无论是在 mRNA 水平还是在蛋白水平。