Spondyloarthropathy Department, Nanyang Nanshi Hospital of He'nan Province, Nanyang, People's Republic of China.
Department of Image, The Affiliated Huai'an Hospital of Xuzhou Medical University and The Second People's Hospital of Huai'an, Huai'an, People's Republic of China.
Environ Toxicol. 2021 Dec;36(12):2541-2550. doi: 10.1002/tox.23368. Epub 2021 Sep 9.
Bergenin is a C-glucoside of 4-O-methyl gallic acid with a variety of biological activities, such as antioxidant and anti-inflammatory. Herein, we investigated the involvement of bergenin in the protective effect against H O -induced oxidative stress and apoptosis in human nucleus pulposus cells (HNPCs) and the underlying mechanisms. HNPCs were cotreated with various concentrations of bergenin and 200 μM H O for 24 h. Cell viability was detected by Cell Counting Kit-8 and lactate dehydrogenase release assays. Reactive oxygen species (ROS) was evaluated utilizing 2',7'-dichlorofluorescein-diacetate. Superoxide dismutase (SOD) and catalase (CAT) activities and glutathione (GSH) levels were measured to assess oxidative stress. Apoptosis was evaluated using terminal deoxynucleotidyl transferase dUTP nick end labeling and caspase-3/7 activity assays. Expression of protein was determined by western blotting. Results indicated that treatment with bergenin significantly alleviated H O -induced viability reduction and ROS overproduction in HNPCs in a dose-dependent manner. Bergenin alleviated H O -induced oxidative stress in HNPCs by increased activity of superoxide dismutase and level of glutathione peroxidase. H O -induced apoptosis and activity of caspase-3/7 were also suppressed by bergenin treatment in HNPCs. Western blotting showed that H O -induced decrease in expression of peroxisome proliferator-activated receptor γ (PPAR-γ) and increase in nuclear factor κB (NF-κB) were inhibited by bergenin. However, the inhibitory effect of bergenin on H O -induced viability reduction, oxidative stress and apoptosis were noticeably abrogated in PPAR-γ knockdown HNPCs. In conclusion, our results indicated that bergenin alleviates H O -induced oxidative stress and apoptosis in HNPCs by activating PPAR-γ and suppressing NF-κB pathway.
Bergenin 是 4-O-甲基没食子酸的 C-葡萄糖苷，具有多种生物活性，如抗氧化和抗炎作用。在此，我们研究了 Bergenin 对人髓核细胞 (HNPCs) 中 H2O2 诱导的氧化应激和细胞凋亡的保护作用及其机制。将不同浓度的 Bergenin 与 200 μM H2O2 共同孵育 24 h。用 Cell Counting Kit-8 和乳酸脱氢酶释放试验检测细胞活力。利用 2',7'-二氯荧光素二乙酸酯评估活性氧 (ROS)。测定超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT) 活性及谷胱甘肽 (GSH) 水平以评估氧化应激。用末端脱氧核苷酸转移酶 dUTP 缺口末端标记和 caspase-3/7 活性测定评估细胞凋亡。用 Western blot 测定蛋白表达。结果表明，Bergenin 以剂量依赖性方式显著减轻 H2O2 诱导的 HNPCs 活力降低和 ROS 过度产生。Bergenin 通过增加超氧化物歧化酶活性和谷胱甘肽过氧化物酶水平缓解 H2O2 诱导的 HNPCs 氧化应激。Bergenin 还抑制 H2O2 诱导的 HNPCs 凋亡和 caspase-3/7 活性。Western blot 显示，Bergenin 抑制 H2O2 诱导的过氧化物酶体增殖物激活受体 γ (PPAR-γ) 表达降低和核因子 κB (NF-κB) 表达升高。然而，在 PPAR-γ 敲低的 HNPCs 中，Bergenin 对 H2O2 诱导的活力降低、氧化应激和凋亡的抑制作用明显减弱。总之，我们的结果表明，Bergenin 通过激活 PPAR-γ 和抑制 NF-κB 通路缓解 H2O2 诱导的 HNPCs 氧化应激和细胞凋亡。
