Procyanidin C1 is a polyphenolic compound, it is found in a variety of vegetables and fruits and has a wide range of biological activities, including antioxidant and anti-inflammatory anticancer roles[1,2]
Procyanidin C is a catechin trimer purified from Cinnamomi Cortex and it showed inhibitory activity against TGF-β-induced EMT[3]. Treatment with procyanidin C1 in BMDMs resulted in a significant decrease in prostaglandin E2 and cyclooxygenase-2 levels, as well as the expression of cell surface molecules (CD80, CD86, and MHC class II), which was induced by LPS[1]. procyanidin C1 induced cell cycle arrest at S-phase and activated check point kinases, Chk1 and 2 in both MCF-7 and MDA-MB- 231 cells. At 48 h treatment procyanidin C1 induced DNA damage. In addition, procyanidin C1 decreased the Bcl2 levels and increased the BAX levels in both MCF-7 and MDA-MB- 231cells, which indicate that the procyanidin C1 inhibits breast cancer cell growth by inhibiting proliferation and by inducing apoptosis[2]
Procyanidin C1, a polyphenolic component of grape seed extract, increases the healthspan and lifespan of mice through its action on senescent cells[4]. In vivo, zebrafish larvae (AB strain) 3 days post-fertilization were incubated with NAC or procyanidins (C, EC, ECG, B1, B2, B3, B4, B1-G, B2-G, C1) in 300 μM H2 O2 for 4 days. Different grape seed procyanidins increased the survival of PC12 cells challenged with H2 O2 , improved the movement behavior disorder of zebrafish caused by H2 O2 , inhibited the increase of ROS and MDA and the decrease of GSH-Px, CAT, and SOD activities, and up-regulated the Nrf2/ARE pathway. The neuroprotective effects of the procyanidin trimer C1 treatment group were greater than the other treatment groups[5]
References:
[1].Byun EB, Sung NY, et al. The procyanidin trimer C1 inhibits LPS-induced MAPK and NF-κB signaling through TLR4 in macrophages. Int Immunopharmacol. 2013;15(2):450-456.
[2].Koteswari LL, Kumari S, et al. A comparative anticancer study on procyanidin C1 against receptor positive and receptor negative breast cancer. Nat Prod Res. 2020;34(22):3267-3274.
[3].Kin R, Kato S, et al. Procyanidin C1 from Cinnamomi Cortex inhibits TGF-β-induced epithelial-to-mesenchymal transition in the A549 lung cancer cell line. Int J Oncol. 2013;43(6):1901-1906.
[4].Xu Q, Fu Q, Li Z, et al. The flavonoid procyanidin C1 has senotherapeutic activity and increases lifespan in mice. Nat Metab. 2021;3(12):1706-1726.
[5].Nakano N, Nishiyama C, Tokura T, et al. Procyanidin C1 from apple extracts inhibits Fc epsilon RI-mediated mast cell activation. Int Arch Allergy Immunol. 2008;147(3):213-221.
原花青素C1是一种多酚类化合物,存在于多种蔬菜和水果中,具有广泛的生物活性,包括抗氧化和抗炎抗癌作用[1,2] /p>\n
原花青素 C 是一种从肉桂皮层纯化的儿茶素三聚体,它对 TGF-β 诱导的 EMT 显示出抑制活性[3]。在 BMDM 中用原花青素 C1 处理导致前列腺素 E2 和环氧合酶 2 水平显着降低,以及由 LPS 诱导的细胞表面分子（CD80、CD86 和 MHC II 类）的表达 [1]。原花青素 C1 在 MCF-7 和 MDA-MB-231 细胞中诱导 S 期细胞周期停滞并激活检查点激酶 Chk1 和 2。在 48 小时处理原花青素 C1 诱导 DNA 损伤。此外,原花青素 C1 降低了 Bcl2 水平,增加了 MCF-7 和 MDA-MB-231 细胞中的 BAX 水平,这表明原花青素 C1 通过抑制增殖和诱导细胞凋亡来抑制乳腺癌细胞生长[2]
原花青素 C1 是葡萄籽提取物的一种多酚成分,可通过其对衰老细胞的作用延长小鼠的健康寿命和寿命[4]。在体内,将受精后 3 天的斑马鱼幼虫（AB 株）与 NAC 或原花青素（C、EC、ECG、B1、B2、B3、B4、B1-G、B2-G、C1）在 300 μM H< sub>2 O2 4 天。不同葡萄籽原花青素提高H2 O2 PC12细胞存活率,改善H2 O引起的斑马鱼运动行为障碍2 ,抑制ROS和MDA的增加以及GSH-Px、CAT和SOD活性的降低,并上调Nrf2/ARE通路。原花青素三聚体C1治疗组的神经保护作用优于其他治疗组[5]
原花青素 C 是一种从肉桂皮层纯化的儿茶素三聚体,它对 TGF-β 诱导的 EMT 显示出抑制活性[3]。在 BMDM 中用原花青素 C1 处理导致前列腺素 E2 和环氧合酶 2 水平显着降低,以及由 LPS 诱导的细胞表面分子（CD80、CD86 和 MHC II 类）的表达 [1]。原花青素 C1 在 MCF-7 和 MDA-MB-231 细胞中诱导 S 期细胞周期停滞并激活检查点激酶 Chk1 和 2。在 48 小时处理原花青素 C1 诱导 DNA 损伤。此外,原花青素 C1 降低了 Bcl2 水平,增加了 MCF-7 和 MDA-MB-231 细胞中的 BAX 水平,这表明原花青素 C1 通过抑制增殖和诱导细胞凋亡来抑制乳腺癌细胞生长[2]
原花青素 C1 是葡萄籽提取物的一种多酚成分,可通过其对衰老细胞的作用延长小鼠的健康寿命和寿命[4]。在体内,将受精后 3 天的斑马鱼幼虫（AB 株）与 NAC 或原花青素（C、EC、ECG、B1、B2、B3、B4、B1-G、B2-G、C1）在 300 μM H< sub>2 O2 4 天。不同葡萄籽原花青素提高H2 O2 PC12细胞存活率,改善H2 O引起的斑马鱼运动行为障碍2 ,抑制ROS和MDA的增加以及GSH-Px、CAT和SOD活性的降低,并上调Nrf2/ARE通路。原花青素三聚体C1治疗组的神经保护作用优于其他治疗组[5]